Kaiser Daily Health Policy Report
Tuesday, August 28, 2007
Prescription Drugs
Physicians Often Ignore, Dismiss Patient Complaints About Possible Side Effects of Statins, Survey Finds
Physicians often ignore or dismiss patient complaints about possible side effects of statins, according to a study published last week in the journal Drug Safety, the Washington Post reports. For the study, researchers led by Beatrice Golomb, an associate professor of medicine at the University of California-San Diego, surveyed 650 patients, most of whom were in their early 60s and lived in the U.S.
Most participants said they complained to their physicians about muscle pain, memory loss, numbness in their hands and feet, or other possible side effects of statins, the study found. However, participants said in most cases their physicians attributed the symptoms to aging, denied their link with statins or dismissed them, according to the study. Golomb said, "Person after person spontaneously (told) us that their doctors told them that symptoms like muscle pain couldn't have come from the drug. We were surprised at how prevalent that experience was."
She attributed the results of the study in part to a lack of awareness about the side effects of statins. "Ad campaigns that preserve statins' miracle drug image are more powerful than education about side effects," Golomb said.
Implications
The study raises concerns about prescription drug safety because, when physicians fail to link symptoms with medications, they do not file adverse event reports with FDA. As a result, FDA might "underestimate the problem, and other doctors and patients may assume the drug is safer than it is," the Post reports.
Jerry Avorn -- a Harvard Medical School professor and author of the book "Powerful Medicines: The Benefits, Risks and Costs of Prescription Drugs" -- said that "there is horrendous underreporting of side effects," adding that 90% to 99% of "serious side effects are not reported by doctors."
The study "points out that doctor reports on side effects [are] a very unreliable means of learning about the true extent of problems," he said, adding, "We ought to have a (better) mechanism for gathering information from patients. A lot of it will be noise, but there may be important signals there as well" (Ganguli, Washington Post, 8/28).
Wednesday, August 29, 2007
Tuesday, August 28, 2007
Kidney Stones?
The Role of Diet in the Prevention
Of Common Kidney Stones
Christy Krieg
Kidney stone formers may
feel doomed to a life of
unpredictable flank pain,periodic surgical intervention,
and concomitant loss of
work and daily pleasures. Indeed,
if untreated, those who have
formed one calcium oxalate stone
have a 50% chance of forming
additional stones within 10 years
(Menon & Resnick, 2002). With
appropriate education, patients
can exercise some control over
stone disease and reduce their
chances of forming stones
through dietary modifications
and medication.
General dietary recommendations
appropriate for patients
who form the most common
metabolic stone types — calcium
oxalate and uric acid — will be discussed
in this article. Patients with
a tendency to form cystine and
brushite stones may also benefit
from some of the same dietary recommendations,
but dietary management
is a small part of an even
more complex treatment regimen
in these instances. Regardless of
stone type, recommendations for
dietary modifications are most
accurate when tailored to the
results of urine stone risk profiles,
or “24-hour urine” studies.
These studies typically provide
total urine volume, urine
calcium, sodium, citrate and uric
Current dietary recommendations for patients who form kidney
stones are discussed. Focusing on the most common kidney stone
types, calcium oxalate and uric acid, the rationale for dietary changes
are described based on the renal and urine physiology.
Christy Krieg, BSN, RN, is a Clinical
Nurse, Methodist Urology, Indianapolis,
IN.
Note: CE Objectives and Evaluation
Form appear on page 457.
acid, as well as pH, and supersaturation
of critical compounds,
among other measurements. The
values, if properly interpreted,
allow the clinician to observe the
patient’s specific abnormalities,
recommend medication and/or
dietary modification, and track
progress through followup studies.
As with many bodily
processes, stone formation is a
complicated and multi-factorial
process. Yet, there is much still to
be understood about stone formation.
For example, we know that
stone formation runs in families,
but while all humans form calcium
oxalate crystals, most do not
form stones (Lemann, 2002). And
while for years calcium stone formers
were instructed to restrict
dietary calcium, there is now significant
evidence against this recommendation
(Borghi et al.,
2002). These observations illustrate
the sometimes counterintuitive
and always complex nature
of stone formation and the need
for ongoing investigation.
Stone recurrence is frustrating
for patients who have made
changes in their lives and yet still
form stones. While diet alone
cannot always control the disease,
dietary measures can
absolutely help supplement
other therapies, and for some
patients are the primary tool for
stone prevention. As a component
of the medical management
for stone disease, the goal of therapy
should be to improve those
factors thought to contribute to
stone formation in the urinary
tract, and thereby reduce the
chance of forming stones, even if
the disease is not eliminated.
Urine Supersaturation
And Stone Formation
Urine volume plays a pivotal
role in the process of stone formation.
In particular, low volume,
highly concentrated urine
contributes to the supersaturation
of elements normally found
in the urine, such as calcium
oxalate. Simply put, when the
solute exceeds the solvent’s ability
to dissolve it, precipitation of
crystals can occur. Consider an
attempt to dissolve sugar in
water: a tablespoon of sugar is
readily dissolved in a glass of
water, but eight tablespoons of
sugar in that same glass will not
completely dissolve, resulting in
the accumulation of crystals in
the bottom of the glass. In this
scenario, the water is saturated
with sugar; the solvent, water,
can dissolve no more solute. It
has exceeded the point of saturation,
and is supersaturated.
Fortunately, urine has the
unique quality of holding more
solute in suspension than does
water and so can accept large
concentrations of solute without
precipitation. The ability of urine
to keep such large concentrations
in solution is, in part, due to the
presence of protective organic
molecules like citrate, as well as
the presence of charged ions
which alter the solubility (Menon
& Resnick, 2002). Despite the fact
that calcium oxalate can be present
in urine in concentrations 7
to 11 times its solubility in water
(Menon & Resnick, 2002), the
point exists at which calcium
oxalate exceeds the unique properties
of urine; crystals will then
form and possibly aggregate to
form stones.
Understanding saturation principles
in the urine, is it not clear
that methods of prevention shall be
focused on both an increase in solvent
and a reduction of solute?
These two concepts are the basis
for the dietary changes described
below.
Assessment of Dietary
Patterns
As dietary history is not part
of the typical urologic patient
history forms, the nurse can
obtain this information through
patient interview. Important information
includes the patient’s
intake of fluids throughout the
day, environmental factors promoting
dehydration, special diets
such as now-popular high-protein
diets, and a propensity to
consume packaged or restaurant
foods which are typically very
high in sodium. What does the
patient drink, how much is consumed,
and how is fluid intake
distributed through the day?
Does he or she work in a hot or
dry environment (such as a hot
factory, outside work in the summer)?
Does he or she prepare
fresh foods at home or tend to eat
convenience foods?
Nurses’ dietary interview can
occur before or after metabolic
testing. Absent metabolic testing,
this interview has even greater
import as it is the only source of
information about dietary habits.
Asking patients to keep a 24-hour
diet record may help identify
patterns of which even the
patient was unaware. Sources of
dietary sodium can be obvious or
insidious. The excess intake of a
patient who consumes a bag of
microwave popcorn every night
is more apparent than the intake
of a patient who drinks sports
drinks after a daily workout;
these are both very high in sodium,
but the latter is less often
recognized.
If the nurse has at his or her
disposal a 24-hour urine study,
dietary anomalies may be more
specifically exposed and documented.
This author views 24-
hour urine studies as “vice recognition
software;” the numbers
show actual urine output, and
indicate dietary sodium, protein,
and oxalate excess. Patients with
low urine volumes may believe
their results are incorrect. They
may say “I drink all the time!”
and yet the output is low. Here
the role of dietary counseling is
critical; the insightful nurse
helps the patient identify volume
consumed, sources of insensible
loss, and ways to ensure
increased urine volume.
DIETARY CHANGES TO
PREVENT AND REDUCE
STONE FORMATION
Increase Fluid Intake
Increasing urine volume can
reduce supersaturation, and is
widely known to help prevent
stone formation. Recommendations
for urinary output vary, but there is
general agreement that it should
exceed two liters per day, while
some even encourage urinary
outputs in excess of three liters
per day (Menon & Resnick, 2002;
Sakhaee, Zerwekh, & Pak, 1980).
A key point is that the dilution of
urine is necessary “24/7,” or all
day, every day. A patient who
voids the recommended two
liters a day between the hours of
8 am and 10 pm, but only 300
milliliters during the remaining
10 hours of the day will have saturated
urine overnight, with the
possibility of precipitation and
aggregation during the sleeping
hours. Patients must accept the
necessity of getting up at least
twice at night to urinate, and
should consume more water each
time they rise to void.
Stress to patients that it is not
the quantity of fluid consumed
that is important, but rather the
fluid voided that should be measured.
Patients living in hot or
dry conditions, or who exercise
and perspire significantly, will
need to drink even more liquid to
maintain adequate urine output.
Many patients ask what fluids
are recommended, and which
are prohibited. The simple
answer is that water is best. For
those with excessive urinary
oxalates, black tea should be
eliminated because black tea is a
high-oxalate beverage. Curhan,
Willett, Rimm, Speizer, and
Stampfer (1998) found, in a retrospective
study of previously nonstone
forming women from the
Nurses’ Health Study, that the
type of beverages consumed
proved relevant for stone formers.
Of the 17 beverages studied,
and after correcting for other contributing
factors, those who
drank one daily 8 ounce glass of
grapefruit juice had a 44%
increased risk of a stone event in
the 8-year period, while the risk
was decreased by 8% to 10% for
each daily 8 ounce serving of coffee
(both caffeinated and non-caffeinated),
tea, or wine. A prospective study had similar
conclusions for men, additionally
showing that beer had a protective
effect and apple juice increased
the risk of stone events (Curhan,
Willett, Rimm, Speigelman, &
Stampfer, 1996). Also, a study published
by Massey and Sutton (2004)
showed a modest positive relationship
between caffeine intake and
urinary calcium levels in stone formers
and non-stone formers, so caffeinated
beverages should be limited
in stone formers. In summary,
stone formers should drink more
water and avoid excess caffeine,
black tea, and grapefruit and apple
juices.
What do these studies mean
for patient education?
Water is the
best beverage for stone formers. It is
non-caloric, non-caffeinated, and
contains insignificant amounts of
solutes. In initial attempts to
increase patients’ fluid intake, it
may be appropriate to advise them
to drink whatever they can consume
in large quantities. However,
warning them of side effects of sugared
and caffeinated beverages in
large quantities is important. The
results discussed above indicate
that consumption of alcoholic
beverages is unlikely to increase
stone risk. Water that tastes good
(filtered, reverse osmosis, bottled)
may be easier to consume than tap
water, so encourage patients to
seek a source of good-tasting
water. There is no clear agreement
on the impact of drinking water’s
mineral content on lithogenesis;
“hard water” may not be problematic
for most patients (Menon &
Resnick, 2002). Again, water in
large quantities should be the
focus of prevention. Lemonade is
often recommended, as it supplies
dietary citrate, a stone inhibitor
and pH buffer when excreted later
in the urine.
Encourage patients to set
consumption goals, carry water
with them at all times, and strive
for pale urine throughout the day
and night. Some patients describe
an initial physiologic
resistance to increased fluid
intake which eases as their bodies
and minds learn the new
habit of extra fluid intake and
output. According to Parks,
Goldfischer, and Coe (2003),
aims by clinicians to increase
patients’ urinary volumes often
fall short, and follow-up metabolic
studies showed an average
increase in urine output of only
0.3 liters per 24 hours. This
increase was associated with a
curious increase in sodium
intake. High urine volumes
should be the goal of all patients
who form stones. In this
instance, more is definitely better.
Most patients find that after
forcing fluids for a couple of
months, their bodies crave fluids
and their habit is to drink more.
Consume Adequate Calcium
High urine calcium, hypercalciuria,
is associated both with
formation of kidney stones and
with osteoporosis. Sufficient calcium
intake is required for the
growth and maintenance of the
skeleton in children and adults.
Reducing urine calcium should
be a goal for stone formers, but
not via dietary restriction. While
reduced dietary calcium can
decrease urine calcium (Lemann,
2002), calcium restriction is no
longer advisable for patients who
form calcium kidney stones as
this puts them at risk of bone disease,
namely osteoporosis. Recall
that bones are in a constant
process of resorption and formation;
adequate calcium is required
for the ongoing rebuilding of bone
material.
Several recent studies have
shown, in fact, that adequate calcium
intake is associated with
decreased stone formation.
Curhan, Willett, Knight, and
Stampfer (2004) found that in
previously non-stone forming
younger women, higher intake of
dietary calcium was related to
lower risk of kidney stone formation.
Additionally, a 5-year randomized
clinical trial of men
with a history of calcium oxalate
stones found that a normal calcium,
decreased sodium, and
decreased animal protein diet
was more effective for reducing
stone events than was a restricted
calcium diet (Borghi et al., 2002).
So, adequate calcium plus
decreased sodium and protein
intake had a significantly more
protective effect against stones
than decreased calcium intake
alone.
Why might increased dietary
calcium reduce the risk of calcium
stone formation? Calcium
and oxalate bind in the gut and
in the urine to form a nonabsorbable
compound. Low dietary
calcium permits greater free
oxalate to be absorbed in the gut
and excreted in the urine, which
may be counterproductive for
calcium oxalate stone formers.
Restricted calcium intake results
in increased urinary oxalates, a
risk for stone formation (Menon
& Resnick, 2002). This is a proposed
cause of the association
between reduced calcium intake
and increased supersaturation of
calcium oxalate (Lemann, 2002).
Clearly, strong research evidence
now supports adequate
calcium intake for patients who
form kidney stones. Low-fat
dairy products, green leafy vegetables,
broccoli, fortified foods,
and almonds are excellent
sources. Patients should consume
enough dietary calcium to
meet (but not exceed) the United
States Recommended Daily
Allowance (RDA) of calcium,
which ranges from 1,000 to 1,200
milligrams daily for adults. The
recommendations are the same
for men and women, but vary by
age group (see Table 1). Patients
should avoid calcium supplements
in favor of calcium-rich
foods; a patient with intolerance
to dairy products may supplement,
but should not exceed the
RDA for his/her age group.
Limit Dietary Oxalates
Oxalate is found in many
foods, but there is considerable
variability in the amount, which
depends upon where the food is
grown. Likewise, individual
absorption of oxalate also varies,
which makes adequate calcium
intake critically important.
Nonetheless, oxalate restriction
should be attempted. The highest
levels of oxalate are found in
chocolate, nuts, beans (including
soybeans), rhubarb, spinach,
beets, and black tea. A thorough
oxalate list can be found on the
Web site of the Oxalosis and
Hyperoxaluria Foundation (http://
www.ohf.org/diet.html). This list
is exhaustive and may be overwhelming
to patients. Stress that
reduction of high oxalate foods is
the goal for typical stone formers
rather than strict avoidance of all
oxalate-containing foods (which
would be very difficult). Followup
24-hour urine studies will demonstrate
the adequacy of patients’
restriction.
Though only 10% to 20% of
urinary oxalates come from
dietary sources (Morton, Iliescu,
& Wilson, 2002), dietary reduction
is commonly advised for calcium
oxalate stone formers. It has
been suggested that because
there is much less oxalate in the
urine than calcium in the urine,
urinary oxalate concentration is
much more critical to the formation
of calcium oxalate crystals
than is the urinary calcium concentration;
reducing urine oxalates
may have a more powerful effect
on stone formation than can reduction
of urine calcium (Morton et
al., 2002). Patients with calcium
oxalate stones, particularly those
with documented hyperoxaluria,
should avoid foods high in
oxalates. Vitamin C is a precursor
to endogenous production of
oxalates, so some clinicians recommend
avoiding mega-doses of
vitamin C. The rare genetic condition
of primary hyperoxaluria is
only slightly impacted by dietary
reduction, and causes serious
medical problems besides kidney
stones.
Limit Sodium Intake
Because calcium and sodium
compete for reabsorption in the
renal tubules, excess sodium
intake and consequent excretion
result in loss of calcium in the
urine. High-sodium diets are
associated with greater calcium
excretion in the urine (Lemann,
2002). Metabolic studies often
reveal exceptionally high urine
calcium over 24 hours, related to
patients’ exceptionally high sodium
excretion. Patients may deny
salt intake, stating, “I never salt
my food!” They quite likely are
ignorant of hidden sodium
sources in the diet. Sodium is a
common preservative in canned
and frozen foods, and is endemic
in restaurant foods. Instruction
on careful inspection of food
labels and wise food choices
helps patients identify and
reduce sodium in their diets.
A notable dietary “ah-ha!”
was the admission by one patient
that, on the day of 24-hour urine
testing, she ate a full jar of pickles
to reduce stress, and then
drank the brine; needless to say,
her urine sodium was very high
on the day of her stress mitigation.
The role of the nurse or dietician
in shedding light on sources
of sodium cannot be underestimated.
Repeated, persistent inquiry
into dietary habits may be necessary.
The goal of therapy should be
a “no added salt diet,” or the equivalent
of 2,000 mg per day or less of
dietary sodium. Reduction of
dietary sodium is difficult and disappointing
to patients. They may
believe they have made significant
reductions and sacrifices, while
their urine sodium remains high.
Consultation with a registered
dietician may help the patient
achieve the specific goal of a sodium
intake of 2,000 milligrams or
less per day.
Limit Animal Protein
The effect of excess animal
protein (purine) is most obvious
for the uric acid stone former.
Uric acid, a byproduct of purine
metabolism, is excreted in large
quantities in the urine. Excess
protein creates urine with high
total urine uric acid, potentially
high supersaturation of urine
uric acid, and a low pH, necessary
for formation of uric acid
stones. There is no inhibitor of
uric acid crystal formation
(Menon & Resnick, 2002), so
dietary measures focus on reducing
uric acid and increasing
urine volume. Reduction of animal
protein to 12 ounces per day
for adults is recommended. This
is plenty to meet the dietary
needs of most Americans, many
of whom typically consume several
more ounces of animal protein
daily than is recommended.
Protein from plant sources
(beans, legumes, etc.) can be substituted
as a dietary alternative
without negative consequences.
Calcium oxalate stone formers
reducing their animal protein
should note the oxalate content
of substitute proteins.
The role of excess protein in
promoting calcium stone formation
is less obvious, but equally
important. High dietary protein
is associated with increased urinary
calcium. Thus, there is a
link between meat consumption
and both uric acid and calcium
stone formation. In fact, vegetarians
form stones at one-third the
rate of those eating a mixed diet
(Lemann, 2002). A study of 18
hypercalciuric stone formers found
that a 15-day protein restriction
had many positive effects on urinary
markers of stone risk.
Namely, significant decreases
were seen in urine calcium, urine
uric acid, urine phosphate, and
urine oxalate. And, for unclear
reasons, a beneficial increase in
urinary citrate was observed
(Giannini et al., 1999). Citrate is a
known inhibitor of calcium
oxalate crystal formation and
also increases pH, which can prevent
uric acid stones. Clearly, the
benefits of protein restriction for
stone formers are many.
Weight Loss
A relationship between weight,
body mass index and risk of calcium
oxalate stone formation was
established in a retrospective
study of health professionals.
Curhan and colleagues (1998)
found that “the prevalence of
stone disease history and the
incidence of stone disease were
directly associated with weight
and body mass index. However,
the magnitude of the associations
was consistently greater among
women” (p. 1645). The value of
weight loss for stone prevention
has not been proven, but given
the benefits of weight loss for
general health, it is certainly
worth mentioning to overweight
patients who form stones.
Educational Resources
There are excellent resources
on the Internet for patients seeking
nutritional information. One stellar
example is NutritionData
(www.nutritiondata.com/). Here
patients can search by general food
category, like “pickle,” to view the
standard sodium content, as well
as a plethora of additional information
regarding vitamin and mineral
content, calories, suggested healthier
substitutes, and even the individual
amino acid compositions of
each protein. The site also provides
detailed information about
thousands of specific brand items
from grocery and fast food restaurants.
Under “Tools,” patients can
search within food categories like
“dairy products” for choices highest
in calcium and lowest in sodium.
This site is complex and may be
overwhelming to patients without
good computer and Web skills, but
is extraordinarily comprehensive;
unfortunately, this site does not list
oxalate content. For that purpose,
refer patients to www.ohf.org.
For patients without Web
access, nurses might find it helpful
to review a general nutrition
book for charts and diagrams to
help patients understand nutrition
content. Show patients a
sample food label from a can of
soup so they know where to find
sodium content on foods at home.
For a simple list of high-oxalate
foods, visit www.gicare.com/
pated/edtgs29.htm.
Conclusion
The dietary measures discussed
have value particularly
for patients who form the most
common types of kidney stones:
calcium oxalate and uric acid.
That said, they may be insufficient
to control the various metabolic
abnormalities present in
individual patients. The most
effective management of kidney
stones includes in-depth metabolic
studies, recommendations
tailored to patients regarding
medications and dietary changes,
and follow-up to ensure changes
are having the desired effect.
Urine studies should be repeated
to judge progress approximately
6 to 8 weeks after initial metabolic
testing recommendations are
implemented. Once a stable state
is reached in which the patient’s
urine demonstrates decreased
risk of stone formation, metabolic
testing should be performed
(along with an x-ray to check for
stone growth) at least annually to
monitor stone risk. The cycle of
stone formation can be altered,
and in some cases broken, with
the aid of effective dietary management.
Every patient need not make
all of these changes to his/her
diet, but in the absence of
patient-specific urine studies,
none of these recommendations
is harmful. Aside from oxalate
consumption, the dietary recommendations
for calcium oxalate
and uric acid stone formers are
the same. Assessing
patients’ dietary habits can shed
light on potential areas of
improvement. For example, a
receptive uric acid stone former
on a high-protein diet for weight
loss could benefit from counseling
on the effects of this diet on
his/her stone disease.
Of course, talking about
dietary changes is easier than actual
implementation. Encourage
patients to make changes at a realistic
pace. Praise even modest
progress and stress the value of
striving for improvement rather
than perfection.
The Bottom Line here is;
•Urinate more than two liters per day.
• Consume enough dietary calcium to meet the US RDA.
• Avoid dietary oxalates (for calcium oxalate stone-formers).
• Limit sodium to 2,000 milligrams per day.
• Limit protein to 12 ounces per day.
• If overweight, lose weight.
Of Common Kidney Stones
Christy Krieg
Kidney stone formers may
feel doomed to a life of
unpredictable flank pain,periodic surgical intervention,
and concomitant loss of
work and daily pleasures. Indeed,
if untreated, those who have
formed one calcium oxalate stone
have a 50% chance of forming
additional stones within 10 years
(Menon & Resnick, 2002). With
appropriate education, patients
can exercise some control over
stone disease and reduce their
chances of forming stones
through dietary modifications
and medication.
General dietary recommendations
appropriate for patients
who form the most common
metabolic stone types — calcium
oxalate and uric acid — will be discussed
in this article. Patients with
a tendency to form cystine and
brushite stones may also benefit
from some of the same dietary recommendations,
but dietary management
is a small part of an even
more complex treatment regimen
in these instances. Regardless of
stone type, recommendations for
dietary modifications are most
accurate when tailored to the
results of urine stone risk profiles,
or “24-hour urine” studies.
These studies typically provide
total urine volume, urine
calcium, sodium, citrate and uric
Current dietary recommendations for patients who form kidney
stones are discussed. Focusing on the most common kidney stone
types, calcium oxalate and uric acid, the rationale for dietary changes
are described based on the renal and urine physiology.
Christy Krieg, BSN, RN, is a Clinical
Nurse, Methodist Urology, Indianapolis,
IN.
Note: CE Objectives and Evaluation
Form appear on page 457.
acid, as well as pH, and supersaturation
of critical compounds,
among other measurements. The
values, if properly interpreted,
allow the clinician to observe the
patient’s specific abnormalities,
recommend medication and/or
dietary modification, and track
progress through followup studies.
As with many bodily
processes, stone formation is a
complicated and multi-factorial
process. Yet, there is much still to
be understood about stone formation.
For example, we know that
stone formation runs in families,
but while all humans form calcium
oxalate crystals, most do not
form stones (Lemann, 2002). And
while for years calcium stone formers
were instructed to restrict
dietary calcium, there is now significant
evidence against this recommendation
(Borghi et al.,
2002). These observations illustrate
the sometimes counterintuitive
and always complex nature
of stone formation and the need
for ongoing investigation.
Stone recurrence is frustrating
for patients who have made
changes in their lives and yet still
form stones. While diet alone
cannot always control the disease,
dietary measures can
absolutely help supplement
other therapies, and for some
patients are the primary tool for
stone prevention. As a component
of the medical management
for stone disease, the goal of therapy
should be to improve those
factors thought to contribute to
stone formation in the urinary
tract, and thereby reduce the
chance of forming stones, even if
the disease is not eliminated.
Urine Supersaturation
And Stone Formation
Urine volume plays a pivotal
role in the process of stone formation.
In particular, low volume,
highly concentrated urine
contributes to the supersaturation
of elements normally found
in the urine, such as calcium
oxalate. Simply put, when the
solute exceeds the solvent’s ability
to dissolve it, precipitation of
crystals can occur. Consider an
attempt to dissolve sugar in
water: a tablespoon of sugar is
readily dissolved in a glass of
water, but eight tablespoons of
sugar in that same glass will not
completely dissolve, resulting in
the accumulation of crystals in
the bottom of the glass. In this
scenario, the water is saturated
with sugar; the solvent, water,
can dissolve no more solute. It
has exceeded the point of saturation,
and is supersaturated.
Fortunately, urine has the
unique quality of holding more
solute in suspension than does
water and so can accept large
concentrations of solute without
precipitation. The ability of urine
to keep such large concentrations
in solution is, in part, due to the
presence of protective organic
molecules like citrate, as well as
the presence of charged ions
which alter the solubility (Menon
& Resnick, 2002). Despite the fact
that calcium oxalate can be present
in urine in concentrations 7
to 11 times its solubility in water
(Menon & Resnick, 2002), the
point exists at which calcium
oxalate exceeds the unique properties
of urine; crystals will then
form and possibly aggregate to
form stones.
Understanding saturation principles
in the urine, is it not clear
that methods of prevention shall be
focused on both an increase in solvent
and a reduction of solute?
These two concepts are the basis
for the dietary changes described
below.
Assessment of Dietary
Patterns
As dietary history is not part
of the typical urologic patient
history forms, the nurse can
obtain this information through
patient interview. Important information
includes the patient’s
intake of fluids throughout the
day, environmental factors promoting
dehydration, special diets
such as now-popular high-protein
diets, and a propensity to
consume packaged or restaurant
foods which are typically very
high in sodium. What does the
patient drink, how much is consumed,
and how is fluid intake
distributed through the day?
Does he or she work in a hot or
dry environment (such as a hot
factory, outside work in the summer)?
Does he or she prepare
fresh foods at home or tend to eat
convenience foods?
Nurses’ dietary interview can
occur before or after metabolic
testing. Absent metabolic testing,
this interview has even greater
import as it is the only source of
information about dietary habits.
Asking patients to keep a 24-hour
diet record may help identify
patterns of which even the
patient was unaware. Sources of
dietary sodium can be obvious or
insidious. The excess intake of a
patient who consumes a bag of
microwave popcorn every night
is more apparent than the intake
of a patient who drinks sports
drinks after a daily workout;
these are both very high in sodium,
but the latter is less often
recognized.
If the nurse has at his or her
disposal a 24-hour urine study,
dietary anomalies may be more
specifically exposed and documented.
This author views 24-
hour urine studies as “vice recognition
software;” the numbers
show actual urine output, and
indicate dietary sodium, protein,
and oxalate excess. Patients with
low urine volumes may believe
their results are incorrect. They
may say “I drink all the time!”
and yet the output is low. Here
the role of dietary counseling is
critical; the insightful nurse
helps the patient identify volume
consumed, sources of insensible
loss, and ways to ensure
increased urine volume.
DIETARY CHANGES TO
PREVENT AND REDUCE
STONE FORMATION
Increase Fluid Intake
Increasing urine volume can
reduce supersaturation, and is
widely known to help prevent
stone formation. Recommendations
for urinary output vary, but there is
general agreement that it should
exceed two liters per day, while
some even encourage urinary
outputs in excess of three liters
per day (Menon & Resnick, 2002;
Sakhaee, Zerwekh, & Pak, 1980).
A key point is that the dilution of
urine is necessary “24/7,” or all
day, every day. A patient who
voids the recommended two
liters a day between the hours of
8 am and 10 pm, but only 300
milliliters during the remaining
10 hours of the day will have saturated
urine overnight, with the
possibility of precipitation and
aggregation during the sleeping
hours. Patients must accept the
necessity of getting up at least
twice at night to urinate, and
should consume more water each
time they rise to void.
Stress to patients that it is not
the quantity of fluid consumed
that is important, but rather the
fluid voided that should be measured.
Patients living in hot or
dry conditions, or who exercise
and perspire significantly, will
need to drink even more liquid to
maintain adequate urine output.
Many patients ask what fluids
are recommended, and which
are prohibited. The simple
answer is that water is best. For
those with excessive urinary
oxalates, black tea should be
eliminated because black tea is a
high-oxalate beverage. Curhan,
Willett, Rimm, Speizer, and
Stampfer (1998) found, in a retrospective
study of previously nonstone
forming women from the
Nurses’ Health Study, that the
type of beverages consumed
proved relevant for stone formers.
Of the 17 beverages studied,
and after correcting for other contributing
factors, those who
drank one daily 8 ounce glass of
grapefruit juice had a 44%
increased risk of a stone event in
the 8-year period, while the risk
was decreased by 8% to 10% for
each daily 8 ounce serving of coffee
(both caffeinated and non-caffeinated),
tea, or wine. A prospective study had similar
conclusions for men, additionally
showing that beer had a protective
effect and apple juice increased
the risk of stone events (Curhan,
Willett, Rimm, Speigelman, &
Stampfer, 1996). Also, a study published
by Massey and Sutton (2004)
showed a modest positive relationship
between caffeine intake and
urinary calcium levels in stone formers
and non-stone formers, so caffeinated
beverages should be limited
in stone formers. In summary,
stone formers should drink more
water and avoid excess caffeine,
black tea, and grapefruit and apple
juices.
What do these studies mean
for patient education?
Water is the
best beverage for stone formers. It is
non-caloric, non-caffeinated, and
contains insignificant amounts of
solutes. In initial attempts to
increase patients’ fluid intake, it
may be appropriate to advise them
to drink whatever they can consume
in large quantities. However,
warning them of side effects of sugared
and caffeinated beverages in
large quantities is important. The
results discussed above indicate
that consumption of alcoholic
beverages is unlikely to increase
stone risk. Water that tastes good
(filtered, reverse osmosis, bottled)
may be easier to consume than tap
water, so encourage patients to
seek a source of good-tasting
water. There is no clear agreement
on the impact of drinking water’s
mineral content on lithogenesis;
“hard water” may not be problematic
for most patients (Menon &
Resnick, 2002). Again, water in
large quantities should be the
focus of prevention. Lemonade is
often recommended, as it supplies
dietary citrate, a stone inhibitor
and pH buffer when excreted later
in the urine.
Encourage patients to set
consumption goals, carry water
with them at all times, and strive
for pale urine throughout the day
and night. Some patients describe
an initial physiologic
resistance to increased fluid
intake which eases as their bodies
and minds learn the new
habit of extra fluid intake and
output. According to Parks,
Goldfischer, and Coe (2003),
aims by clinicians to increase
patients’ urinary volumes often
fall short, and follow-up metabolic
studies showed an average
increase in urine output of only
0.3 liters per 24 hours. This
increase was associated with a
curious increase in sodium
intake. High urine volumes
should be the goal of all patients
who form stones. In this
instance, more is definitely better.
Most patients find that after
forcing fluids for a couple of
months, their bodies crave fluids
and their habit is to drink more.
Consume Adequate Calcium
High urine calcium, hypercalciuria,
is associated both with
formation of kidney stones and
with osteoporosis. Sufficient calcium
intake is required for the
growth and maintenance of the
skeleton in children and adults.
Reducing urine calcium should
be a goal for stone formers, but
not via dietary restriction. While
reduced dietary calcium can
decrease urine calcium (Lemann,
2002), calcium restriction is no
longer advisable for patients who
form calcium kidney stones as
this puts them at risk of bone disease,
namely osteoporosis. Recall
that bones are in a constant
process of resorption and formation;
adequate calcium is required
for the ongoing rebuilding of bone
material.
Several recent studies have
shown, in fact, that adequate calcium
intake is associated with
decreased stone formation.
Curhan, Willett, Knight, and
Stampfer (2004) found that in
previously non-stone forming
younger women, higher intake of
dietary calcium was related to
lower risk of kidney stone formation.
Additionally, a 5-year randomized
clinical trial of men
with a history of calcium oxalate
stones found that a normal calcium,
decreased sodium, and
decreased animal protein diet
was more effective for reducing
stone events than was a restricted
calcium diet (Borghi et al., 2002).
So, adequate calcium plus
decreased sodium and protein
intake had a significantly more
protective effect against stones
than decreased calcium intake
alone.
Why might increased dietary
calcium reduce the risk of calcium
stone formation? Calcium
and oxalate bind in the gut and
in the urine to form a nonabsorbable
compound. Low dietary
calcium permits greater free
oxalate to be absorbed in the gut
and excreted in the urine, which
may be counterproductive for
calcium oxalate stone formers.
Restricted calcium intake results
in increased urinary oxalates, a
risk for stone formation (Menon
& Resnick, 2002). This is a proposed
cause of the association
between reduced calcium intake
and increased supersaturation of
calcium oxalate (Lemann, 2002).
Clearly, strong research evidence
now supports adequate
calcium intake for patients who
form kidney stones. Low-fat
dairy products, green leafy vegetables,
broccoli, fortified foods,
and almonds are excellent
sources. Patients should consume
enough dietary calcium to
meet (but not exceed) the United
States Recommended Daily
Allowance (RDA) of calcium,
which ranges from 1,000 to 1,200
milligrams daily for adults. The
recommendations are the same
for men and women, but vary by
age group (see Table 1). Patients
should avoid calcium supplements
in favor of calcium-rich
foods; a patient with intolerance
to dairy products may supplement,
but should not exceed the
RDA for his/her age group.
Limit Dietary Oxalates
Oxalate is found in many
foods, but there is considerable
variability in the amount, which
depends upon where the food is
grown. Likewise, individual
absorption of oxalate also varies,
which makes adequate calcium
intake critically important.
Nonetheless, oxalate restriction
should be attempted. The highest
levels of oxalate are found in
chocolate, nuts, beans (including
soybeans), rhubarb, spinach,
beets, and black tea. A thorough
oxalate list can be found on the
Web site of the Oxalosis and
Hyperoxaluria Foundation (http://
www.ohf.org/diet.html). This list
is exhaustive and may be overwhelming
to patients. Stress that
reduction of high oxalate foods is
the goal for typical stone formers
rather than strict avoidance of all
oxalate-containing foods (which
would be very difficult). Followup
24-hour urine studies will demonstrate
the adequacy of patients’
restriction.
Though only 10% to 20% of
urinary oxalates come from
dietary sources (Morton, Iliescu,
& Wilson, 2002), dietary reduction
is commonly advised for calcium
oxalate stone formers. It has
been suggested that because
there is much less oxalate in the
urine than calcium in the urine,
urinary oxalate concentration is
much more critical to the formation
of calcium oxalate crystals
than is the urinary calcium concentration;
reducing urine oxalates
may have a more powerful effect
on stone formation than can reduction
of urine calcium (Morton et
al., 2002). Patients with calcium
oxalate stones, particularly those
with documented hyperoxaluria,
should avoid foods high in
oxalates. Vitamin C is a precursor
to endogenous production of
oxalates, so some clinicians recommend
avoiding mega-doses of
vitamin C. The rare genetic condition
of primary hyperoxaluria is
only slightly impacted by dietary
reduction, and causes serious
medical problems besides kidney
stones.
Limit Sodium Intake
Because calcium and sodium
compete for reabsorption in the
renal tubules, excess sodium
intake and consequent excretion
result in loss of calcium in the
urine. High-sodium diets are
associated with greater calcium
excretion in the urine (Lemann,
2002). Metabolic studies often
reveal exceptionally high urine
calcium over 24 hours, related to
patients’ exceptionally high sodium
excretion. Patients may deny
salt intake, stating, “I never salt
my food!” They quite likely are
ignorant of hidden sodium
sources in the diet. Sodium is a
common preservative in canned
and frozen foods, and is endemic
in restaurant foods. Instruction
on careful inspection of food
labels and wise food choices
helps patients identify and
reduce sodium in their diets.
A notable dietary “ah-ha!”
was the admission by one patient
that, on the day of 24-hour urine
testing, she ate a full jar of pickles
to reduce stress, and then
drank the brine; needless to say,
her urine sodium was very high
on the day of her stress mitigation.
The role of the nurse or dietician
in shedding light on sources
of sodium cannot be underestimated.
Repeated, persistent inquiry
into dietary habits may be necessary.
The goal of therapy should be
a “no added salt diet,” or the equivalent
of 2,000 mg per day or less of
dietary sodium. Reduction of
dietary sodium is difficult and disappointing
to patients. They may
believe they have made significant
reductions and sacrifices, while
their urine sodium remains high.
Consultation with a registered
dietician may help the patient
achieve the specific goal of a sodium
intake of 2,000 milligrams or
less per day.
Limit Animal Protein
The effect of excess animal
protein (purine) is most obvious
for the uric acid stone former.
Uric acid, a byproduct of purine
metabolism, is excreted in large
quantities in the urine. Excess
protein creates urine with high
total urine uric acid, potentially
high supersaturation of urine
uric acid, and a low pH, necessary
for formation of uric acid
stones. There is no inhibitor of
uric acid crystal formation
(Menon & Resnick, 2002), so
dietary measures focus on reducing
uric acid and increasing
urine volume. Reduction of animal
protein to 12 ounces per day
for adults is recommended. This
is plenty to meet the dietary
needs of most Americans, many
of whom typically consume several
more ounces of animal protein
daily than is recommended.
Protein from plant sources
(beans, legumes, etc.) can be substituted
as a dietary alternative
without negative consequences.
Calcium oxalate stone formers
reducing their animal protein
should note the oxalate content
of substitute proteins.
The role of excess protein in
promoting calcium stone formation
is less obvious, but equally
important. High dietary protein
is associated with increased urinary
calcium. Thus, there is a
link between meat consumption
and both uric acid and calcium
stone formation. In fact, vegetarians
form stones at one-third the
rate of those eating a mixed diet
(Lemann, 2002). A study of 18
hypercalciuric stone formers found
that a 15-day protein restriction
had many positive effects on urinary
markers of stone risk.
Namely, significant decreases
were seen in urine calcium, urine
uric acid, urine phosphate, and
urine oxalate. And, for unclear
reasons, a beneficial increase in
urinary citrate was observed
(Giannini et al., 1999). Citrate is a
known inhibitor of calcium
oxalate crystal formation and
also increases pH, which can prevent
uric acid stones. Clearly, the
benefits of protein restriction for
stone formers are many.
Weight Loss
A relationship between weight,
body mass index and risk of calcium
oxalate stone formation was
established in a retrospective
study of health professionals.
Curhan and colleagues (1998)
found that “the prevalence of
stone disease history and the
incidence of stone disease were
directly associated with weight
and body mass index. However,
the magnitude of the associations
was consistently greater among
women” (p. 1645). The value of
weight loss for stone prevention
has not been proven, but given
the benefits of weight loss for
general health, it is certainly
worth mentioning to overweight
patients who form stones.
Educational Resources
There are excellent resources
on the Internet for patients seeking
nutritional information. One stellar
example is NutritionData
(www.nutritiondata.com/). Here
patients can search by general food
category, like “pickle,” to view the
standard sodium content, as well
as a plethora of additional information
regarding vitamin and mineral
content, calories, suggested healthier
substitutes, and even the individual
amino acid compositions of
each protein. The site also provides
detailed information about
thousands of specific brand items
from grocery and fast food restaurants.
Under “Tools,” patients can
search within food categories like
“dairy products” for choices highest
in calcium and lowest in sodium.
This site is complex and may be
overwhelming to patients without
good computer and Web skills, but
is extraordinarily comprehensive;
unfortunately, this site does not list
oxalate content. For that purpose,
refer patients to www.ohf.org.
For patients without Web
access, nurses might find it helpful
to review a general nutrition
book for charts and diagrams to
help patients understand nutrition
content. Show patients a
sample food label from a can of
soup so they know where to find
sodium content on foods at home.
For a simple list of high-oxalate
foods, visit www.gicare.com/
pated/edtgs29.htm.
Conclusion
The dietary measures discussed
have value particularly
for patients who form the most
common types of kidney stones:
calcium oxalate and uric acid.
That said, they may be insufficient
to control the various metabolic
abnormalities present in
individual patients. The most
effective management of kidney
stones includes in-depth metabolic
studies, recommendations
tailored to patients regarding
medications and dietary changes,
and follow-up to ensure changes
are having the desired effect.
Urine studies should be repeated
to judge progress approximately
6 to 8 weeks after initial metabolic
testing recommendations are
implemented. Once a stable state
is reached in which the patient’s
urine demonstrates decreased
risk of stone formation, metabolic
testing should be performed
(along with an x-ray to check for
stone growth) at least annually to
monitor stone risk. The cycle of
stone formation can be altered,
and in some cases broken, with
the aid of effective dietary management.
Every patient need not make
all of these changes to his/her
diet, but in the absence of
patient-specific urine studies,
none of these recommendations
is harmful. Aside from oxalate
consumption, the dietary recommendations
for calcium oxalate
and uric acid stone formers are
the same. Assessing
patients’ dietary habits can shed
light on potential areas of
improvement. For example, a
receptive uric acid stone former
on a high-protein diet for weight
loss could benefit from counseling
on the effects of this diet on
his/her stone disease.
Of course, talking about
dietary changes is easier than actual
implementation. Encourage
patients to make changes at a realistic
pace. Praise even modest
progress and stress the value of
striving for improvement rather
than perfection.
The Bottom Line here is;
•Urinate more than two liters per day.
• Consume enough dietary calcium to meet the US RDA.
• Avoid dietary oxalates (for calcium oxalate stone-formers).
• Limit sodium to 2,000 milligrams per day.
• Limit protein to 12 ounces per day.
• If overweight, lose weight.
Diet and Kidney Stones
The Role of Diet in the Prevention
Of Common Kidney Stones
Christy Krieg
Kidney stone formers may
feel doomed to a life of
unpredictable flank pain,periodic surgical intervention,
and concomitant loss of
work and daily pleasures. Indeed,
if untreated, those who have
formed one calcium oxalate stone
have a 50% chance of forming
additional stones within 10 years
(Menon & Resnick, 2002). With
appropriate education, patients
can exercise some control over
stone disease and reduce their
chances of forming stones
through dietary modifications
and medication.
General dietary recommendations
appropriate for patients
who form the most common
metabolic stone types — calcium
oxalate and uric acid — will be discussed
in this article. Patients with
a tendency to form cystine and
brushite stones may also benefit
from some of the same dietary recommendations,
but dietary management
is a small part of an even
more complex treatment regimen
in these instances. Regardless of
stone type, recommendations for
dietary modifications are most
accurate when tailored to the
results of urine stone risk profiles,
or “24-hour urine” studies.
These studies typically provide
total urine volume, urine
calcium, sodium, citrate and uric
Current dietary recommendations for patients who form kidney
stones are discussed. Focusing on the most common kidney stone
types, calcium oxalate and uric acid, the rationale for dietary changes
are described based on the renal and urine physiology.
Christy Krieg, BSN, RN, is a Clinical
Nurse, Methodist Urology, Indianapolis,
IN.
Note: CE Objectives and Evaluation
Form appear on page 457.
acid, as well as pH, and supersaturation
of critical compounds,
among other measurements. The
values, if properly interpreted,
allow the clinician to observe the
patient’s specific abnormalities,
recommend medication and/or
dietary modification, and track
progress through followup studies.
As with many bodily
processes, stone formation is a
complicated and multi-factorial
process. Yet, there is much still to
be understood about stone formation.
For example, we know that
stone formation runs in families,
but while all humans form calcium
oxalate crystals, most do not
form stones (Lemann, 2002). And
while for years calcium stone formers
were instructed to restrict
dietary calcium, there is now significant
evidence against this recommendation
(Borghi et al.,
2002). These observations illustrate
the sometimes counterintuitive
and always complex nature
of stone formation and the need
for ongoing investigation.
Stone recurrence is frustrating
for patients who have made
changes in their lives and yet still
form stones. While diet alone
cannot always control the disease,
dietary measures can
absolutely help supplement
other therapies, and for some
patients are the primary tool for
stone prevention. As a component
of the medical management
for stone disease, the goal of therapy
should be to improve those
factors thought to contribute to
stone formation in the urinary
tract, and thereby reduce the
chance of forming stones, even if
the disease is not eliminated.
Urine Supersaturation
And Stone Formation
Urine volume plays a pivotal
role in the process of stone formation.
In particular, low volume,
highly concentrated urine
contributes to the supersaturation
of elements normally found
in the urine, such as calcium
oxalate. Simply put, when the
solute exceeds the solvent’s ability
to dissolve it, precipitation of
crystals can occur. Consider an
attempt to dissolve sugar in
water: a tablespoon of sugar is
readily dissolved in a glass of
water, but eight tablespoons of
sugar in that same glass will not
completely dissolve, resulting in
the accumulation of crystals in
the bottom of the glass. In this
scenario, the water is saturated
with sugar; the solvent, water,
can dissolve no more solute. It
has exceeded the point of saturation,
and is supersaturated.
Fortunately, urine has the
unique quality of holding more
solute in suspension than does
water and so can accept large
concentrations of solute without
precipitation. The ability of urine
to keep such large concentrations
in solution is, in part, due to the
presence of protective organic
molecules like citrate, as well as
the presence of charged ions
which alter the solubility (Menon
& Resnick, 2002). Despite the fact
that calcium oxalate can be present
in urine in concentrations 7
to 11 times its solubility in water
(Menon & Resnick, 2002), the
point exists at which calcium
oxalate exceeds the unique properties
of urine; crystals will then
form and possibly aggregate to
form stones.
Understanding saturation principles
in the urine, is it not clear
that methods of prevention shall be
focused on both an increase in solvent
and a reduction of solute?
These two concepts are the basis
for the dietary changes described
below.
Assessment of Dietary
Patterns
As dietary history is not part
of the typical urologic patient
history forms, the nurse can
obtain this information through
patient interview. Important information
includes the patient’s
intake of fluids throughout the
day, environmental factors promoting
dehydration, special diets
such as now-popular high-protein
diets, and a propensity to
consume packaged or restaurant
foods which are typically very
high in sodium. What does the
patient drink, how much is consumed,
and how is fluid intake
distributed through the day?
Does he or she work in a hot or
dry environment (such as a hot
factory, outside work in the summer)?
Does he or she prepare
fresh foods at home or tend to eat
convenience foods?
Nurses’ dietary interview can
occur before or after metabolic
testing. Absent metabolic testing,
this interview has even greater
import as it is the only source of
information about dietary habits.
Asking patients to keep a 24-hour
diet record may help identify
patterns of which even the
patient was unaware. Sources of
dietary sodium can be obvious or
insidious. The excess intake of a
patient who consumes a bag of
microwave popcorn every night
is more apparent than the intake
of a patient who drinks sports
drinks after a daily workout;
these are both very high in sodium,
but the latter is less often
recognized.
If the nurse has at his or her
disposal a 24-hour urine study,
dietary anomalies may be more
specifically exposed and documented.
This author views 24-
hour urine studies as “vice recognition
software;” the numbers
show actual urine output, and
indicate dietary sodium, protein,
and oxalate excess. Patients with
low urine volumes may believe
their results are incorrect. They
may say “I drink all the time!”
and yet the output is low. Here
the role of dietary counseling is
critical; the insightful nurse
helps the patient identify volume
consumed, sources of insensible
loss, and ways to ensure
increased urine volume.
DIETARY CHANGES TO
PREVENT AND REDUCE
STONE FORMATION
Increase Fluid Intake
Increasing urine volume can
reduce supersaturation, and is
widely known to help prevent
stone formation. Recommendations
for urinary output vary, but there is
general agreement that it should
exceed two liters per day, while
some even encourage urinary
outputs in excess of three liters
per day (Menon & Resnick, 2002;
Sakhaee, Zerwekh, & Pak, 1980).
A key point is that the dilution of
urine is necessary “24/7,” or all
day, every day. A patient who
voids the recommended two
liters a day between the hours of
8 am and 10 pm, but only 300
milliliters during the remaining
10 hours of the day will have saturated
urine overnight, with the
possibility of precipitation and
aggregation during the sleeping
hours. Patients must accept the
necessity of getting up at least
twice at night to urinate, and
should consume more water each
time they rise to void.
Stress to patients that it is not
the quantity of fluid consumed
that is important, but rather the
fluid voided that should be measured.
Patients living in hot or
dry conditions, or who exercise
and perspire significantly, will
need to drink even more liquid to
maintain adequate urine output.
Many patients ask what fluids
are recommended, and which
are prohibited. The simple
answer is that water is best. For
those with excessive urinary
oxalates, black tea should be
eliminated because black tea is a
high-oxalate beverage. Curhan,
Willett, Rimm, Speizer, and
Stampfer (1998) found, in a retrospective
study of previously nonstone
forming women from the
Nurses’ Health Study, that the
type of beverages consumed
proved relevant for stone formers.
Of the 17 beverages studied,
and after correcting for other contributing
factors, those who
drank one daily 8 ounce glass of
grapefruit juice had a 44%
increased risk of a stone event in
the 8-year period, while the risk
was decreased by 8% to 10% for
each daily 8 ounce serving of coffee
(both caffeinated and non-caffeinated),
tea, or wine. A prospective study had similar
conclusions for men, additionally
showing that beer had a protective
effect and apple juice increased
the risk of stone events (Curhan,
Willett, Rimm, Speigelman, &
Stampfer, 1996). Also, a study published
by Massey and Sutton (2004)
showed a modest positive relationship
between caffeine intake and
urinary calcium levels in stone formers
and non-stone formers, so caffeinated
beverages should be limited
in stone formers. In summary,
stone formers should drink more
water and avoid excess caffeine,
black tea, and grapefruit and apple
juices.
What do these studies mean
for patient education?
Water is the
best beverage for stone formers. It is
non-caloric, non-caffeinated, and
contains insignificant amounts of
solutes. In initial attempts to
increase patients’ fluid intake, it
may be appropriate to advise them
to drink whatever they can consume
in large quantities. However,
warning them of side effects of sugared
and caffeinated beverages in
large quantities is important. The
results discussed above indicate
that consumption of alcoholic
beverages is unlikely to increase
stone risk. Water that tastes good
(filtered, reverse osmosis, bottled)
may be easier to consume than tap
water, so encourage patients to
seek a source of good-tasting
water. There is no clear agreement
on the impact of drinking water’s
mineral content on lithogenesis;
“hard water” may not be problematic
for most patients (Menon &
Resnick, 2002). Again, water in
large quantities should be the
focus of prevention. Lemonade is
often recommended, as it supplies
dietary citrate, a stone inhibitor
and pH buffer when excreted later
in the urine.
Encourage patients to set
consumption goals, carry water
with them at all times, and strive
for pale urine throughout the day
and night. Some patients describe
an initial physiologic
resistance to increased fluid
intake which eases as their bodies
and minds learn the new
habit of extra fluid intake and
output. According to Parks,
Goldfischer, and Coe (2003),
aims by clinicians to increase
patients’ urinary volumes often
fall short, and follow-up metabolic
studies showed an average
increase in urine output of only
0.3 liters per 24 hours. This
increase was associated with a
curious increase in sodium
intake. High urine volumes
should be the goal of all patients
who form stones. In this
instance, more is definitely better.
Most patients find that after
forcing fluids for a couple of
months, their bodies crave fluids
and their habit is to drink more.
Consume Adequate Calcium
High urine calcium, hypercalciuria,
is associated both with
formation of kidney stones and
with osteoporosis. Sufficient calcium
intake is required for the
growth and maintenance of the
skeleton in children and adults.
Reducing urine calcium should
be a goal for stone formers, but
not via dietary restriction. While
reduced dietary calcium can
decrease urine calcium (Lemann,
2002), calcium restriction is no
longer advisable for patients who
form calcium kidney stones as
this puts them at risk of bone disease,
namely osteoporosis. Recall
that bones are in a constant
process of resorption and formation;
adequate calcium is required
for the ongoing rebuilding of bone
material.
Several recent studies have
shown, in fact, that adequate calcium
intake is associated with
decreased stone formation.
Curhan, Willett, Knight, and
Stampfer (2004) found that in
previously non-stone forming
younger women, higher intake of
dietary calcium was related to
lower risk of kidney stone formation.
Additionally, a 5-year randomized
clinical trial of men
with a history of calcium oxalate
stones found that a normal calcium,
decreased sodium, and
decreased animal protein diet
was more effective for reducing
stone events than was a restricted
calcium diet (Borghi et al., 2002).
So, adequate calcium plus
decreased sodium and protein
intake had a significantly more
protective effect against stones
than decreased calcium intake
alone.
Why might increased dietary
calcium reduce the risk of calcium
stone formation? Calcium
and oxalate bind in the gut and
in the urine to form a nonabsorbable
compound. Low dietary
calcium permits greater free
oxalate to be absorbed in the gut
and excreted in the urine, which
may be counterproductive for
calcium oxalate stone formers.
Restricted calcium intake results
in increased urinary oxalates, a
risk for stone formation (Menon
& Resnick, 2002). This is a proposed
cause of the association
between reduced calcium intake
and increased supersaturation of
calcium oxalate (Lemann, 2002).
Clearly, strong research evidence
now supports adequate
calcium intake for patients who
form kidney stones. Low-fat
dairy products, green leafy vegetables,
broccoli, fortified foods,
and almonds are excellent
sources. Patients should consume
enough dietary calcium to
meet (but not exceed) the United
States Recommended Daily
Allowance (RDA) of calcium,
which ranges from 1,000 to 1,200
milligrams daily for adults. The
recommendations are the same
for men and women, but vary by
age group (see Table 1). Patients
should avoid calcium supplements
in favor of calcium-rich
foods; a patient with intolerance
to dairy products may supplement,
but should not exceed the
RDA for his/her age group.
Limit Dietary Oxalates
Oxalate is found in many
foods, but there is considerable
variability in the amount, which
depends upon where the food is
grown. Likewise, individual
absorption of oxalate also varies,
which makes adequate calcium
intake critically important.
Nonetheless, oxalate restriction
should be attempted. The highest
levels of oxalate are found in
chocolate, nuts, beans (including
soybeans), rhubarb, spinach,
beets, and black tea. A thorough
oxalate list can be found on the
Web site of the Oxalosis and
Hyperoxaluria Foundation (http://
www.ohf.org/diet.html). This list
is exhaustive and may be overwhelming
to patients. Stress that
reduction of high oxalate foods is
the goal for typical stone formers
rather than strict avoidance of all
oxalate-containing foods (which
would be very difficult). Followup
24-hour urine studies will demonstrate
the adequacy of patients’
restriction.
Though only 10% to 20% of
urinary oxalates come from
dietary sources (Morton, Iliescu,
& Wilson, 2002), dietary reduction
is commonly advised for calcium
oxalate stone formers. It has
been suggested that because
there is much less oxalate in the
urine than calcium in the urine,
urinary oxalate concentration is
much more critical to the formation
of calcium oxalate crystals
than is the urinary calcium concentration;
reducing urine oxalates
may have a more powerful effect
on stone formation than can reduction
of urine calcium (Morton et
al., 2002). Patients with calcium
oxalate stones, particularly those
with documented hyperoxaluria,
should avoid foods high in
oxalates. Vitamin C is a precursor
to endogenous production of
oxalates, so some clinicians recommend
avoiding mega-doses of
vitamin C. The rare genetic condition
of primary hyperoxaluria is
only slightly impacted by dietary
reduction, and causes serious
medical problems besides kidney
stones.
Limit Sodium Intake
Because calcium and sodium
compete for reabsorption in the
renal tubules, excess sodium
intake and consequent excretion
result in loss of calcium in the
urine. High-sodium diets are
associated with greater calcium
excretion in the urine (Lemann,
2002). Metabolic studies often
reveal exceptionally high urine
calcium over 24 hours, related to
patients’ exceptionally high sodium
excretion. Patients may deny
salt intake, stating, “I never salt
my food!” They quite likely are
ignorant of hidden sodium
sources in the diet. Sodium is a
common preservative in canned
and frozen foods, and is endemic
in restaurant foods. Instruction
on careful inspection of food
labels and wise food choices
helps patients identify and
reduce sodium in their diets.
A notable dietary “ah-ha!”
was the admission by one patient
that, on the day of 24-hour urine
testing, she ate a full jar of pickles
to reduce stress, and then
drank the brine; needless to say,
her urine sodium was very high
on the day of her stress mitigation.
The role of the nurse or dietician
in shedding light on sources
of sodium cannot be underestimated.
Repeated, persistent inquiry
into dietary habits may be necessary.
The goal of therapy should be
a “no added salt diet,” or the equivalent
of 2,000 mg per day or less of
dietary sodium. Reduction of
dietary sodium is difficult and disappointing
to patients. They may
believe they have made significant
reductions and sacrifices, while
their urine sodium remains high.
Consultation with a registered
dietician may help the patient
achieve the specific goal of a sodium
intake of 2,000 milligrams or
less per day.
Limit Animal Protein
The effect of excess animal
protein (purine) is most obvious
for the uric acid stone former.
Uric acid, a byproduct of purine
metabolism, is excreted in large
quantities in the urine. Excess
protein creates urine with high
total urine uric acid, potentially
high supersaturation of urine
uric acid, and a low pH, necessary
for formation of uric acid
stones. There is no inhibitor of
uric acid crystal formation
(Menon & Resnick, 2002), so
dietary measures focus on reducing
uric acid and increasing
urine volume. Reduction of animal
protein to 12 ounces per day
for adults is recommended. This
is plenty to meet the dietary
needs of most Americans, many
of whom typically consume several
more ounces of animal protein
daily than is recommended.
Protein from plant sources
(beans, legumes, etc.) can be substituted
as a dietary alternative
without negative consequences.
Calcium oxalate stone formers
reducing their animal protein
should note the oxalate content
of substitute proteins.
The role of excess protein in
promoting calcium stone formation
is less obvious, but equally
important. High dietary protein
is associated with increased urinary
calcium. Thus, there is a
link between meat consumption
and both uric acid and calcium
stone formation. In fact, vegetarians
form stones at one-third the
rate of those eating a mixed diet
(Lemann, 2002). A study of 18
hypercalciuric stone formers found
that a 15-day protein restriction
had many positive effects on urinary
markers of stone risk.
Namely, significant decreases
were seen in urine calcium, urine
uric acid, urine phosphate, and
urine oxalate. And, for unclear
reasons, a beneficial increase in
urinary citrate was observed
(Giannini et al., 1999). Citrate is a
known inhibitor of calcium
oxalate crystal formation and
also increases pH, which can prevent
uric acid stones. Clearly, the
benefits of protein restriction for
stone formers are many.
Weight Loss
A relationship between weight,
body mass index and risk of calcium
oxalate stone formation was
established in a retrospective
study of health professionals.
Curhan and colleagues (1998)
found that “the prevalence of
stone disease history and the
incidence of stone disease were
directly associated with weight
and body mass index. However,
the magnitude of the associations
was consistently greater among
women” (p. 1645). The value of
weight loss for stone prevention
has not been proven, but given
the benefits of weight loss for
general health, it is certainly
worth mentioning to overweight
patients who form stones.
Educational Resources
There are excellent resources
on the Internet for patients seeking
nutritional information. One stellar
example is NutritionData
(www.nutritiondata.com/). Here
patients can search by general food
category, like “pickle,” to view the
standard sodium content, as well
as a plethora of additional information
regarding vitamin and mineral
content, calories, suggested healthier
substitutes, and even the individual
amino acid compositions of
each protein. The site also provides
detailed information about
thousands of specific brand items
from grocery and fast food restaurants.
Under “Tools,” patients can
search within food categories like
“dairy products” for choices highest
in calcium and lowest in sodium.
This site is complex and may be
overwhelming to patients without
good computer and Web skills, but
is extraordinarily comprehensive;
unfortunately, this site does not list
oxalate content. For that purpose,
refer patients to www.ohf.org.
For patients without Web
access, nurses might find it helpful
to review a general nutrition
book for charts and diagrams to
help patients understand nutrition
content. Show patients a
sample food label from a can of
soup so they know where to find
sodium content on foods at home.
For a simple list of high-oxalate
foods, visit www.gicare.com/
pated/edtgs29.htm.
Conclusion
The dietary measures discussed
have value particularly
for patients who form the most
common types of kidney stones:
calcium oxalate and uric acid.
That said, they may be insufficient
to control the various metabolic
abnormalities present in
individual patients. The most
effective management of kidney
stones includes in-depth metabolic
studies, recommendations
tailored to patients regarding
medications and dietary changes,
and follow-up to ensure changes
are having the desired effect.
Urine studies should be repeated
to judge progress approximately
6 to 8 weeks after initial metabolic
testing recommendations are
implemented. Once a stable state
is reached in which the patient’s
urine demonstrates decreased
risk of stone formation, metabolic
testing should be performed
(along with an x-ray to check for
stone growth) at least annually to
monitor stone risk. The cycle of
stone formation can be altered,
and in some cases broken, with
the aid of effective dietary management.
Every patient need not make
all of these changes to his/her
diet, but in the absence of
patient-specific urine studies,
none of these recommendations
is harmful. Aside from oxalate
consumption, the dietary recommendations
for calcium oxalate
and uric acid stone formers are
the same. Assessing
patients’ dietary habits can shed
light on potential areas of
improvement. For example, a
receptive uric acid stone former
on a high-protein diet for weight
loss could benefit from counseling
on the effects of this diet on
his/her stone disease.
Of course, talking about
dietary changes is easier than actual
implementation. Encourage
patients to make changes at a realistic
pace. Praise even modest
progress and stress the value of
striving for improvement rather
than perfection.
The Bottom Line here is;
•Urinate more than two liters per day.
• Consume enough dietary calcium to meet the US RDA.
• Avoid dietary oxalates (for calcium oxalate stone-formers).
• Limit sodium to 2,000 milligrams per day.
• Limit protein to 12 ounces per day.
• If overweight, lose weight.
Of Common Kidney Stones
Christy Krieg
Kidney stone formers may
feel doomed to a life of
unpredictable flank pain,periodic surgical intervention,
and concomitant loss of
work and daily pleasures. Indeed,
if untreated, those who have
formed one calcium oxalate stone
have a 50% chance of forming
additional stones within 10 years
(Menon & Resnick, 2002). With
appropriate education, patients
can exercise some control over
stone disease and reduce their
chances of forming stones
through dietary modifications
and medication.
General dietary recommendations
appropriate for patients
who form the most common
metabolic stone types — calcium
oxalate and uric acid — will be discussed
in this article. Patients with
a tendency to form cystine and
brushite stones may also benefit
from some of the same dietary recommendations,
but dietary management
is a small part of an even
more complex treatment regimen
in these instances. Regardless of
stone type, recommendations for
dietary modifications are most
accurate when tailored to the
results of urine stone risk profiles,
or “24-hour urine” studies.
These studies typically provide
total urine volume, urine
calcium, sodium, citrate and uric
Current dietary recommendations for patients who form kidney
stones are discussed. Focusing on the most common kidney stone
types, calcium oxalate and uric acid, the rationale for dietary changes
are described based on the renal and urine physiology.
Christy Krieg, BSN, RN, is a Clinical
Nurse, Methodist Urology, Indianapolis,
IN.
Note: CE Objectives and Evaluation
Form appear on page 457.
acid, as well as pH, and supersaturation
of critical compounds,
among other measurements. The
values, if properly interpreted,
allow the clinician to observe the
patient’s specific abnormalities,
recommend medication and/or
dietary modification, and track
progress through followup studies.
As with many bodily
processes, stone formation is a
complicated and multi-factorial
process. Yet, there is much still to
be understood about stone formation.
For example, we know that
stone formation runs in families,
but while all humans form calcium
oxalate crystals, most do not
form stones (Lemann, 2002). And
while for years calcium stone formers
were instructed to restrict
dietary calcium, there is now significant
evidence against this recommendation
(Borghi et al.,
2002). These observations illustrate
the sometimes counterintuitive
and always complex nature
of stone formation and the need
for ongoing investigation.
Stone recurrence is frustrating
for patients who have made
changes in their lives and yet still
form stones. While diet alone
cannot always control the disease,
dietary measures can
absolutely help supplement
other therapies, and for some
patients are the primary tool for
stone prevention. As a component
of the medical management
for stone disease, the goal of therapy
should be to improve those
factors thought to contribute to
stone formation in the urinary
tract, and thereby reduce the
chance of forming stones, even if
the disease is not eliminated.
Urine Supersaturation
And Stone Formation
Urine volume plays a pivotal
role in the process of stone formation.
In particular, low volume,
highly concentrated urine
contributes to the supersaturation
of elements normally found
in the urine, such as calcium
oxalate. Simply put, when the
solute exceeds the solvent’s ability
to dissolve it, precipitation of
crystals can occur. Consider an
attempt to dissolve sugar in
water: a tablespoon of sugar is
readily dissolved in a glass of
water, but eight tablespoons of
sugar in that same glass will not
completely dissolve, resulting in
the accumulation of crystals in
the bottom of the glass. In this
scenario, the water is saturated
with sugar; the solvent, water,
can dissolve no more solute. It
has exceeded the point of saturation,
and is supersaturated.
Fortunately, urine has the
unique quality of holding more
solute in suspension than does
water and so can accept large
concentrations of solute without
precipitation. The ability of urine
to keep such large concentrations
in solution is, in part, due to the
presence of protective organic
molecules like citrate, as well as
the presence of charged ions
which alter the solubility (Menon
& Resnick, 2002). Despite the fact
that calcium oxalate can be present
in urine in concentrations 7
to 11 times its solubility in water
(Menon & Resnick, 2002), the
point exists at which calcium
oxalate exceeds the unique properties
of urine; crystals will then
form and possibly aggregate to
form stones.
Understanding saturation principles
in the urine, is it not clear
that methods of prevention shall be
focused on both an increase in solvent
and a reduction of solute?
These two concepts are the basis
for the dietary changes described
below.
Assessment of Dietary
Patterns
As dietary history is not part
of the typical urologic patient
history forms, the nurse can
obtain this information through
patient interview. Important information
includes the patient’s
intake of fluids throughout the
day, environmental factors promoting
dehydration, special diets
such as now-popular high-protein
diets, and a propensity to
consume packaged or restaurant
foods which are typically very
high in sodium. What does the
patient drink, how much is consumed,
and how is fluid intake
distributed through the day?
Does he or she work in a hot or
dry environment (such as a hot
factory, outside work in the summer)?
Does he or she prepare
fresh foods at home or tend to eat
convenience foods?
Nurses’ dietary interview can
occur before or after metabolic
testing. Absent metabolic testing,
this interview has even greater
import as it is the only source of
information about dietary habits.
Asking patients to keep a 24-hour
diet record may help identify
patterns of which even the
patient was unaware. Sources of
dietary sodium can be obvious or
insidious. The excess intake of a
patient who consumes a bag of
microwave popcorn every night
is more apparent than the intake
of a patient who drinks sports
drinks after a daily workout;
these are both very high in sodium,
but the latter is less often
recognized.
If the nurse has at his or her
disposal a 24-hour urine study,
dietary anomalies may be more
specifically exposed and documented.
This author views 24-
hour urine studies as “vice recognition
software;” the numbers
show actual urine output, and
indicate dietary sodium, protein,
and oxalate excess. Patients with
low urine volumes may believe
their results are incorrect. They
may say “I drink all the time!”
and yet the output is low. Here
the role of dietary counseling is
critical; the insightful nurse
helps the patient identify volume
consumed, sources of insensible
loss, and ways to ensure
increased urine volume.
DIETARY CHANGES TO
PREVENT AND REDUCE
STONE FORMATION
Increase Fluid Intake
Increasing urine volume can
reduce supersaturation, and is
widely known to help prevent
stone formation. Recommendations
for urinary output vary, but there is
general agreement that it should
exceed two liters per day, while
some even encourage urinary
outputs in excess of three liters
per day (Menon & Resnick, 2002;
Sakhaee, Zerwekh, & Pak, 1980).
A key point is that the dilution of
urine is necessary “24/7,” or all
day, every day. A patient who
voids the recommended two
liters a day between the hours of
8 am and 10 pm, but only 300
milliliters during the remaining
10 hours of the day will have saturated
urine overnight, with the
possibility of precipitation and
aggregation during the sleeping
hours. Patients must accept the
necessity of getting up at least
twice at night to urinate, and
should consume more water each
time they rise to void.
Stress to patients that it is not
the quantity of fluid consumed
that is important, but rather the
fluid voided that should be measured.
Patients living in hot or
dry conditions, or who exercise
and perspire significantly, will
need to drink even more liquid to
maintain adequate urine output.
Many patients ask what fluids
are recommended, and which
are prohibited. The simple
answer is that water is best. For
those with excessive urinary
oxalates, black tea should be
eliminated because black tea is a
high-oxalate beverage. Curhan,
Willett, Rimm, Speizer, and
Stampfer (1998) found, in a retrospective
study of previously nonstone
forming women from the
Nurses’ Health Study, that the
type of beverages consumed
proved relevant for stone formers.
Of the 17 beverages studied,
and after correcting for other contributing
factors, those who
drank one daily 8 ounce glass of
grapefruit juice had a 44%
increased risk of a stone event in
the 8-year period, while the risk
was decreased by 8% to 10% for
each daily 8 ounce serving of coffee
(both caffeinated and non-caffeinated),
tea, or wine. A prospective study had similar
conclusions for men, additionally
showing that beer had a protective
effect and apple juice increased
the risk of stone events (Curhan,
Willett, Rimm, Speigelman, &
Stampfer, 1996). Also, a study published
by Massey and Sutton (2004)
showed a modest positive relationship
between caffeine intake and
urinary calcium levels in stone formers
and non-stone formers, so caffeinated
beverages should be limited
in stone formers. In summary,
stone formers should drink more
water and avoid excess caffeine,
black tea, and grapefruit and apple
juices.
What do these studies mean
for patient education?
Water is the
best beverage for stone formers. It is
non-caloric, non-caffeinated, and
contains insignificant amounts of
solutes. In initial attempts to
increase patients’ fluid intake, it
may be appropriate to advise them
to drink whatever they can consume
in large quantities. However,
warning them of side effects of sugared
and caffeinated beverages in
large quantities is important. The
results discussed above indicate
that consumption of alcoholic
beverages is unlikely to increase
stone risk. Water that tastes good
(filtered, reverse osmosis, bottled)
may be easier to consume than tap
water, so encourage patients to
seek a source of good-tasting
water. There is no clear agreement
on the impact of drinking water’s
mineral content on lithogenesis;
“hard water” may not be problematic
for most patients (Menon &
Resnick, 2002). Again, water in
large quantities should be the
focus of prevention. Lemonade is
often recommended, as it supplies
dietary citrate, a stone inhibitor
and pH buffer when excreted later
in the urine.
Encourage patients to set
consumption goals, carry water
with them at all times, and strive
for pale urine throughout the day
and night. Some patients describe
an initial physiologic
resistance to increased fluid
intake which eases as their bodies
and minds learn the new
habit of extra fluid intake and
output. According to Parks,
Goldfischer, and Coe (2003),
aims by clinicians to increase
patients’ urinary volumes often
fall short, and follow-up metabolic
studies showed an average
increase in urine output of only
0.3 liters per 24 hours. This
increase was associated with a
curious increase in sodium
intake. High urine volumes
should be the goal of all patients
who form stones. In this
instance, more is definitely better.
Most patients find that after
forcing fluids for a couple of
months, their bodies crave fluids
and their habit is to drink more.
Consume Adequate Calcium
High urine calcium, hypercalciuria,
is associated both with
formation of kidney stones and
with osteoporosis. Sufficient calcium
intake is required for the
growth and maintenance of the
skeleton in children and adults.
Reducing urine calcium should
be a goal for stone formers, but
not via dietary restriction. While
reduced dietary calcium can
decrease urine calcium (Lemann,
2002), calcium restriction is no
longer advisable for patients who
form calcium kidney stones as
this puts them at risk of bone disease,
namely osteoporosis. Recall
that bones are in a constant
process of resorption and formation;
adequate calcium is required
for the ongoing rebuilding of bone
material.
Several recent studies have
shown, in fact, that adequate calcium
intake is associated with
decreased stone formation.
Curhan, Willett, Knight, and
Stampfer (2004) found that in
previously non-stone forming
younger women, higher intake of
dietary calcium was related to
lower risk of kidney stone formation.
Additionally, a 5-year randomized
clinical trial of men
with a history of calcium oxalate
stones found that a normal calcium,
decreased sodium, and
decreased animal protein diet
was more effective for reducing
stone events than was a restricted
calcium diet (Borghi et al., 2002).
So, adequate calcium plus
decreased sodium and protein
intake had a significantly more
protective effect against stones
than decreased calcium intake
alone.
Why might increased dietary
calcium reduce the risk of calcium
stone formation? Calcium
and oxalate bind in the gut and
in the urine to form a nonabsorbable
compound. Low dietary
calcium permits greater free
oxalate to be absorbed in the gut
and excreted in the urine, which
may be counterproductive for
calcium oxalate stone formers.
Restricted calcium intake results
in increased urinary oxalates, a
risk for stone formation (Menon
& Resnick, 2002). This is a proposed
cause of the association
between reduced calcium intake
and increased supersaturation of
calcium oxalate (Lemann, 2002).
Clearly, strong research evidence
now supports adequate
calcium intake for patients who
form kidney stones. Low-fat
dairy products, green leafy vegetables,
broccoli, fortified foods,
and almonds are excellent
sources. Patients should consume
enough dietary calcium to
meet (but not exceed) the United
States Recommended Daily
Allowance (RDA) of calcium,
which ranges from 1,000 to 1,200
milligrams daily for adults. The
recommendations are the same
for men and women, but vary by
age group (see Table 1). Patients
should avoid calcium supplements
in favor of calcium-rich
foods; a patient with intolerance
to dairy products may supplement,
but should not exceed the
RDA for his/her age group.
Limit Dietary Oxalates
Oxalate is found in many
foods, but there is considerable
variability in the amount, which
depends upon where the food is
grown. Likewise, individual
absorption of oxalate also varies,
which makes adequate calcium
intake critically important.
Nonetheless, oxalate restriction
should be attempted. The highest
levels of oxalate are found in
chocolate, nuts, beans (including
soybeans), rhubarb, spinach,
beets, and black tea. A thorough
oxalate list can be found on the
Web site of the Oxalosis and
Hyperoxaluria Foundation (http://
www.ohf.org/diet.html). This list
is exhaustive and may be overwhelming
to patients. Stress that
reduction of high oxalate foods is
the goal for typical stone formers
rather than strict avoidance of all
oxalate-containing foods (which
would be very difficult). Followup
24-hour urine studies will demonstrate
the adequacy of patients’
restriction.
Though only 10% to 20% of
urinary oxalates come from
dietary sources (Morton, Iliescu,
& Wilson, 2002), dietary reduction
is commonly advised for calcium
oxalate stone formers. It has
been suggested that because
there is much less oxalate in the
urine than calcium in the urine,
urinary oxalate concentration is
much more critical to the formation
of calcium oxalate crystals
than is the urinary calcium concentration;
reducing urine oxalates
may have a more powerful effect
on stone formation than can reduction
of urine calcium (Morton et
al., 2002). Patients with calcium
oxalate stones, particularly those
with documented hyperoxaluria,
should avoid foods high in
oxalates. Vitamin C is a precursor
to endogenous production of
oxalates, so some clinicians recommend
avoiding mega-doses of
vitamin C. The rare genetic condition
of primary hyperoxaluria is
only slightly impacted by dietary
reduction, and causes serious
medical problems besides kidney
stones.
Limit Sodium Intake
Because calcium and sodium
compete for reabsorption in the
renal tubules, excess sodium
intake and consequent excretion
result in loss of calcium in the
urine. High-sodium diets are
associated with greater calcium
excretion in the urine (Lemann,
2002). Metabolic studies often
reveal exceptionally high urine
calcium over 24 hours, related to
patients’ exceptionally high sodium
excretion. Patients may deny
salt intake, stating, “I never salt
my food!” They quite likely are
ignorant of hidden sodium
sources in the diet. Sodium is a
common preservative in canned
and frozen foods, and is endemic
in restaurant foods. Instruction
on careful inspection of food
labels and wise food choices
helps patients identify and
reduce sodium in their diets.
A notable dietary “ah-ha!”
was the admission by one patient
that, on the day of 24-hour urine
testing, she ate a full jar of pickles
to reduce stress, and then
drank the brine; needless to say,
her urine sodium was very high
on the day of her stress mitigation.
The role of the nurse or dietician
in shedding light on sources
of sodium cannot be underestimated.
Repeated, persistent inquiry
into dietary habits may be necessary.
The goal of therapy should be
a “no added salt diet,” or the equivalent
of 2,000 mg per day or less of
dietary sodium. Reduction of
dietary sodium is difficult and disappointing
to patients. They may
believe they have made significant
reductions and sacrifices, while
their urine sodium remains high.
Consultation with a registered
dietician may help the patient
achieve the specific goal of a sodium
intake of 2,000 milligrams or
less per day.
Limit Animal Protein
The effect of excess animal
protein (purine) is most obvious
for the uric acid stone former.
Uric acid, a byproduct of purine
metabolism, is excreted in large
quantities in the urine. Excess
protein creates urine with high
total urine uric acid, potentially
high supersaturation of urine
uric acid, and a low pH, necessary
for formation of uric acid
stones. There is no inhibitor of
uric acid crystal formation
(Menon & Resnick, 2002), so
dietary measures focus on reducing
uric acid and increasing
urine volume. Reduction of animal
protein to 12 ounces per day
for adults is recommended. This
is plenty to meet the dietary
needs of most Americans, many
of whom typically consume several
more ounces of animal protein
daily than is recommended.
Protein from plant sources
(beans, legumes, etc.) can be substituted
as a dietary alternative
without negative consequences.
Calcium oxalate stone formers
reducing their animal protein
should note the oxalate content
of substitute proteins.
The role of excess protein in
promoting calcium stone formation
is less obvious, but equally
important. High dietary protein
is associated with increased urinary
calcium. Thus, there is a
link between meat consumption
and both uric acid and calcium
stone formation. In fact, vegetarians
form stones at one-third the
rate of those eating a mixed diet
(Lemann, 2002). A study of 18
hypercalciuric stone formers found
that a 15-day protein restriction
had many positive effects on urinary
markers of stone risk.
Namely, significant decreases
were seen in urine calcium, urine
uric acid, urine phosphate, and
urine oxalate. And, for unclear
reasons, a beneficial increase in
urinary citrate was observed
(Giannini et al., 1999). Citrate is a
known inhibitor of calcium
oxalate crystal formation and
also increases pH, which can prevent
uric acid stones. Clearly, the
benefits of protein restriction for
stone formers are many.
Weight Loss
A relationship between weight,
body mass index and risk of calcium
oxalate stone formation was
established in a retrospective
study of health professionals.
Curhan and colleagues (1998)
found that “the prevalence of
stone disease history and the
incidence of stone disease were
directly associated with weight
and body mass index. However,
the magnitude of the associations
was consistently greater among
women” (p. 1645). The value of
weight loss for stone prevention
has not been proven, but given
the benefits of weight loss for
general health, it is certainly
worth mentioning to overweight
patients who form stones.
Educational Resources
There are excellent resources
on the Internet for patients seeking
nutritional information. One stellar
example is NutritionData
(www.nutritiondata.com/). Here
patients can search by general food
category, like “pickle,” to view the
standard sodium content, as well
as a plethora of additional information
regarding vitamin and mineral
content, calories, suggested healthier
substitutes, and even the individual
amino acid compositions of
each protein. The site also provides
detailed information about
thousands of specific brand items
from grocery and fast food restaurants.
Under “Tools,” patients can
search within food categories like
“dairy products” for choices highest
in calcium and lowest in sodium.
This site is complex and may be
overwhelming to patients without
good computer and Web skills, but
is extraordinarily comprehensive;
unfortunately, this site does not list
oxalate content. For that purpose,
refer patients to www.ohf.org.
For patients without Web
access, nurses might find it helpful
to review a general nutrition
book for charts and diagrams to
help patients understand nutrition
content. Show patients a
sample food label from a can of
soup so they know where to find
sodium content on foods at home.
For a simple list of high-oxalate
foods, visit www.gicare.com/
pated/edtgs29.htm.
Conclusion
The dietary measures discussed
have value particularly
for patients who form the most
common types of kidney stones:
calcium oxalate and uric acid.
That said, they may be insufficient
to control the various metabolic
abnormalities present in
individual patients. The most
effective management of kidney
stones includes in-depth metabolic
studies, recommendations
tailored to patients regarding
medications and dietary changes,
and follow-up to ensure changes
are having the desired effect.
Urine studies should be repeated
to judge progress approximately
6 to 8 weeks after initial metabolic
testing recommendations are
implemented. Once a stable state
is reached in which the patient’s
urine demonstrates decreased
risk of stone formation, metabolic
testing should be performed
(along with an x-ray to check for
stone growth) at least annually to
monitor stone risk. The cycle of
stone formation can be altered,
and in some cases broken, with
the aid of effective dietary management.
Every patient need not make
all of these changes to his/her
diet, but in the absence of
patient-specific urine studies,
none of these recommendations
is harmful. Aside from oxalate
consumption, the dietary recommendations
for calcium oxalate
and uric acid stone formers are
the same. Assessing
patients’ dietary habits can shed
light on potential areas of
improvement. For example, a
receptive uric acid stone former
on a high-protein diet for weight
loss could benefit from counseling
on the effects of this diet on
his/her stone disease.
Of course, talking about
dietary changes is easier than actual
implementation. Encourage
patients to make changes at a realistic
pace. Praise even modest
progress and stress the value of
striving for improvement rather
than perfection.
The Bottom Line here is;
•Urinate more than two liters per day.
• Consume enough dietary calcium to meet the US RDA.
• Avoid dietary oxalates (for calcium oxalate stone-formers).
• Limit sodium to 2,000 milligrams per day.
• Limit protein to 12 ounces per day.
• If overweight, lose weight.
Monday, August 27, 2007
We Keep Getting Fatter
Obesity rates climb in most states
By KEVIN FREKING, Associated Press
Loosen the belt buckle another notch: Obesity rates continued their climb in 31 states last year. No state showed a decline.
Mississippi became the first state to crack the 30 percent barrier for adult residents considered to be obese. West Virginia and Alabama are just slightly behind, according to the Trust for America's Health, a research group that focuses on disease prevention.
Colorado continued its reign as the leanest state in the nation with an obesity rate projected at 17.6 percent.
This year's report, for the first time, looked at rates of overweight children ages 10 to 17. The District of Columbia had the highest percentage — 22.8 percent. Utah had the lowest percentage of overweight youth — 8.5 percent.
Health officials say the latest state rankings provide evidence that the nation has a public health crisis on its hands.
Unfortunately, we're treating it like a mere inconvenience instead of the emergency that it is," said Dr. James Marks, senior vice president at the Robert Wood Johnson Foundation,a philanthropy devoted to improving health care.
Officials at the Trust for America's Health advocate for the government to play a larger role in preventing obesity. People who are overweight are at an increased risk for diabetes, heart problems and other chronic diseases that contribute to greater health care costs.
"It's one of those issues where everyone believes this is an epidemic, but it's not getting the level of political and policymaker attention that it ought to," said Jeffrey Levi, the organization's executive director. "As every candidate for president talks about health care reform and controlling health care cost costs, if we don't hone in on this issue, none of their proposals are going to be affordable."
At the same time, many believe weight is a personal choice and responsibility. Levi doesn't dispute that notion, but he said society can help people make good choices.
"If we want kids to eat healthier food, we have to invest the money for school nutrition programs so that school lunches are healthier," he said. "If we want people to be more physically active, then there have to be safe places to be active. That's not just a class issues. We've designed suburban communities where there are no sidewalks for anybody to go out and take a walk."
To measure obesity rates, Trust for America's Health compares data from 2003-2005 with 2004-2006. It combines data from three years to improve the accuracy of projections. The data come from a survey of height and weight taken over the telephone. Because the information comes from a personal estimate, some believe it is conservative.
Indeed, the Centers for Disease Control and Prevention released a study last year noting a national obesity rate of about 32 percent — a higher rate than was cited for any of the states in the Trust for America's Health report. The CDC's estimate came from weighing people rather than relying on telephone interviews, officials explained.
Generally, anyone with a body mass index greater than 30 is considered obese. The index is a ratio that takes into account height and weight. The overweight range is 25 to 29.9. Normal is 18.5 to 24.9. People with a large amount of lean muscle mass, such as athletes, can show a large body mass index without having an unhealthy level of fat.
A lack of exercise is a huge factor in obesity rates. The Centers for Disease Control and Prevention found last year that more than 22 percent of Americans did not engage in any physical activity in the past month. The percentage is greater than 30 percent in four states: Mississippi, Louisiana, Kentucky and Tennessee.
Meanwhile, Minnesotans led the way when it came to exercise. An estimated 15.4 percent of the state's residents did not engage an any physical exercise — the best rate in the nation. Still, the state ranked 28th overall when it came to the percentage of obese adults.
Another factor in obesity rates is poverty. The five poorest states were all in the top 10 when it came to obesity rates. An exception to that rule was the District of Columbia and New Mexico. Both had high poverty rates, but also one of the better obesity rates among adults.
Officials said the report is not designed to stigmatize states with high obesity rates but to stir them into action.
"These are the states where the urgency is the greatest. They need not to wait for others to lead. They need to become the leaders," Marks said. "It's the only way that they can restore the health of their children and their families. It's the only way that they can improve their economic competitiveness."
By KEVIN FREKING, Associated Press
Loosen the belt buckle another notch: Obesity rates continued their climb in 31 states last year. No state showed a decline.
Mississippi became the first state to crack the 30 percent barrier for adult residents considered to be obese. West Virginia and Alabama are just slightly behind, according to the Trust for America's Health, a research group that focuses on disease prevention.
Colorado continued its reign as the leanest state in the nation with an obesity rate projected at 17.6 percent.
This year's report, for the first time, looked at rates of overweight children ages 10 to 17. The District of Columbia had the highest percentage — 22.8 percent. Utah had the lowest percentage of overweight youth — 8.5 percent.
Health officials say the latest state rankings provide evidence that the nation has a public health crisis on its hands.
Unfortunately, we're treating it like a mere inconvenience instead of the emergency that it is," said Dr. James Marks, senior vice president at the Robert Wood Johnson Foundation,a philanthropy devoted to improving health care.
Officials at the Trust for America's Health advocate for the government to play a larger role in preventing obesity. People who are overweight are at an increased risk for diabetes, heart problems and other chronic diseases that contribute to greater health care costs.
"It's one of those issues where everyone believes this is an epidemic, but it's not getting the level of political and policymaker attention that it ought to," said Jeffrey Levi, the organization's executive director. "As every candidate for president talks about health care reform and controlling health care cost costs, if we don't hone in on this issue, none of their proposals are going to be affordable."
At the same time, many believe weight is a personal choice and responsibility. Levi doesn't dispute that notion, but he said society can help people make good choices.
"If we want kids to eat healthier food, we have to invest the money for school nutrition programs so that school lunches are healthier," he said. "If we want people to be more physically active, then there have to be safe places to be active. That's not just a class issues. We've designed suburban communities where there are no sidewalks for anybody to go out and take a walk."
To measure obesity rates, Trust for America's Health compares data from 2003-2005 with 2004-2006. It combines data from three years to improve the accuracy of projections. The data come from a survey of height and weight taken over the telephone. Because the information comes from a personal estimate, some believe it is conservative.
Indeed, the Centers for Disease Control and Prevention released a study last year noting a national obesity rate of about 32 percent — a higher rate than was cited for any of the states in the Trust for America's Health report. The CDC's estimate came from weighing people rather than relying on telephone interviews, officials explained.
Generally, anyone with a body mass index greater than 30 is considered obese. The index is a ratio that takes into account height and weight. The overweight range is 25 to 29.9. Normal is 18.5 to 24.9. People with a large amount of lean muscle mass, such as athletes, can show a large body mass index without having an unhealthy level of fat.
A lack of exercise is a huge factor in obesity rates. The Centers for Disease Control and Prevention found last year that more than 22 percent of Americans did not engage in any physical activity in the past month. The percentage is greater than 30 percent in four states: Mississippi, Louisiana, Kentucky and Tennessee.
Meanwhile, Minnesotans led the way when it came to exercise. An estimated 15.4 percent of the state's residents did not engage an any physical exercise — the best rate in the nation. Still, the state ranked 28th overall when it came to the percentage of obese adults.
Another factor in obesity rates is poverty. The five poorest states were all in the top 10 when it came to obesity rates. An exception to that rule was the District of Columbia and New Mexico. Both had high poverty rates, but also one of the better obesity rates among adults.
Officials said the report is not designed to stigmatize states with high obesity rates but to stir them into action.
"These are the states where the urgency is the greatest. They need not to wait for others to lead. They need to become the leaders," Marks said. "It's the only way that they can restore the health of their children and their families. It's the only way that they can improve their economic competitiveness."
Friday, August 17, 2007
Whole grains may lower odds of high blood pressure
Women who get plenty of whole grains in their diet may lower their risk of developing high blood pressure, a large study suggests.
Researchers found that middle-aged and older women who ate the most whole grains were less likely than those with the lowest intakes to develop high blood pressure over the next 10 years.
The benefit was modest. Women who consumed the most whole grains had an 11-percent lower risk of high blood pressure than those with the lowest intakes.
But the findings add to evidence of the cardiovascular benefits of whole grains such as oatmeal, bran and brown rice. Past studies have tied diets rich in these foods to lower risks of heart disease and stroke.
The fiber and other nutrients in whole grains may help lower cholesterol, blood sugar and insulin levels, as well as improve blood vessel functioning and reduce inflammation in the circulatory system. Whether whole grains benefit blood pressure has been unclear, however.
For the current study, researchers at Harvard University in Boston used data from the Women's Health Study, which has followed nearly 40,000 U.S. female health professionals since 1992. Upon entering the study, the women completed detailed questionnaires on their diet habits, including their usual intake of whole-grain foods like dark bread, popcorn, oatmeal and whole-grain breakfast cereals.
Of the nearly 30,000 women who were free of high blood pressure at the outset, those who ate the most whole grains had a lower risk of developing the condition. The apparent protective effect held when the researchers considered other factors, like weight, smoking and exercise habits.
In contrast, refined grains -- like pasta, white bread and other foods made from white flour -- were unrelated to high blood pressure risk, according to the researchers, led by Dr. Lu Wang.
Unlike whole grains, refined grains are largely stripped of the fiber- and nutrient-rich bran and germ components of the plant. This difference may explain why only whole grains were related to lower blood pressure, according to Wang's team.
The findings, the researchers conclude, suggest that people may do their blood pressure and heart health some good by replacing refined-grain foods with whole grains.
SOURCE: American Journal of Clinical Nutrition, August 2007.
Women who get plenty of whole grains in their diet may lower their risk of developing high blood pressure, a large study suggests.
Researchers found that middle-aged and older women who ate the most whole grains were less likely than those with the lowest intakes to develop high blood pressure over the next 10 years.
The benefit was modest. Women who consumed the most whole grains had an 11-percent lower risk of high blood pressure than those with the lowest intakes.
But the findings add to evidence of the cardiovascular benefits of whole grains such as oatmeal, bran and brown rice. Past studies have tied diets rich in these foods to lower risks of heart disease and stroke.
The fiber and other nutrients in whole grains may help lower cholesterol, blood sugar and insulin levels, as well as improve blood vessel functioning and reduce inflammation in the circulatory system. Whether whole grains benefit blood pressure has been unclear, however.
For the current study, researchers at Harvard University in Boston used data from the Women's Health Study, which has followed nearly 40,000 U.S. female health professionals since 1992. Upon entering the study, the women completed detailed questionnaires on their diet habits, including their usual intake of whole-grain foods like dark bread, popcorn, oatmeal and whole-grain breakfast cereals.
Of the nearly 30,000 women who were free of high blood pressure at the outset, those who ate the most whole grains had a lower risk of developing the condition. The apparent protective effect held when the researchers considered other factors, like weight, smoking and exercise habits.
In contrast, refined grains -- like pasta, white bread and other foods made from white flour -- were unrelated to high blood pressure risk, according to the researchers, led by Dr. Lu Wang.
Unlike whole grains, refined grains are largely stripped of the fiber- and nutrient-rich bran and germ components of the plant. This difference may explain why only whole grains were related to lower blood pressure, according to Wang's team.
The findings, the researchers conclude, suggest that people may do their blood pressure and heart health some good by replacing refined-grain foods with whole grains.
SOURCE: American Journal of Clinical Nutrition, August 2007.
Wednesday, August 15, 2007
Brain Food from Wikipedia
Nootropic
Nootropics, popularly referred to as "smart drugs" and "smart nutrients", are substances which boost human cognitive abilities (the functions and capacities of the brain). The word nootropic was coined in 1964 by the Romanian Dr. Corneliu E. Giurgea, derived from the Greek words noos, or "mind," and tropein meaning "to bend/turn." Typically, nootropics are alleged to work by increasing the brain's supply of neurochemicals (neurotransmitters, enzymes, and hormones), by improving the brain's oxygen supply, or by stimulating nerve growth.
Most alleged nootropic substances are nutrients or plant components (herbs, roots, beans, bark, etc.), available over the counter at health food and grocery stores, and are used as nutritional supplements. Some nootropics are drugs, used to treat people with cognitive learning difficulties, neural degradation (Alzheimer's disease or Parkinson's disease), and for cases of oxygen deficit to prevent hypoxia. These drugs have a variety of human enhancement applications as well, are marketed heavily on the World Wide Web, and are used by many people in personal cognitive enhancement regimens.
While scientific studies support some of the claimed benefits, it is worth noting that many of the claims attributed to most nootropics have not been formally tested.
General strategies
Neurotransmitter support - supplying the body with the precursors and cofactors it needs to produce neurotransmitters.
Note that cardiovascular exercise performed on a regular basis also has nootropic effects, by increasing the body's capacity to supply brain cells with oxygen.
Nootropic substances
Nootropic drugs are generally only available by prescription or through personal importation. The other nootropic substances listed below are either nutritional supplements or plant components, and are generally available over the counter at health food and grocery stores. The term "drug" here is used as a legal designation, and does not indicate greater efficacy. With nootropics, the effects, effectiveness, and potency differ from substance to substance and from individual to individual. See the substance descriptions below for more detail.
Replenishing and increasing neurotransmitters
Thinking is a biologically demanding task. It involves the firing of neurons, which requires ample neurotransmitters, and even though these are reuseable to some extent, they do get depleted. Depletion of neurotransmitters generally results in reduced mental performance, which may include difficulty concentrating, slowed reasoning, decreased learning efficiency, impaired recall, reduced coordination, lowered moods, inability to cope, increased response times, and mental fatigue. This also generally increases the likelihood of human error on tasks and activities performed. Stress causes neurotransmitters to be depleted even faster. The brain's neurotransmitters need to be replenished frequently, made by the body from substances ingested in the diet. Maintaining neurochemicals at optimal levels has a corresponding effect on brain performance, supporting improved mental agility and stamina, even beyond the individual's normal limits.
As the brain ages, its ability to produce and maintain youthful levels of neurotransmitters declines. Thus, the theory is that providing the brain with ample raw materials necessary to make neurotransmitters can restore them to more youthful levels and thus help maintain cognitive function at vigorous youthful levels as well.
Cholinergics
Cholinergics are substances that affect the neurotransmitter acetylcholine or the components of the nervous system that use acetylcholine. Acetylcholine facilitates memory, concentration, focus, and high-order thought processes (abstract thought, calculation, innovation, etc.). Increasing the availability of this neurotransmitter in the brain may improve these functions and increase the duration in which they may be engaged without slowing down or stopping. Oversupplying the brain with acetylcholine may have the opposite effect, temporarily reducing rather than improving mental performance. Cholinergic nootropics include acetylcholine precursors and cofactors, and acetylcholinesterase inhibitors:
• Acetyl-L-carnitine (ALCAR) - Amino acid. Precursor of acetylcholine (donating the acetyl portion to the acetylcholine molecule). It is synergistic with lipoic acid.
• Centrophenoxine (Lucidril) - Drug. Cholinergic agent, enhances color perception.
• Choline - precursor to acetylcholine (an essential component of the acetylcholine molecule).
o Alpha-GPC (L-alpha glycerylphosphorylcholine, Choline alfoscerate) - most effective choline precursor, readily crosses the blood-brain barrier.
o CDP-Choline (Cytidine Diphosphate Choline) - choline precursor, tends to be less expensive and similar in effect to Alpha GPC.
o Choline bitartrate - precursor of acetylcholine, anti-depressant.
o Choline citrate - precursor of the neurotransmitter acetylcholine, anti-depressant.
• DMAE - approved treatment for ADD/ADHD, precursor of acetylcholine, cholinergic agent, removes lipofuscin from the brain, anti-depressant.
• Huperzine A - potent acetylcholinesterase inhibitor derived from Chinese club-moss.
• Lecithin - contains phosphatidylcholine, precursor of acetylcholine.
• Pyrrolidone derivatives:
o Piracetam (Nootropil) - Prescription drug (in Europe). The original (first), and most commonly taken nootropic drug. It is a cholinergic agent, synergistic with DMAE, centrophenoxine, choline, and Hydergine. Increases brain cell metabolism and energy levels, and speeds up interhemispheric flow of information (left-right brain hemisphere communication). Increases alertness, improves concentration, and enhances memory. Protects neurons from hypoxia, and stimulates growth of acetylcholine receptors. May also cause nerves to regenerate. Piracetam markedly decreases the formation of neuronal lipofuscin. It improves posture in elderly people. It is not regulated in the US.
o Aniracetam - Drug. Analog of piracetam, and 4 to 8 times more potent. Like piracetam, aniracetam protects against some memory impairing chemicals, such as diethyldithiocarbamate and clonidine. Also like piracetam, aniracetam may enhance memory in aging adults by increasing levels of brain biogenic monoamines, which are beneficial to learning and memory. Both racetams have possible therapeutic use in treating fetal alcohol syndrome. Aniracetam increases vigilance.
o Etiracetam - It increases vigilance.
o Nefiracetam - Drug. Analog of piracetam, and facilitates hippocampal neurotransmission.
o Oxiracetam - Drug. Analog of piracetam, and 2 to 4 times stronger. Improves memory, concentration, and vigilance. When fed to pregnant rats, the offspring of those rats were more intelligent than the offspring of rats fed a saline solution placebo.
o Pramiracetam - Drug. Fifteen times stronger than piracetam, of which it is an analog.
• Vitamin B5 - cofactor in the conversion of choline into acetylcholine, cholinergic agent, increases stamina (including mental stamina).
Excess acetylcholine is considered by many to be potentially harmful; see cholinesterase inhibitor.
Dopaminergics
Dopaminergics are substances that affect the neurotransmitter dopamine or the components of the nervous system that use dopamine. Dopamine is produced in the synthesis of all catecholamine neurotransmitters, and is the rate limiting step for this synthesis. Dopaminergic nootropics include dopamine precursors and cofactors, and dopamine reuptake inhibitors:
• L-dopa - Prescription drug. Precursor to the neurotransmitter dopamine, anti-depressant.
• Phenylalanine (requires Vitamin B6 and Vitamin C) - Essential amino acid. Precursor to dopamine, anti-depressant, sleep reducer.
• Theanine - Found in tea. Increases serotonin and dopamine levels in the brain. Increases alpha-wave based alert relaxation.
• Tyrosine (requires Vitamin B6 and Vitamin C) - Amino acid. Precursor to dopamine, anti-depressant, sleep reducer.
• Vitamin C- improves cardiovascular elasticity and integrity, membrane stabilizer and major anti-oxidant (protects brain cells and prevents brain cell death), cofactor in the production of the neurotransmitters dopamine and serotonin.
• Vitamin B6 - co-factor used by the body to produce dopamine.
• Yohimbe - Bark. Boosts dopamine levels as much as 80%, though how it does this is not yet understood. Aphrodisiac. Yohimbe poses some health risks through its side-effects: it is a neuro-paralytic which slows down breathing and induces acidosis, some symptoms of which are malaise, nausea, and vomiting. Contraindicated for users of megadoses of acidic vitamins or nutrients.
• Deprenyl - Inhibits MAO B (an enzyme that breaks down dopamine) thus raising dopamine by partially inhibiting its breakdown.
• Tolcapone - Inhibits COMT (an enzyme that breaks down the neurotransmitters dopamine, epinephrine, and norepinephrine) and increases performance in tasks depending on working memory in individuals with the val/val and val/met genotype of the val158Met polymorphism of the catechol-O-methyltransferase gene, while decreasing it in presence of the met/met version. Tolcapone presents the risk of deadly side effects.
Serotonergics
Serotonergics are substances that affect the neurotransmitter serotonin or the components of the nervous system that use serotonin. Serotonergic nootropics include serotonin precursors and cofactors, and serotonin reuptake inhibitors:
• 5-HTP - more bioavailable form of tryptophan, precursor to the neurotransmitter serotonin, promotes relaxed poise and sound sleep.
• Griffonia simplicifolia a natural source of 5-HTP (an alternative in countries where 5-HTP not legal, freely available.)
• Tryptophan (requires Vitamin B6 and Vitamin C) - Essential amino acid. Precursor to serotonin, found in high concentration in bananas and poultry (especially turkey), also in milk, promotes relaxed poise and sound sleep.
• 5HT2A agonists such as LSD and 2C-T-7 have been shown to produce nootropic effects when used at a dose much lower than a hallucinogenic dose. (e.g. 10 μg for LSD and 1 mg 2C-T-7, 1/25 of a normal recreational dose )
Anti-depression, adaptogenic and mood stabilization
Depression and depressed mood negatively affect cognitive performance. Feelings of sadness, guilt, helplessness, hopelessness, anxiety, and fear caused by depression detract from productive thought, while apathy (which is also induced by depression) is the lack of motivation and driving moods (like curiosity, interest, determination, etc.) Other symptoms include disturbed sleep patterns, mental fatigue and loss of energy, trouble concentrating or making decisions, and a generalized slowing and obtunding of cognition, including memory. Obviously, removing these effects improves intelligence and mental performance, and therefore, counteracting and preventing depression are effective nootropic strategies. There is a high correlation between depression and a reduction or depletion of neurotransmitters (dopamine, acetylcholine, and serotonin) in the brain, therefore it is no surprise that increasing the brain's supply of neurotransmitters alleviates (or at least reduces the symptoms of) most depressions. Stress is another major factor in neurotransmitter depletion, being both a cause and effect of it (creating a vicious downward spiral), therefore stress management and anti-stress substances are also very useful nootropic strategies.
All of the "nergics" listed above have been found to increase stress tolerance and alleviate depression (by replenishing or increasing the brain's supply of specific neurotransmitters)[citation needed], especially when used in precursor/co-factor combinations[citation needed].
Below are additional more nootropics which affect mood and stress:
• Ashwagandha (Withania somnifera) - Root. Also known as Indian ginseng. Adaptogen used as a tonic to normalize body processes and reduce stress and anxiety.
• Inositol - Is a B-vitamin like substance with anti-anxiety effects. It is believed to produce its anti-anxiety effects by improving the binding of gabaergics to GABAA receptors. Inositol is a sugar, and is therefore an alternative energy source for brain and muscle tissues. It produces a sugar high without a sugar low, making it especially suited for sweetening tea (instead of sugar). It is also a membrane stabilizer which can strengthen (and therefore help protect) neurons.
• Lemon Balm (Melissa officinalis) - Herb. Anti-depressant.
• Rhodiola Rosea - Herb. Adaptogen; elevates mood, alleviates depression. Promotes mental energy and stamina, reduces fatigue.
• St John's Wort - Herb. The active components: hypericin and hyperforin, are clinically indicated to be effective in cases of mild to medium depression.
• Ginseng, Siberian (Eleutherococcus senticosus) - Root. Anti-anxiety adaptogen that normalizes physical stress and mental consequences.
• Selegiline (Deprenyl) - Along with Piracetam and Meclofenoxate, Deprenyl decreases the amount of lipofuscin pigment and ceroid pigment accumulations in the brain by improving cellular recycling activities. Therefore, these nootropics may slow age-related diseases in the brain.
• Sutherlandia frutescens - Herb. Adaptogen, blood detoxifier.
• Tea - Herb. Contains theophylline and theanine. Increases alpha-wave based alert relaxation (relieves stress).
• Theanine - Amino acid. Found in tea. Increases serotonin and dopamine levels in the brain. Increases alpha-wave based alert relaxation.
• Vasopressin - Drug. Memory hormone produced by the pituitary gland which improves both memory encoding and recall. Rapidly counters chronic apathy syndrome and drug-induced vasopressin depletion.
• Nicotinic acid (vitamin B3) - Essential nutrient. Mild enhancer of concentration and memory. Vasodilator. Mood stabilizer, with a powerful anti-anxiety effect — perhaps the best and most immediate stress reliever available (note that other forms of vitamin B do not have this effect). Side effects: gastric upset (which is easily prevented and relieved with antacids), reduced blood pressure and flushing of the skin (caused by vasodilation), and itchy sensation in the skin caused by histamine release.
Brain energy and improved oxygen supply
• Acetyl-L-carnitine (ALCAR) - Amino acid. Transports fatty acids through cellular membranes and cytosol into cells' mitochondria, where the fats undergo oxidation to produce ATP, the universal energy molecule. Synergistic with lipoic acid.
• Chromium- stabilises blood sugar levels promoting concentration.
• Coenzyme q-10 syn. Ubiquinone - increases oxygen transport through the mitochondria of the cells. Appears to slow age-related dementia.
• Creatine - increases brain energy levels via ATP production.
• Inositol -
• Lipoic acid - synergistic with Acetyl-L-carnitine.
• Piracetam - improves alertness, blood flow, oxygen supply, and stroke recovery.
• Pyritinol (Enerbol) - Drug. Enhances oxygen and glucose uptake in the brain, and allows glucose to pass more easily through the blood-brain barrier. It is also a powerful anti-oxidant which scavenges hydroxyl radicals created in the very processes it is involved in.
• Vinpocetine - micro-circulation enhancer, improves oxygen supply to brain cells.
Mental agility, concentration, stamina, and focus
• Adrafinil (Olmifon) - Drug.
• Caffeine - improves concentration, idea production, but hinders memory encoding. Also produces the jitters. Caffeine is the most widely used psychoactive substance in the world, it may be susceptible to strong levels of tolerance.
• Coffee - Bean. Contains caffeine; brewed coffee is high in antioxidants.
• Nicergoline - Drug. Nicergoline is an ergoloid mesylate derivative used to treat senile dementia. It has also been found to increase mental agility and enhance clarity and perception. It increases vigilance. Increases arterial flow and use of oxygen and glucose in the brain.
• Nicotine - stimulus barrier (aids in concentration). Stimulus barrier rebound effect (an unpleasant side effect).
• Cocaine - Drug
• Methylphenidate (Ritalin) - Drug
• Dextroamphetamine - (Adderall, Dexedrine) - Drug
• Modafinil - (Provigil) - Drug.
• Piracetam - improves alertness, socialization, and co-operation in the brain impaired from age, dementia, and reduced blood flow.
• Phenibut -
• Theophylline -
• Amphetamine -
Purported memory enhancement and learning improvement
All of the "nergics" listed above are purported to improve memory (encoding and recall), As do all nootropics which improve general brain performance in categories such as the brain energy and oxygen supply, and nerve growth stimulantion and protection. Other agents purported to have these specific benefits are mentioned in their own sections.
Other nootropics with specific effects on memory encoding and recall include:
• Bacopa monniera (Brahmi) - Herb. Elevates curiosity, enhances memory and concentration. Brahmi also protects against amnesia inducing chemicals such as scopolamine or loss of memory due to electro convulsive shocks. It is a traditional ayurvedic medicine.
• Piracetam - improves memory, Alzheimer's, dementia, dyslexia and Down's syndrome
• Rosemary - Herb. Rosemary has a very old, albeit unverified, reputation for improving memory.
• Vasopressin - Hormone, prescription drug.
• Dextroamphetamine- Adderall, Dexedrine.[13]
Nerve growth stimulation and brain cell protection
• Acetyl-L-carnitine (ALCAR) - Amino acid. Inhibits lipofuscin formation.
• Bacopa monnieri (Brahmi) - Herb. Improves protein synthesis in brain cell repair and new dendritic growth.
• Selegiline (Deprenyl) - Drug. Brain cell protectant, delays senescence of brain cells, proven to increase maximum life span in laboratory rats.
• Ergoloid mesylates (Hydergine) - Drug. Mimics nerve growth factor (NGF), and is a powerful anti-oxidant capable of delaying brain death in cases of heart failure and stroke by several minutes with regular use. It increases vigilance.
• Idebenone - stimulates nerve growth, and has same effects as Coenzyme q-10 - boosters claim that CoQ10 has "harmful side-effects", a claim which has not been demonstrated in published peer-reviewed studies.
• Inositol - Membrane stabilizer. Strengthens neurons, making them less susceptible to damage.
• Pyritinol (Enerbol) - Drug. Powerful anti-oxidant which scavenges hydroxyl radicals. Also enhances oxygen and glucose uptake in the brain, and allows glucose to pass more easily through the blood-brain barrier. Improves general brain function.
• Rasagiline (Azilect) - Drug. Treats Parkinson’s disease either as monotherapy (by itself) or in addition to levodopa therapy. Promotes increased and sustained levels of dopamine by selectively inhibiting an enzyme, monoamine oxidase-B.
• Vitamin C - Membrane stabilizer, involved in collagen synthesis. Strengthens neurons, making them less susceptible to damage. Vitamin C is also a co-factor in the brain's production of dopamine.
Recreational drugs with purported nootropic effects
See also: Controlled substances act and Misuse of Drugs Act 1971
• Amphetamines (Adderall, Dexedrine) - Schedule II / Class B drugs. Prescribed for attention-deficit disorders, narcolepsy, and certain cases of obesity; and issued as an anti-fatigue pill for pilots in the armed forces. These also heighten alertness, mental focus, vigilance, stamina, and sex drive. They are highly addictive, and have many side effects. Personal importation is prohibited. Using these recreationally or for performance enhancement is illegal in most countries.
• Cannabis is reported to heighten the ability of the senses, as well as heighten alpha wave activity in the brain associated with creativity.
• LSD - Schedule I / Class A drug. At minuscule doses (1 μg) the drug has effects similar to Hydergine. The ability of the senses are expanded to such an overwhelming degree that what is being sensed seems qualitatively different. Left brain and right brain activity is heightened to produce an extremely heightened creativity. Also produces hallucinogenic and entheogenic effects at doses as low as 20–30 μg (micrograms), with the likelihood of having a bad trip increasing as dose is increased if these effects are undesired. May also cause cognitive shifts, synesthesia, and flashbacks. The drug sometimes spurs long-term or even permanent changes in a user's personality and life perspective. (For more details, see Albert Hofmann: LSD - My Problem Child.)
• 4-methylaminorex
• Pemoline
• Psilocybin and Psilocin
• MDPV
• Mescaline
Other nootropics
• Adafenoxate - Has an anti-anxiety effect for rats and possibly the same for humans.
• Butea frondosa - "The plant Butea frondosa has been indicated in the Indian system of medicine as a plant augmenting memory and as a rejuvenator. ... B. frondosa possesses anti-stress and weak nootropic activity."
• BMY 21502 - Injured animals treated with BMY-21502 at one week post-injury showed significant improvement in post-injury learning ability compared to injured animals treated with vehicle. Paradoxically, in uninjured control animals BMY-21502 treatment appeared to worsen learning scores. The results of this study indicate that BMY-21502 may be useful for attenuating the dysfunction in learning ability that occurs following TBI.
• Cabergoline (Dostinex) -
• Celastrus panicaltus - Herb.
• Cerebrolysin - A neuroprotective nootropic agent, might affect Alzheimer's disease pathology. Currently in clinical trials
• Coluracetam - It may also have potential use in prevention and treatment of ischemic retinopathy and retinal and optic nerve injury.
• Desmopressin (DDAVP) - Drug. Analog of vasopressin (the anti-diuretic and memory hormone)
• DHEA - Hormone created by the adrenal glands; Precursor to Estrogen and Testosterone
• Dostinex -
• Fasoracetam -
• Essential Fatty Acids- Eicosapentaenoic acid (EPA) and docosahexaenoic acid (DPA) are the best known. EPA in particular, has an anti-depressant function and is positively indicated in trials with autism and learning difficulties.
• Fipexide (Vigilor) - It protects against some memory impairing chemicals, such as diethyldithiocarbamate and clonidine.
• Galantamine - Drug.
• Gerovital H3 -
• Ginkgo biloba - Root. Increases blood flow to the extremities and the brain, nootropic effects are disputed.
• Gotu Kola - Herb and root.
• Meclofenoxate - Has an anti-anxiety effect for rats and possibly the same for humans. Like Fipexide, it protects against some memory impairing chemicals, such as diethyldithiocarbamate and clonidine. Like many racetams, it may treat fetal alcohol syndrome.
• Milacemide - Drug.
• Nimodipine -
• Ondansetron -
• Oxiracetam (Neuromet) -
• Phenytoin (Dilantin) -
• Phosphatidylserine- reduces age-related memory loss and promotes concentration.
• Picamilon - Drug.
• Pikamilone -
• Pregnenolone - Hormone; Precursor to DHEA;
• Pyroglutamate -
• Semax - A neuropeptide (stimulator of the nervous system) developed from a short fragment of ACTH, Pro8-Gly9-Pro10 ACTH(4-10). Claims of significant increase in salvation of neurons are made
• Somatotropin -
• Sulbutiamine (Arcalion) - Drug.
• Xanthinol -
Brain foods
Some regular food items are rich sources of substances with alleged nootropic benefits:
• Nuts, in particular walnuts, are rich sources of alpha-linolenic acid (ALA), a type of omega-3 fatty acid. A mixture of walnuts served with dried fruit pieces is known in some regions as student food (orig. German: Studentenfutter) and is there popularily recommended as a snack for students and other mental workers.
• Oily fish, such as salmon or fresh tuna (not tuna canned in oil) are also good sources of omega-3 fatty acids such as eicosapentaenoic acid and docosahexaenoic acid, whose lack in diet has been associated with increased risk of mental illnesses such as depression, aggressive behavior, schizophrenia, or hyper-activity in children.
Links
• BetterBrain Nootropics Index
• Business Week Online - "I Can't Remember" September 1, 2003
• CerebralHealth.com
• Slashdot |Cognitive Enhancement Drugs
• Brain Foods
• List of Nootropic drugs at Erowid.org
• The Scientist - Seeking Smart Drugs by Eugene Russo October 28, 2002
Psychoanaleptics: psychostimulants, agents used for ADHD and nootropics (N06B)
Centrally acting sympathomimetics
Amphetamine - Dexamphetamine - Dextromethamphetamine - Levomethamphetamine - Pemoline - Fencamfamin - Modafinil - Fenozolone - Atomoxetine - Fenetylline
Xanthine derivatives
Caffeine - Propentofylline
Other psychostimulants and nootropics Racetams (Piracetam, Oxiracetam, Aniracetam, Pramiracetam) - Meclofenoxate - Pyritinol - Deanol - Fipexide - Citicoline - Pirisudanol - Linopirdine - Nizofenone - Acetylcarnitine - Idebenone - Prolintane - Pipradrol - Adrafinil -
Nootropics, popularly referred to as "smart drugs" and "smart nutrients", are substances which boost human cognitive abilities (the functions and capacities of the brain). The word nootropic was coined in 1964 by the Romanian Dr. Corneliu E. Giurgea, derived from the Greek words noos, or "mind," and tropein meaning "to bend/turn." Typically, nootropics are alleged to work by increasing the brain's supply of neurochemicals (neurotransmitters, enzymes, and hormones), by improving the brain's oxygen supply, or by stimulating nerve growth.
Most alleged nootropic substances are nutrients or plant components (herbs, roots, beans, bark, etc.), available over the counter at health food and grocery stores, and are used as nutritional supplements. Some nootropics are drugs, used to treat people with cognitive learning difficulties, neural degradation (Alzheimer's disease or Parkinson's disease), and for cases of oxygen deficit to prevent hypoxia. These drugs have a variety of human enhancement applications as well, are marketed heavily on the World Wide Web, and are used by many people in personal cognitive enhancement regimens.
While scientific studies support some of the claimed benefits, it is worth noting that many of the claims attributed to most nootropics have not been formally tested.
General strategies
Neurotransmitter support - supplying the body with the precursors and cofactors it needs to produce neurotransmitters.
Note that cardiovascular exercise performed on a regular basis also has nootropic effects, by increasing the body's capacity to supply brain cells with oxygen.
Nootropic substances
Nootropic drugs are generally only available by prescription or through personal importation. The other nootropic substances listed below are either nutritional supplements or plant components, and are generally available over the counter at health food and grocery stores. The term "drug" here is used as a legal designation, and does not indicate greater efficacy. With nootropics, the effects, effectiveness, and potency differ from substance to substance and from individual to individual. See the substance descriptions below for more detail.
Replenishing and increasing neurotransmitters
Thinking is a biologically demanding task. It involves the firing of neurons, which requires ample neurotransmitters, and even though these are reuseable to some extent, they do get depleted. Depletion of neurotransmitters generally results in reduced mental performance, which may include difficulty concentrating, slowed reasoning, decreased learning efficiency, impaired recall, reduced coordination, lowered moods, inability to cope, increased response times, and mental fatigue. This also generally increases the likelihood of human error on tasks and activities performed. Stress causes neurotransmitters to be depleted even faster. The brain's neurotransmitters need to be replenished frequently, made by the body from substances ingested in the diet. Maintaining neurochemicals at optimal levels has a corresponding effect on brain performance, supporting improved mental agility and stamina, even beyond the individual's normal limits.
As the brain ages, its ability to produce and maintain youthful levels of neurotransmitters declines. Thus, the theory is that providing the brain with ample raw materials necessary to make neurotransmitters can restore them to more youthful levels and thus help maintain cognitive function at vigorous youthful levels as well.
Cholinergics
Cholinergics are substances that affect the neurotransmitter acetylcholine or the components of the nervous system that use acetylcholine. Acetylcholine facilitates memory, concentration, focus, and high-order thought processes (abstract thought, calculation, innovation, etc.). Increasing the availability of this neurotransmitter in the brain may improve these functions and increase the duration in which they may be engaged without slowing down or stopping. Oversupplying the brain with acetylcholine may have the opposite effect, temporarily reducing rather than improving mental performance. Cholinergic nootropics include acetylcholine precursors and cofactors, and acetylcholinesterase inhibitors:
• Acetyl-L-carnitine (ALCAR) - Amino acid. Precursor of acetylcholine (donating the acetyl portion to the acetylcholine molecule). It is synergistic with lipoic acid.
• Centrophenoxine (Lucidril) - Drug. Cholinergic agent, enhances color perception.
• Choline - precursor to acetylcholine (an essential component of the acetylcholine molecule).
o Alpha-GPC (L-alpha glycerylphosphorylcholine, Choline alfoscerate) - most effective choline precursor, readily crosses the blood-brain barrier.
o CDP-Choline (Cytidine Diphosphate Choline) - choline precursor, tends to be less expensive and similar in effect to Alpha GPC.
o Choline bitartrate - precursor of acetylcholine, anti-depressant.
o Choline citrate - precursor of the neurotransmitter acetylcholine, anti-depressant.
• DMAE - approved treatment for ADD/ADHD, precursor of acetylcholine, cholinergic agent, removes lipofuscin from the brain, anti-depressant.
• Huperzine A - potent acetylcholinesterase inhibitor derived from Chinese club-moss.
• Lecithin - contains phosphatidylcholine, precursor of acetylcholine.
• Pyrrolidone derivatives:
o Piracetam (Nootropil) - Prescription drug (in Europe). The original (first), and most commonly taken nootropic drug. It is a cholinergic agent, synergistic with DMAE, centrophenoxine, choline, and Hydergine. Increases brain cell metabolism and energy levels, and speeds up interhemispheric flow of information (left-right brain hemisphere communication). Increases alertness, improves concentration, and enhances memory. Protects neurons from hypoxia, and stimulates growth of acetylcholine receptors. May also cause nerves to regenerate. Piracetam markedly decreases the formation of neuronal lipofuscin. It improves posture in elderly people. It is not regulated in the US.
o Aniracetam - Drug. Analog of piracetam, and 4 to 8 times more potent. Like piracetam, aniracetam protects against some memory impairing chemicals, such as diethyldithiocarbamate and clonidine. Also like piracetam, aniracetam may enhance memory in aging adults by increasing levels of brain biogenic monoamines, which are beneficial to learning and memory. Both racetams have possible therapeutic use in treating fetal alcohol syndrome. Aniracetam increases vigilance.
o Etiracetam - It increases vigilance.
o Nefiracetam - Drug. Analog of piracetam, and facilitates hippocampal neurotransmission.
o Oxiracetam - Drug. Analog of piracetam, and 2 to 4 times stronger. Improves memory, concentration, and vigilance. When fed to pregnant rats, the offspring of those rats were more intelligent than the offspring of rats fed a saline solution placebo.
o Pramiracetam - Drug. Fifteen times stronger than piracetam, of which it is an analog.
• Vitamin B5 - cofactor in the conversion of choline into acetylcholine, cholinergic agent, increases stamina (including mental stamina).
Excess acetylcholine is considered by many to be potentially harmful; see cholinesterase inhibitor.
Dopaminergics
Dopaminergics are substances that affect the neurotransmitter dopamine or the components of the nervous system that use dopamine. Dopamine is produced in the synthesis of all catecholamine neurotransmitters, and is the rate limiting step for this synthesis. Dopaminergic nootropics include dopamine precursors and cofactors, and dopamine reuptake inhibitors:
• L-dopa - Prescription drug. Precursor to the neurotransmitter dopamine, anti-depressant.
• Phenylalanine (requires Vitamin B6 and Vitamin C) - Essential amino acid. Precursor to dopamine, anti-depressant, sleep reducer.
• Theanine - Found in tea. Increases serotonin and dopamine levels in the brain. Increases alpha-wave based alert relaxation.
• Tyrosine (requires Vitamin B6 and Vitamin C) - Amino acid. Precursor to dopamine, anti-depressant, sleep reducer.
• Vitamin C- improves cardiovascular elasticity and integrity, membrane stabilizer and major anti-oxidant (protects brain cells and prevents brain cell death), cofactor in the production of the neurotransmitters dopamine and serotonin.
• Vitamin B6 - co-factor used by the body to produce dopamine.
• Yohimbe - Bark. Boosts dopamine levels as much as 80%, though how it does this is not yet understood. Aphrodisiac. Yohimbe poses some health risks through its side-effects: it is a neuro-paralytic which slows down breathing and induces acidosis, some symptoms of which are malaise, nausea, and vomiting. Contraindicated for users of megadoses of acidic vitamins or nutrients.
• Deprenyl - Inhibits MAO B (an enzyme that breaks down dopamine) thus raising dopamine by partially inhibiting its breakdown.
• Tolcapone - Inhibits COMT (an enzyme that breaks down the neurotransmitters dopamine, epinephrine, and norepinephrine) and increases performance in tasks depending on working memory in individuals with the val/val and val/met genotype of the val158Met polymorphism of the catechol-O-methyltransferase gene, while decreasing it in presence of the met/met version. Tolcapone presents the risk of deadly side effects.
Serotonergics
Serotonergics are substances that affect the neurotransmitter serotonin or the components of the nervous system that use serotonin. Serotonergic nootropics include serotonin precursors and cofactors, and serotonin reuptake inhibitors:
• 5-HTP - more bioavailable form of tryptophan, precursor to the neurotransmitter serotonin, promotes relaxed poise and sound sleep.
• Griffonia simplicifolia a natural source of 5-HTP (an alternative in countries where 5-HTP not legal, freely available.)
• Tryptophan (requires Vitamin B6 and Vitamin C) - Essential amino acid. Precursor to serotonin, found in high concentration in bananas and poultry (especially turkey), also in milk, promotes relaxed poise and sound sleep.
• 5HT2A agonists such as LSD and 2C-T-7 have been shown to produce nootropic effects when used at a dose much lower than a hallucinogenic dose. (e.g. 10 μg for LSD and 1 mg 2C-T-7, 1/25 of a normal recreational dose )
Anti-depression, adaptogenic and mood stabilization
Depression and depressed mood negatively affect cognitive performance. Feelings of sadness, guilt, helplessness, hopelessness, anxiety, and fear caused by depression detract from productive thought, while apathy (which is also induced by depression) is the lack of motivation and driving moods (like curiosity, interest, determination, etc.) Other symptoms include disturbed sleep patterns, mental fatigue and loss of energy, trouble concentrating or making decisions, and a generalized slowing and obtunding of cognition, including memory. Obviously, removing these effects improves intelligence and mental performance, and therefore, counteracting and preventing depression are effective nootropic strategies. There is a high correlation between depression and a reduction or depletion of neurotransmitters (dopamine, acetylcholine, and serotonin) in the brain, therefore it is no surprise that increasing the brain's supply of neurotransmitters alleviates (or at least reduces the symptoms of) most depressions. Stress is another major factor in neurotransmitter depletion, being both a cause and effect of it (creating a vicious downward spiral), therefore stress management and anti-stress substances are also very useful nootropic strategies.
All of the "nergics" listed above have been found to increase stress tolerance and alleviate depression (by replenishing or increasing the brain's supply of specific neurotransmitters)[citation needed], especially when used in precursor/co-factor combinations[citation needed].
Below are additional more nootropics which affect mood and stress:
• Ashwagandha (Withania somnifera) - Root. Also known as Indian ginseng. Adaptogen used as a tonic to normalize body processes and reduce stress and anxiety.
• Inositol - Is a B-vitamin like substance with anti-anxiety effects. It is believed to produce its anti-anxiety effects by improving the binding of gabaergics to GABAA receptors. Inositol is a sugar, and is therefore an alternative energy source for brain and muscle tissues. It produces a sugar high without a sugar low, making it especially suited for sweetening tea (instead of sugar). It is also a membrane stabilizer which can strengthen (and therefore help protect) neurons.
• Lemon Balm (Melissa officinalis) - Herb. Anti-depressant.
• Rhodiola Rosea - Herb. Adaptogen; elevates mood, alleviates depression. Promotes mental energy and stamina, reduces fatigue.
• St John's Wort - Herb. The active components: hypericin and hyperforin, are clinically indicated to be effective in cases of mild to medium depression.
• Ginseng, Siberian (Eleutherococcus senticosus) - Root. Anti-anxiety adaptogen that normalizes physical stress and mental consequences.
• Selegiline (Deprenyl) - Along with Piracetam and Meclofenoxate, Deprenyl decreases the amount of lipofuscin pigment and ceroid pigment accumulations in the brain by improving cellular recycling activities. Therefore, these nootropics may slow age-related diseases in the brain.
• Sutherlandia frutescens - Herb. Adaptogen, blood detoxifier.
• Tea - Herb. Contains theophylline and theanine. Increases alpha-wave based alert relaxation (relieves stress).
• Theanine - Amino acid. Found in tea. Increases serotonin and dopamine levels in the brain. Increases alpha-wave based alert relaxation.
• Vasopressin - Drug. Memory hormone produced by the pituitary gland which improves both memory encoding and recall. Rapidly counters chronic apathy syndrome and drug-induced vasopressin depletion.
• Nicotinic acid (vitamin B3) - Essential nutrient. Mild enhancer of concentration and memory. Vasodilator. Mood stabilizer, with a powerful anti-anxiety effect — perhaps the best and most immediate stress reliever available (note that other forms of vitamin B do not have this effect). Side effects: gastric upset (which is easily prevented and relieved with antacids), reduced blood pressure and flushing of the skin (caused by vasodilation), and itchy sensation in the skin caused by histamine release.
Brain energy and improved oxygen supply
• Acetyl-L-carnitine (ALCAR) - Amino acid. Transports fatty acids through cellular membranes and cytosol into cells' mitochondria, where the fats undergo oxidation to produce ATP, the universal energy molecule. Synergistic with lipoic acid.
• Chromium- stabilises blood sugar levels promoting concentration.
• Coenzyme q-10 syn. Ubiquinone - increases oxygen transport through the mitochondria of the cells. Appears to slow age-related dementia.
• Creatine - increases brain energy levels via ATP production.
• Inositol -
• Lipoic acid - synergistic with Acetyl-L-carnitine.
• Piracetam - improves alertness, blood flow, oxygen supply, and stroke recovery.
• Pyritinol (Enerbol) - Drug. Enhances oxygen and glucose uptake in the brain, and allows glucose to pass more easily through the blood-brain barrier. It is also a powerful anti-oxidant which scavenges hydroxyl radicals created in the very processes it is involved in.
• Vinpocetine - micro-circulation enhancer, improves oxygen supply to brain cells.
Mental agility, concentration, stamina, and focus
• Adrafinil (Olmifon) - Drug.
• Caffeine - improves concentration, idea production, but hinders memory encoding. Also produces the jitters. Caffeine is the most widely used psychoactive substance in the world, it may be susceptible to strong levels of tolerance.
• Coffee - Bean. Contains caffeine; brewed coffee is high in antioxidants.
• Nicergoline - Drug. Nicergoline is an ergoloid mesylate derivative used to treat senile dementia. It has also been found to increase mental agility and enhance clarity and perception. It increases vigilance. Increases arterial flow and use of oxygen and glucose in the brain.
• Nicotine - stimulus barrier (aids in concentration). Stimulus barrier rebound effect (an unpleasant side effect).
• Cocaine - Drug
• Methylphenidate (Ritalin) - Drug
• Dextroamphetamine - (Adderall, Dexedrine) - Drug
• Modafinil - (Provigil) - Drug.
• Piracetam - improves alertness, socialization, and co-operation in the brain impaired from age, dementia, and reduced blood flow.
• Phenibut -
• Theophylline -
• Amphetamine -
Purported memory enhancement and learning improvement
All of the "nergics" listed above are purported to improve memory (encoding and recall), As do all nootropics which improve general brain performance in categories such as the brain energy and oxygen supply, and nerve growth stimulantion and protection. Other agents purported to have these specific benefits are mentioned in their own sections.
Other nootropics with specific effects on memory encoding and recall include:
• Bacopa monniera (Brahmi) - Herb. Elevates curiosity, enhances memory and concentration. Brahmi also protects against amnesia inducing chemicals such as scopolamine or loss of memory due to electro convulsive shocks. It is a traditional ayurvedic medicine.
• Piracetam - improves memory, Alzheimer's, dementia, dyslexia and Down's syndrome
• Rosemary - Herb. Rosemary has a very old, albeit unverified, reputation for improving memory.
• Vasopressin - Hormone, prescription drug.
• Dextroamphetamine- Adderall, Dexedrine.[13]
Nerve growth stimulation and brain cell protection
• Acetyl-L-carnitine (ALCAR) - Amino acid. Inhibits lipofuscin formation.
• Bacopa monnieri (Brahmi) - Herb. Improves protein synthesis in brain cell repair and new dendritic growth.
• Selegiline (Deprenyl) - Drug. Brain cell protectant, delays senescence of brain cells, proven to increase maximum life span in laboratory rats.
• Ergoloid mesylates (Hydergine) - Drug. Mimics nerve growth factor (NGF), and is a powerful anti-oxidant capable of delaying brain death in cases of heart failure and stroke by several minutes with regular use. It increases vigilance.
• Idebenone - stimulates nerve growth, and has same effects as Coenzyme q-10 - boosters claim that CoQ10 has "harmful side-effects", a claim which has not been demonstrated in published peer-reviewed studies.
• Inositol - Membrane stabilizer. Strengthens neurons, making them less susceptible to damage.
• Pyritinol (Enerbol) - Drug. Powerful anti-oxidant which scavenges hydroxyl radicals. Also enhances oxygen and glucose uptake in the brain, and allows glucose to pass more easily through the blood-brain barrier. Improves general brain function.
• Rasagiline (Azilect) - Drug. Treats Parkinson’s disease either as monotherapy (by itself) or in addition to levodopa therapy. Promotes increased and sustained levels of dopamine by selectively inhibiting an enzyme, monoamine oxidase-B.
• Vitamin C - Membrane stabilizer, involved in collagen synthesis. Strengthens neurons, making them less susceptible to damage. Vitamin C is also a co-factor in the brain's production of dopamine.
Recreational drugs with purported nootropic effects
See also: Controlled substances act and Misuse of Drugs Act 1971
• Amphetamines (Adderall, Dexedrine) - Schedule II / Class B drugs. Prescribed for attention-deficit disorders, narcolepsy, and certain cases of obesity; and issued as an anti-fatigue pill for pilots in the armed forces. These also heighten alertness, mental focus, vigilance, stamina, and sex drive. They are highly addictive, and have many side effects. Personal importation is prohibited. Using these recreationally or for performance enhancement is illegal in most countries.
• Cannabis is reported to heighten the ability of the senses, as well as heighten alpha wave activity in the brain associated with creativity.
• LSD - Schedule I / Class A drug. At minuscule doses (1 μg) the drug has effects similar to Hydergine. The ability of the senses are expanded to such an overwhelming degree that what is being sensed seems qualitatively different. Left brain and right brain activity is heightened to produce an extremely heightened creativity. Also produces hallucinogenic and entheogenic effects at doses as low as 20–30 μg (micrograms), with the likelihood of having a bad trip increasing as dose is increased if these effects are undesired. May also cause cognitive shifts, synesthesia, and flashbacks. The drug sometimes spurs long-term or even permanent changes in a user's personality and life perspective. (For more details, see Albert Hofmann: LSD - My Problem Child.)
• 4-methylaminorex
• Pemoline
• Psilocybin and Psilocin
• MDPV
• Mescaline
Other nootropics
• Adafenoxate - Has an anti-anxiety effect for rats and possibly the same for humans.
• Butea frondosa - "The plant Butea frondosa has been indicated in the Indian system of medicine as a plant augmenting memory and as a rejuvenator. ... B. frondosa possesses anti-stress and weak nootropic activity."
• BMY 21502 - Injured animals treated with BMY-21502 at one week post-injury showed significant improvement in post-injury learning ability compared to injured animals treated with vehicle. Paradoxically, in uninjured control animals BMY-21502 treatment appeared to worsen learning scores. The results of this study indicate that BMY-21502 may be useful for attenuating the dysfunction in learning ability that occurs following TBI.
• Cabergoline (Dostinex) -
• Celastrus panicaltus - Herb.
• Cerebrolysin - A neuroprotective nootropic agent, might affect Alzheimer's disease pathology. Currently in clinical trials
• Coluracetam - It may also have potential use in prevention and treatment of ischemic retinopathy and retinal and optic nerve injury.
• Desmopressin (DDAVP) - Drug. Analog of vasopressin (the anti-diuretic and memory hormone)
• DHEA - Hormone created by the adrenal glands; Precursor to Estrogen and Testosterone
• Dostinex -
• Fasoracetam -
• Essential Fatty Acids- Eicosapentaenoic acid (EPA) and docosahexaenoic acid (DPA) are the best known. EPA in particular, has an anti-depressant function and is positively indicated in trials with autism and learning difficulties.
• Fipexide (Vigilor) - It protects against some memory impairing chemicals, such as diethyldithiocarbamate and clonidine.
• Galantamine - Drug.
• Gerovital H3 -
• Ginkgo biloba - Root. Increases blood flow to the extremities and the brain, nootropic effects are disputed.
• Gotu Kola - Herb and root.
• Meclofenoxate - Has an anti-anxiety effect for rats and possibly the same for humans. Like Fipexide, it protects against some memory impairing chemicals, such as diethyldithiocarbamate and clonidine. Like many racetams, it may treat fetal alcohol syndrome.
• Milacemide - Drug.
• Nimodipine -
• Ondansetron -
• Oxiracetam (Neuromet) -
• Phenytoin (Dilantin) -
• Phosphatidylserine- reduces age-related memory loss and promotes concentration.
• Picamilon - Drug.
• Pikamilone -
• Pregnenolone - Hormone; Precursor to DHEA;
• Pyroglutamate -
• Semax - A neuropeptide (stimulator of the nervous system) developed from a short fragment of ACTH, Pro8-Gly9-Pro10 ACTH(4-10). Claims of significant increase in salvation of neurons are made
• Somatotropin -
• Sulbutiamine (Arcalion) - Drug.
• Xanthinol -
Brain foods
Some regular food items are rich sources of substances with alleged nootropic benefits:
• Nuts, in particular walnuts, are rich sources of alpha-linolenic acid (ALA), a type of omega-3 fatty acid. A mixture of walnuts served with dried fruit pieces is known in some regions as student food (orig. German: Studentenfutter) and is there popularily recommended as a snack for students and other mental workers.
• Oily fish, such as salmon or fresh tuna (not tuna canned in oil) are also good sources of omega-3 fatty acids such as eicosapentaenoic acid and docosahexaenoic acid, whose lack in diet has been associated with increased risk of mental illnesses such as depression, aggressive behavior, schizophrenia, or hyper-activity in children.
Links
• BetterBrain Nootropics Index
• Business Week Online - "I Can't Remember" September 1, 2003
• CerebralHealth.com
• Slashdot |Cognitive Enhancement Drugs
• Brain Foods
• List of Nootropic drugs at Erowid.org
• The Scientist - Seeking Smart Drugs by Eugene Russo October 28, 2002
Psychoanaleptics: psychostimulants, agents used for ADHD and nootropics (N06B)
Centrally acting sympathomimetics
Amphetamine - Dexamphetamine - Dextromethamphetamine - Levomethamphetamine - Pemoline - Fencamfamin - Modafinil - Fenozolone - Atomoxetine - Fenetylline
Xanthine derivatives
Caffeine - Propentofylline
Other psychostimulants and nootropics Racetams (Piracetam, Oxiracetam, Aniracetam, Pramiracetam) - Meclofenoxate - Pyritinol - Deanol - Fipexide - Citicoline - Pirisudanol - Linopirdine - Nizofenone - Acetylcarnitine - Idebenone - Prolintane - Pipradrol - Adrafinil -
The Mens Health Article on Fish Oil
Note to VitalChoice.com visitors: We have inserted our own comments between brackets [ ] in a few places. This article was accessed online August 7, 2007 at http://health.msn.com/general/articlepage.aspx?cp-documentid=100166680>1=10212
The Government's Big Fish Story
Scientists worldwide are praising a nutrient so powerful that it may help combat dozens of diseases. But don't expect an endorsement from our policy makers: They say we can do without.
By Sabrina Rubin Erdely and Denny Watkins, Men's Health.
When Randal McCloy was rushed to West Virginia University Ruby Memorial Hospital's intensive-care unit, he was practically dead. The 27-year-old coal miner had spent 41 hours buried 2 ½ miles underground after an explosion in the Sago, West Virginia, mine where he'd been working. His 12 oxygen-starved colleagues had all perished.
"As far as we know, he survived the longest exposure to carbon monoxide poisoning," says Julian Bailes, M.D., the neurosurgeon assigned to the case. McCloy was in a coma and in deep shock, his heart barely beating, one of his lungs collapsed, his liver and both kidneys shut down. Even if he somehow managed to pull through, doctors predicted McCloy would be severely brain damaged, since the carbon monoxide had stripped the protective myelin sheath from most of his brain's neurons. "It's very difficult to come back from a brain injury," says Dr. Bailes. "There's no drug that can help that."
While McCloy was being given oxygen infusions in a hyperbaric chamber, Dr. Bailes was struck by inspiration: He ordered a daily dose of 15,000 milligrams (mg) docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) for the miner. In layman's terms?
"Fish oil," says Dr. Bailes.
Several weeks passed. Then, unexpectedly, McCloy emerged from his coma. This in itself was amazing, but he wasn't done. In the weeks that followed, he stunned even the most optimistic experts by recovering his memory and gradually regaining his ability to walk, talk, and see, a turnaround that many in the medical field called miraculous.
Although Dr. Bailes believes the hyperbaric chamber may have worked some magic on the myelin, he thinks much of the credit belongs elsewhere. "The omega-3s helped rebuild the damaged gray and white matter of his brain," says Dr. Bailes, who now takes his own medicine, swallowing a fish-oil supplement each morning. On his orders, McCloy, still recuperating at home, continues to take fish oil daily. "I would say he should be on it for a lifetime," says Dr. Bailes. "But then, I think everybody should."
Maybe what fish oil needed all along was a better publicist. After all, this isn't the medical community's first infatuation with omega-3s. Back in 1970, a pair of Danish researchers, Hans Olaf Bang and Jørn Dyerberg, traveled to Greenland to uncover why the Eskimo population there had a low incidence of heart disease despite subsisting on a high-fat diet. Their finding: The Eskimos' blood contained high levels of omega-3s, establishing the first link to heart health. But even though this discovery spurred additional omega-3 research throughout the '70s and '80s, the public remained more interested in other nutrients—none of which had the unfortunate words "fish" or "fatty" in their names.
There are three types of omega-3s: DHA and EPA, found in fish and marine algae (which is where the fish get them), and alpha-linolenic acid (ALA), which is found in plants, seeds, and nuts. All three have health benefits, but those attributed to DHA and EPA have sparked renewed interest in recent years. Studies show that this tag team may not only reduce a person's risk of heart disease and stroke but also possibly help prevent ailments as diverse as arthritis, Alzheimer's disease, asthma, autoimmune disorders, and attention-deficit/hyperactivity disorder—and those are just the A's. Researchers are now exploring if these multifunctional fats can, among other things, ward off cancer and even make prison inmates less violent. It's enough to make omega-3 geeks downright giddy.
"Omega-3s are fantastic!" says Jing X. Kang, M.D., Ph.D., a Harvard University researcher who made the news by genetically engineering pigs to produce omega-3s in their meat. "Not just for your heart but also for brain function, immunity function, women's health, children's health—I'm amazed at how important they are."
In fact, some experts argue that omega-3s should be labeled essential nutrients as necessary to health as, say, vitamins A and D. "They're involved in the metabolism of each individual cell," says Artemis P. Simopoulos, M.D., a physician and the president of the Center for Genetics, Nutrition and Health in Washington, D.C. "They're part of your body's basic nutrition."
But while some see omega-3s as a nutritional no-brainer, others find them surprisingly controversial. "Omega-3s are way, way overhyped," says Marion Nestle, Ph.D., M.P.H., a professor of nutrition and public health at New York University and the author of What to Eat. "The research so far has been mixed. I'll grant that they're healthy, but I don't think if you don't eat them you're going to die of a heart attack."
[Note: We respect Dr. Nestle’s public battle against junk food and in favor of whole food nutrition, so we were surprised by the thoughtless nature of her comment. The issue is not whether you need to eat omega-3s to avoid dying of a heart attack tomorrow, but whether you will be healthier overall by eating amounts greater than most Americans do, and there is little doubt of that.]
The government has been equally cautious. So far, the Food and Drug Administration has issued only a tepid statement that "supportive but not conclusive research" indicates that DHA and EPA are good for your heart. And the Food and Nutrition Board—the scientific panel that, funded mostly by federal money, creates Daily Recommended Intakes (DRI) for essential nutrients—has shrugged off the issue altogether. It crowned ALA essential, but ignored DHA and EPA. "We didn't feel the data were sufficient," says Linda Meyers, Ph.D., director of the board. It's precisely the sort of comment that leaves omega-3 researchers flabbergasted.
"They're in the Dark Ages," says Bill Lands, Ph.D., a retired National Institutes of Health (NIH) biochemist who has written extensively about omega-3s and is widely considered the field's elder statesman. "The science was very clear 15 years ago. But they're not interested in science. All they're interested in doing is preserving the status quo, when they could be saving lives."
[Note: Dr. Lands has been a science advisor to Vital Choice since 2005.]
I stare down at the fish lying on the laboratory countertop. It stares back with one dead eye. Hours ago it was swimming in the Chesapeake Bay with 2 million of its brethren; tomorrow they'll all be squashed in a giant screw press to make 10,000 gallons of oil destined for fish-oil capsules and omega-3 fortified foods.
"Not very glamorous, is he?" says Jane Crowther, senior director of Omega Protein's Health and Science Center. It's hard to disagree: I've come to the nation's largest fish-oil refinery, in Reedville, Virginia, and now that I'm face to fin with what a poster on the wall calls "MENHADEN...THE WONDERFISH!" I'm not exactly awestruck. Bony, oily, and without much meat, the menhaden isn't even considered edible by most people. And yet, hidden inside is a substance that some anthropologists claim was critical to our very evolution; without it, they say, we'd still have brains like chimps'.
Ask most scientists and they'll tell you that Stone Age man evolved on the African savannas, developing his big, complex brain as a result of all the animals he'd hunt and eat. But most scientists would be wrong, according to Michael Crawford, Ph.D., who, along with researchers from the USDA, conducted a 2002 study challenging the prevailing theory, which he calls "a load of rubbish."
Crawford, the director of London's Institute of Brain Chemistry and Human Nutrition, argues that many other savanna mammals also subsisted on meat, but none developed our megabrains. "And with their strong jaws and sharp teeth, they were far better equipped to eat flesh than we were," he says. Yet relative to their growing bodies, those animals' brains actually shrank, while man's brain expanded from a 1-pound processor to a 3-pound supercomputer.
What were we dining on that the rest of the Paleolithic crowd wasn't? Crawford has a three-letter answer: DHA. "The human brain is soaking in DHA," he says. "It is the only substance that supports that level of neural development and cognitive function."
And lo and behold, paleontologists have found evidence that early man lived along the coasts of southern Africa, leaving behind mounds of fossilized shells and other table scraps. Crawford points out that catching fish would have been a heck of a lot easier than snaring four-legged prey. Children and pregnant women could wade in and collect mollusks themselves, feeding young brains in the process. Studies show that DHA helps secure the connections between brain cells, especially in utero, when pregnant women can increase their babies' IQs by as many as six points.
While the savanna-versus-seashore debate will continue (Emory University researchers recently fired their own scientific salvo at Crawford's theory), no one can dispute that we're veritable meat-eating machines today. The average American ate only 16.2 pounds of fish in 2005, but consumed 195 pounds of meat. And although our livers can manufacture tiny amounts of DHA and EPA when we eat lots of ALA-rich nuts and seeds, these aren't exactly our favorite foods, either.
Changing agricultural techniques have worsened the situation. The natural omega-3 contents of meat, milk, and eggs have plummeted now that our livestock no longer graze on ALA-rich grass, instead consuming corn, wheat, and other grains that are loaded with another group of fatty acids, called omega-6s. In fact, the disappearance of omega-3s from our diets has coincided with an upsurge in omega-6s, mainly in the form of cereals, grains, and processed foods made with hydrogenated oils. Dr. Simopoulos estimates that in caveman days, we ate an equal amount of the two types, but that the average American now eats 16 times more omega-6s than omega-3s.
"That's what's really killing us," says Lands. "The balance of 6 and 3 got out of whack." These two types of fatty acids have a biochemical yin-and-yang relationship: While omega-3s reduce our body's inflammation response, omega-6s encourage it. Each fatty acid is crucial: For example, if your inflammatory response is too weak, you won't be able to fight infection properly. And in theory, the push and pull should create perfect balance. Instead, the excess of omega-6s in our diets may have left us in a perpetual state of inflammation.
"The reason you take ibuprofen and Celebrex and all those nonsteroidals is to prevent the manufacture of these inflammation molecules in the first place," says Joseph Hibbeln, M.D., a neuroscientist with the NIH. "The mental picture I have is of the Dutch boy with his finger in the dike, where the finger is expensive pharmacology, and the flood is omega-6s."
Andrew McGeehin had limped for the past half century. "Stupid football," mutters the 83-year-old resident of Allentown, Pennsylvania. He tore up his right knee in his 30s, and despite surgery and drugs, the pain gradually became enough to wake him at night. Finally, McGeehin's orthopedist, Thomas Meade, M.D., suggested that he take an omega-3 supplement.
"I wasn't expecting much. But I figured I'd tried everything else," says McGeehin, who began swallowing fish oil along with his usual dose of the anti-inflammatory drug Voltaren. One week later, McGeehin was startled to realize that the stiffness in his knee was gone. He was able to walk with the easy, fluid stride of a younger man.
"Dr. Meade must be a genius!" McGeehin says today, though Dr. Meade himself explains it more modestly: "I read the literature. There's a plethora of evidence supporting the benefit of omega-3s for joint pain." He cites a 2006 University of Pittsburgh study of 125 people with neck and back pain, in which 60 percent of participants reported having less pain after taking omega-3s. And clinical studies on rheumatoid arthritis suggest that patients who take a daily dose may be able to cut back on their meds.
Indeed, in the 2 years in which Dr. Meade has been recommending omega-3s to his patients, he's seen a major shift in his orthopedic practice. "I almost never prescribe anti-inflammatories now," he says. "My staff kids me that I'll put us out of business with fish oil."
Omega-3s act as a sort of internal ice pack, in part because they spur our bodies to produce several inflammation-lowering substances. "Omega-3s work along the same biochemical pathway as a COX-2 inhibitor, such as Vioxx, but farther upstream," says Dr. Meade, meaning that omega-3s treat the underlying problem rather than the symptoms. And emerging research indicates that this powerful ability to ease inflammation is one of the ways omega-3s may help prevent a number of ailments, including:
Heart attack and stroke.
Cardiologists now believe that chronic inflammation triggers the release of artery-blocking plaque. In the most definitive study to date, published in the Lancet, heart-attack survivors who took 900 mg fish oil daily were 30 percent less likely to die of a second heart attack, and 20 percent less likely to suffer a stroke, than those who skipped the supplement.
Omega-3s can guard your arteries in other ways, too, since they also lower triglycerides and make blood vessels more elastic. Add in their ability to improve electrical communication between cardiac cells, thereby preventing arrhythmia, and you can see why omega-3s are a standard part of cardiac care in Europe. If you have a heart attack in Italy, France, Britain, or Spain, the hospital will even send you home with a prescription for Omacor, a "medication" that's superpurified DHA and EPA.
Alzheimer's disease.
Though not yet conclusive, research suggests that runaway brain inflammation may cause Alzheimer's disease. In a 2007 study published in the American Journal of Clinical Nutrition, elderly men who consumed 350 mg DHA and EPA daily experienced less cognitive decline than those who swallowed only 15 mg a day. And researchers at the Rush Institute for Healthy Aging, in Chicago, found that people who ate fish at least once a week were significantly less likely to develop Alzheimer's disease than those who ate more turf than surf.
Prostate cancer.
It's estimated that chronic inflammation is the culprit in 20 percent of all cancers, and that may include many cases of prostate cancer. In a 2003 Harvard study that tracked nearly 48,000 men over 12 years, researchers discovered that the men who ate fish three times a week were 25 percent less likely to develop metastatic prostate cancer than those who dined on less. However, a recent (and hotly debated) study review in the Journal of the American Medical Association says clear proof of cancer protection is still lacking.
Depression.
Could fish be the ultimate mood food? Ohio State University researchers recently analyzed blood samples from 43 older adults and found that a high omega-6 to low omega-3 ratio corresponded to elevated inflammation and more symptoms of depression. This and previous research suggest that eating more fatty fish or supplementing with omega-3s could help us beat the blues.
In the world of nutrition, few events make a scientist's palms sweat as much as the release of a newly revised DRI list.
Before the Food and Nutrition Board announced its most recent DRI for fatty acids, in 2002, some experts were optimistic that omega-3s would make the cut, given the research strides made over the previous decade. Instead, DHA and EPA were nowhere to be found—snubbed yet again by the larger scientific community. Even worse, the new DRI recommended that adults continue eating 10 times as many omega-6s as omega-3s, a ratio that practically gave omega-3 researchers a heart attack.
But Alice Lichtenstein, D.Sc., a Tufts University public-health professor who was on the panel that voted DHA down, doesn't see what all the fuss is about. "There just wasn't enough data to go on," she says. "What's out there is a little difficult to interpret."
Part of the problem she's referring to is that some studies didn't account for the amount of omega-6s that research participants consumed (too much blunts the effects of omega-3s), and other supplement studies didn't adjust for how much fish their participants ate. The differences make the studies hard to compare.
"It's all over the place," says Sharon Akabas, Ph.D., codirector of the master's program at Columbia University's institute of human nutrition, which held a symposium on this very problem. "It's like dealing with a moving target." Also, since most omega-3 research has focused on curing the sick, no one has yet pinned down how much DHA and EPA keeps healthy people well. Without that magic number, the Food and Nutrition Board says, its hands are tied.
The board's cautious approach is typical of how slow our government is to accept scientific change, say advocates of omega-3s. For example, although the World Health Organization endorsed adding DHA to infant formula back in 1994, it took the FDA until 2002 to approve the move. "Fifty-nine countries added DHA to infant formula before we did," says Dr. Simopoulos. "Mexico and China were ahead of us! And that's because our government is 20 years behind when it comes to the science."
Nevertheless, Meyers insists that the Food and Nutrition Board is just being thorough. "Anything in nutrition is going to lead to controversy," she says. "No matter the issue, some people will say we don't go far enough and others will say we go too far."
Perhaps, but it's revealing that even though important studies have come out since the board's 2002 list, it has no plans to revisit the status of DHA, despite the fact that at least one panelist has changed her mind. "There's a growing consensus that we should be eating more DHA for sure, as well as EPA," says Penny Kris-Etherton, Ph.D., a Penn State University professor of nutrition. "I would like to see stronger dietary recommendations than we currently have."
Columbia's Akabas agrees, which is why her Institute of Nutrition has come out with a bold endorsement. "We think the whole U.S. population would benefit from an upward shift in omega-3 intake, and we don't see any downside," she says. "So our recommendation is to not wait until the research becomes definitive. It's time to examine the development of a DRI."
One group that isn't waiting around for the blessing of the Food and Nutrition Board is the food manufacturers. Companies are already adding fish oil—minus the fish odor—to everyday products such as yogurt, frozen pizza, and orange juice. Most recently, Hormel Foods announced that it was entering this arena by partnering with a North Carolina research firm. What this also means, however, is that our government's greatest nutrition minds are being scooped by the maker of Spam.
Pick the Perfect Fish-Oil Supplement
Purity
When Consumerlab.com tested 41 fish-oil supplements, none was found to contain unsafe levels of mercury, PCBs, or dioxins. One explanation is that many brands are now molecularly distilled to remove any possible contaminants.
[Note: Vital Choice Sockeye Salmon Oil is certified free of harmful levels of contaminants by NSF. It does not need to be distilled because Sockeye are naturally very pure fish, because they eat low on the food chain, and their diets are largely vegetarian.]
Dosage
Ignore the total milligrams (mg) of fish oil, and focus instead on the combined eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). You want a supplement that contains at least 500 mg per dose or serving. If you're on blood thinners, talk to your doctor about the best dosage.
[Note: High-dose fish oil is not needed to raise blood levels of omega-3s to the range recommend by experts. It just takes a few weeks longer to reach these levels when taking a “natural” dose fish oil like Vital Choice Sockeye Salmon Oil, which provides about 260 mg of DHA and EPA per capsule. We recommend taking two to four capsules per day, to reach the dose level recommended by experts.]
Form
Your choice is basically capsules or a liquid. They're equally effective at delivering omega-3s to your bloodstream, so go with the form you think you'll take on a daily basis.
[Note: Vital Choice offers Salmon Oil in fish-gelatin capsules and in liquid form.]
Fish Burp
Some people experience this as their stomachs dissolve the fish-oil capsule. Beat the burp by buying enteric-coated capsules or freezing regular capsules. Either strategy will cause the fish oil to be released in your intestine instead, says William Harris, Ph.D., a professor of medicine and biomedical sciences at the University of South Dakota.
[Note: Vital Choice Sockeye Salmon Oil is available with added lemon oil to reduce fishy burps.]
Ratio
The ratio of EPA to DHA used in research varies, but most supplements are made with a 3:2 split. This translates to 300 mg EPA and 200 mg DHA in a 500 mg supplement.
Source
Any fish oil will do, be it from mackerel or menhaden, salmon or sardines. Supplements made from algae oil contain only DHA, and those made from flaxseed oil have alpha-linolenic acid (ALA), only a little of which can be converted into EPA and DHA by your body.
Antioxidants
Once inside your body, omega-3s can quickly lose their power due to oxidation. Look for vitamin E, a.k.a. tocopherol, an antioxidant that can neutralize free radicals.
[Note: Vital Choice Sockeye Salmon Oil contains naturally occurring astaxanthin, the potent antioxidant pigment that makes salmon flesh red-orange. It is many times more powerful than vitamin E, so we do not need to add tocopherols to our oil to protect it.]
The Government's Big Fish Story
Scientists worldwide are praising a nutrient so powerful that it may help combat dozens of diseases. But don't expect an endorsement from our policy makers: They say we can do without.
By Sabrina Rubin Erdely and Denny Watkins, Men's Health.
When Randal McCloy was rushed to West Virginia University Ruby Memorial Hospital's intensive-care unit, he was practically dead. The 27-year-old coal miner had spent 41 hours buried 2 ½ miles underground after an explosion in the Sago, West Virginia, mine where he'd been working. His 12 oxygen-starved colleagues had all perished.
"As far as we know, he survived the longest exposure to carbon monoxide poisoning," says Julian Bailes, M.D., the neurosurgeon assigned to the case. McCloy was in a coma and in deep shock, his heart barely beating, one of his lungs collapsed, his liver and both kidneys shut down. Even if he somehow managed to pull through, doctors predicted McCloy would be severely brain damaged, since the carbon monoxide had stripped the protective myelin sheath from most of his brain's neurons. "It's very difficult to come back from a brain injury," says Dr. Bailes. "There's no drug that can help that."
While McCloy was being given oxygen infusions in a hyperbaric chamber, Dr. Bailes was struck by inspiration: He ordered a daily dose of 15,000 milligrams (mg) docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) for the miner. In layman's terms?
"Fish oil," says Dr. Bailes.
Several weeks passed. Then, unexpectedly, McCloy emerged from his coma. This in itself was amazing, but he wasn't done. In the weeks that followed, he stunned even the most optimistic experts by recovering his memory and gradually regaining his ability to walk, talk, and see, a turnaround that many in the medical field called miraculous.
Although Dr. Bailes believes the hyperbaric chamber may have worked some magic on the myelin, he thinks much of the credit belongs elsewhere. "The omega-3s helped rebuild the damaged gray and white matter of his brain," says Dr. Bailes, who now takes his own medicine, swallowing a fish-oil supplement each morning. On his orders, McCloy, still recuperating at home, continues to take fish oil daily. "I would say he should be on it for a lifetime," says Dr. Bailes. "But then, I think everybody should."
Maybe what fish oil needed all along was a better publicist. After all, this isn't the medical community's first infatuation with omega-3s. Back in 1970, a pair of Danish researchers, Hans Olaf Bang and Jørn Dyerberg, traveled to Greenland to uncover why the Eskimo population there had a low incidence of heart disease despite subsisting on a high-fat diet. Their finding: The Eskimos' blood contained high levels of omega-3s, establishing the first link to heart health. But even though this discovery spurred additional omega-3 research throughout the '70s and '80s, the public remained more interested in other nutrients—none of which had the unfortunate words "fish" or "fatty" in their names.
There are three types of omega-3s: DHA and EPA, found in fish and marine algae (which is where the fish get them), and alpha-linolenic acid (ALA), which is found in plants, seeds, and nuts. All three have health benefits, but those attributed to DHA and EPA have sparked renewed interest in recent years. Studies show that this tag team may not only reduce a person's risk of heart disease and stroke but also possibly help prevent ailments as diverse as arthritis, Alzheimer's disease, asthma, autoimmune disorders, and attention-deficit/hyperactivity disorder—and those are just the A's. Researchers are now exploring if these multifunctional fats can, among other things, ward off cancer and even make prison inmates less violent. It's enough to make omega-3 geeks downright giddy.
"Omega-3s are fantastic!" says Jing X. Kang, M.D., Ph.D., a Harvard University researcher who made the news by genetically engineering pigs to produce omega-3s in their meat. "Not just for your heart but also for brain function, immunity function, women's health, children's health—I'm amazed at how important they are."
In fact, some experts argue that omega-3s should be labeled essential nutrients as necessary to health as, say, vitamins A and D. "They're involved in the metabolism of each individual cell," says Artemis P. Simopoulos, M.D., a physician and the president of the Center for Genetics, Nutrition and Health in Washington, D.C. "They're part of your body's basic nutrition."
But while some see omega-3s as a nutritional no-brainer, others find them surprisingly controversial. "Omega-3s are way, way overhyped," says Marion Nestle, Ph.D., M.P.H., a professor of nutrition and public health at New York University and the author of What to Eat. "The research so far has been mixed. I'll grant that they're healthy, but I don't think if you don't eat them you're going to die of a heart attack."
[Note: We respect Dr. Nestle’s public battle against junk food and in favor of whole food nutrition, so we were surprised by the thoughtless nature of her comment. The issue is not whether you need to eat omega-3s to avoid dying of a heart attack tomorrow, but whether you will be healthier overall by eating amounts greater than most Americans do, and there is little doubt of that.]
The government has been equally cautious. So far, the Food and Drug Administration has issued only a tepid statement that "supportive but not conclusive research" indicates that DHA and EPA are good for your heart. And the Food and Nutrition Board—the scientific panel that, funded mostly by federal money, creates Daily Recommended Intakes (DRI) for essential nutrients—has shrugged off the issue altogether. It crowned ALA essential, but ignored DHA and EPA. "We didn't feel the data were sufficient," says Linda Meyers, Ph.D., director of the board. It's precisely the sort of comment that leaves omega-3 researchers flabbergasted.
"They're in the Dark Ages," says Bill Lands, Ph.D., a retired National Institutes of Health (NIH) biochemist who has written extensively about omega-3s and is widely considered the field's elder statesman. "The science was very clear 15 years ago. But they're not interested in science. All they're interested in doing is preserving the status quo, when they could be saving lives."
[Note: Dr. Lands has been a science advisor to Vital Choice since 2005.]
I stare down at the fish lying on the laboratory countertop. It stares back with one dead eye. Hours ago it was swimming in the Chesapeake Bay with 2 million of its brethren; tomorrow they'll all be squashed in a giant screw press to make 10,000 gallons of oil destined for fish-oil capsules and omega-3 fortified foods.
"Not very glamorous, is he?" says Jane Crowther, senior director of Omega Protein's Health and Science Center. It's hard to disagree: I've come to the nation's largest fish-oil refinery, in Reedville, Virginia, and now that I'm face to fin with what a poster on the wall calls "MENHADEN...THE WONDERFISH!" I'm not exactly awestruck. Bony, oily, and without much meat, the menhaden isn't even considered edible by most people. And yet, hidden inside is a substance that some anthropologists claim was critical to our very evolution; without it, they say, we'd still have brains like chimps'.
Ask most scientists and they'll tell you that Stone Age man evolved on the African savannas, developing his big, complex brain as a result of all the animals he'd hunt and eat. But most scientists would be wrong, according to Michael Crawford, Ph.D., who, along with researchers from the USDA, conducted a 2002 study challenging the prevailing theory, which he calls "a load of rubbish."
Crawford, the director of London's Institute of Brain Chemistry and Human Nutrition, argues that many other savanna mammals also subsisted on meat, but none developed our megabrains. "And with their strong jaws and sharp teeth, they were far better equipped to eat flesh than we were," he says. Yet relative to their growing bodies, those animals' brains actually shrank, while man's brain expanded from a 1-pound processor to a 3-pound supercomputer.
What were we dining on that the rest of the Paleolithic crowd wasn't? Crawford has a three-letter answer: DHA. "The human brain is soaking in DHA," he says. "It is the only substance that supports that level of neural development and cognitive function."
And lo and behold, paleontologists have found evidence that early man lived along the coasts of southern Africa, leaving behind mounds of fossilized shells and other table scraps. Crawford points out that catching fish would have been a heck of a lot easier than snaring four-legged prey. Children and pregnant women could wade in and collect mollusks themselves, feeding young brains in the process. Studies show that DHA helps secure the connections between brain cells, especially in utero, when pregnant women can increase their babies' IQs by as many as six points.
While the savanna-versus-seashore debate will continue (Emory University researchers recently fired their own scientific salvo at Crawford's theory), no one can dispute that we're veritable meat-eating machines today. The average American ate only 16.2 pounds of fish in 2005, but consumed 195 pounds of meat. And although our livers can manufacture tiny amounts of DHA and EPA when we eat lots of ALA-rich nuts and seeds, these aren't exactly our favorite foods, either.
Changing agricultural techniques have worsened the situation. The natural omega-3 contents of meat, milk, and eggs have plummeted now that our livestock no longer graze on ALA-rich grass, instead consuming corn, wheat, and other grains that are loaded with another group of fatty acids, called omega-6s. In fact, the disappearance of omega-3s from our diets has coincided with an upsurge in omega-6s, mainly in the form of cereals, grains, and processed foods made with hydrogenated oils. Dr. Simopoulos estimates that in caveman days, we ate an equal amount of the two types, but that the average American now eats 16 times more omega-6s than omega-3s.
"That's what's really killing us," says Lands. "The balance of 6 and 3 got out of whack." These two types of fatty acids have a biochemical yin-and-yang relationship: While omega-3s reduce our body's inflammation response, omega-6s encourage it. Each fatty acid is crucial: For example, if your inflammatory response is too weak, you won't be able to fight infection properly. And in theory, the push and pull should create perfect balance. Instead, the excess of omega-6s in our diets may have left us in a perpetual state of inflammation.
"The reason you take ibuprofen and Celebrex and all those nonsteroidals is to prevent the manufacture of these inflammation molecules in the first place," says Joseph Hibbeln, M.D., a neuroscientist with the NIH. "The mental picture I have is of the Dutch boy with his finger in the dike, where the finger is expensive pharmacology, and the flood is omega-6s."
Andrew McGeehin had limped for the past half century. "Stupid football," mutters the 83-year-old resident of Allentown, Pennsylvania. He tore up his right knee in his 30s, and despite surgery and drugs, the pain gradually became enough to wake him at night. Finally, McGeehin's orthopedist, Thomas Meade, M.D., suggested that he take an omega-3 supplement.
"I wasn't expecting much. But I figured I'd tried everything else," says McGeehin, who began swallowing fish oil along with his usual dose of the anti-inflammatory drug Voltaren. One week later, McGeehin was startled to realize that the stiffness in his knee was gone. He was able to walk with the easy, fluid stride of a younger man.
"Dr. Meade must be a genius!" McGeehin says today, though Dr. Meade himself explains it more modestly: "I read the literature. There's a plethora of evidence supporting the benefit of omega-3s for joint pain." He cites a 2006 University of Pittsburgh study of 125 people with neck and back pain, in which 60 percent of participants reported having less pain after taking omega-3s. And clinical studies on rheumatoid arthritis suggest that patients who take a daily dose may be able to cut back on their meds.
Indeed, in the 2 years in which Dr. Meade has been recommending omega-3s to his patients, he's seen a major shift in his orthopedic practice. "I almost never prescribe anti-inflammatories now," he says. "My staff kids me that I'll put us out of business with fish oil."
Omega-3s act as a sort of internal ice pack, in part because they spur our bodies to produce several inflammation-lowering substances. "Omega-3s work along the same biochemical pathway as a COX-2 inhibitor, such as Vioxx, but farther upstream," says Dr. Meade, meaning that omega-3s treat the underlying problem rather than the symptoms. And emerging research indicates that this powerful ability to ease inflammation is one of the ways omega-3s may help prevent a number of ailments, including:
Heart attack and stroke.
Cardiologists now believe that chronic inflammation triggers the release of artery-blocking plaque. In the most definitive study to date, published in the Lancet, heart-attack survivors who took 900 mg fish oil daily were 30 percent less likely to die of a second heart attack, and 20 percent less likely to suffer a stroke, than those who skipped the supplement.
Omega-3s can guard your arteries in other ways, too, since they also lower triglycerides and make blood vessels more elastic. Add in their ability to improve electrical communication between cardiac cells, thereby preventing arrhythmia, and you can see why omega-3s are a standard part of cardiac care in Europe. If you have a heart attack in Italy, France, Britain, or Spain, the hospital will even send you home with a prescription for Omacor, a "medication" that's superpurified DHA and EPA.
Alzheimer's disease.
Though not yet conclusive, research suggests that runaway brain inflammation may cause Alzheimer's disease. In a 2007 study published in the American Journal of Clinical Nutrition, elderly men who consumed 350 mg DHA and EPA daily experienced less cognitive decline than those who swallowed only 15 mg a day. And researchers at the Rush Institute for Healthy Aging, in Chicago, found that people who ate fish at least once a week were significantly less likely to develop Alzheimer's disease than those who ate more turf than surf.
Prostate cancer.
It's estimated that chronic inflammation is the culprit in 20 percent of all cancers, and that may include many cases of prostate cancer. In a 2003 Harvard study that tracked nearly 48,000 men over 12 years, researchers discovered that the men who ate fish three times a week were 25 percent less likely to develop metastatic prostate cancer than those who dined on less. However, a recent (and hotly debated) study review in the Journal of the American Medical Association says clear proof of cancer protection is still lacking.
Depression.
Could fish be the ultimate mood food? Ohio State University researchers recently analyzed blood samples from 43 older adults and found that a high omega-6 to low omega-3 ratio corresponded to elevated inflammation and more symptoms of depression. This and previous research suggest that eating more fatty fish or supplementing with omega-3s could help us beat the blues.
In the world of nutrition, few events make a scientist's palms sweat as much as the release of a newly revised DRI list.
Before the Food and Nutrition Board announced its most recent DRI for fatty acids, in 2002, some experts were optimistic that omega-3s would make the cut, given the research strides made over the previous decade. Instead, DHA and EPA were nowhere to be found—snubbed yet again by the larger scientific community. Even worse, the new DRI recommended that adults continue eating 10 times as many omega-6s as omega-3s, a ratio that practically gave omega-3 researchers a heart attack.
But Alice Lichtenstein, D.Sc., a Tufts University public-health professor who was on the panel that voted DHA down, doesn't see what all the fuss is about. "There just wasn't enough data to go on," she says. "What's out there is a little difficult to interpret."
Part of the problem she's referring to is that some studies didn't account for the amount of omega-6s that research participants consumed (too much blunts the effects of omega-3s), and other supplement studies didn't adjust for how much fish their participants ate. The differences make the studies hard to compare.
"It's all over the place," says Sharon Akabas, Ph.D., codirector of the master's program at Columbia University's institute of human nutrition, which held a symposium on this very problem. "It's like dealing with a moving target." Also, since most omega-3 research has focused on curing the sick, no one has yet pinned down how much DHA and EPA keeps healthy people well. Without that magic number, the Food and Nutrition Board says, its hands are tied.
The board's cautious approach is typical of how slow our government is to accept scientific change, say advocates of omega-3s. For example, although the World Health Organization endorsed adding DHA to infant formula back in 1994, it took the FDA until 2002 to approve the move. "Fifty-nine countries added DHA to infant formula before we did," says Dr. Simopoulos. "Mexico and China were ahead of us! And that's because our government is 20 years behind when it comes to the science."
Nevertheless, Meyers insists that the Food and Nutrition Board is just being thorough. "Anything in nutrition is going to lead to controversy," she says. "No matter the issue, some people will say we don't go far enough and others will say we go too far."
Perhaps, but it's revealing that even though important studies have come out since the board's 2002 list, it has no plans to revisit the status of DHA, despite the fact that at least one panelist has changed her mind. "There's a growing consensus that we should be eating more DHA for sure, as well as EPA," says Penny Kris-Etherton, Ph.D., a Penn State University professor of nutrition. "I would like to see stronger dietary recommendations than we currently have."
Columbia's Akabas agrees, which is why her Institute of Nutrition has come out with a bold endorsement. "We think the whole U.S. population would benefit from an upward shift in omega-3 intake, and we don't see any downside," she says. "So our recommendation is to not wait until the research becomes definitive. It's time to examine the development of a DRI."
One group that isn't waiting around for the blessing of the Food and Nutrition Board is the food manufacturers. Companies are already adding fish oil—minus the fish odor—to everyday products such as yogurt, frozen pizza, and orange juice. Most recently, Hormel Foods announced that it was entering this arena by partnering with a North Carolina research firm. What this also means, however, is that our government's greatest nutrition minds are being scooped by the maker of Spam.
Pick the Perfect Fish-Oil Supplement
Purity
When Consumerlab.com tested 41 fish-oil supplements, none was found to contain unsafe levels of mercury, PCBs, or dioxins. One explanation is that many brands are now molecularly distilled to remove any possible contaminants.
[Note: Vital Choice Sockeye Salmon Oil is certified free of harmful levels of contaminants by NSF. It does not need to be distilled because Sockeye are naturally very pure fish, because they eat low on the food chain, and their diets are largely vegetarian.]
Dosage
Ignore the total milligrams (mg) of fish oil, and focus instead on the combined eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). You want a supplement that contains at least 500 mg per dose or serving. If you're on blood thinners, talk to your doctor about the best dosage.
[Note: High-dose fish oil is not needed to raise blood levels of omega-3s to the range recommend by experts. It just takes a few weeks longer to reach these levels when taking a “natural” dose fish oil like Vital Choice Sockeye Salmon Oil, which provides about 260 mg of DHA and EPA per capsule. We recommend taking two to four capsules per day, to reach the dose level recommended by experts.]
Form
Your choice is basically capsules or a liquid. They're equally effective at delivering omega-3s to your bloodstream, so go with the form you think you'll take on a daily basis.
[Note: Vital Choice offers Salmon Oil in fish-gelatin capsules and in liquid form.]
Fish Burp
Some people experience this as their stomachs dissolve the fish-oil capsule. Beat the burp by buying enteric-coated capsules or freezing regular capsules. Either strategy will cause the fish oil to be released in your intestine instead, says William Harris, Ph.D., a professor of medicine and biomedical sciences at the University of South Dakota.
[Note: Vital Choice Sockeye Salmon Oil is available with added lemon oil to reduce fishy burps.]
Ratio
The ratio of EPA to DHA used in research varies, but most supplements are made with a 3:2 split. This translates to 300 mg EPA and 200 mg DHA in a 500 mg supplement.
Source
Any fish oil will do, be it from mackerel or menhaden, salmon or sardines. Supplements made from algae oil contain only DHA, and those made from flaxseed oil have alpha-linolenic acid (ALA), only a little of which can be converted into EPA and DHA by your body.
Antioxidants
Once inside your body, omega-3s can quickly lose their power due to oxidation. Look for vitamin E, a.k.a. tocopherol, an antioxidant that can neutralize free radicals.
[Note: Vital Choice Sockeye Salmon Oil contains naturally occurring astaxanthin, the potent antioxidant pigment that makes salmon flesh red-orange. It is many times more powerful than vitamin E, so we do not need to add tocopherols to our oil to protect it.]
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