the Lipid Spin (Spring 2007)

Transcription

A Publication of the National Lipid Association
THE
Lipid Spin
The Official Publication of the National Lipid Association
Volume 4 • Issue 1 • Spring 2007
Clinical Insights
The Impact of Supplements/
Nutraceuticals (Functional Foods)
on Lipid Levels: What Works?
And How Well?
Mary McGowan, MD
Director: Cholesterol Treatment Center
Concord Hospital
Concord, NH
Assistant Professor of Medicine
University of Massachusetts Medical Center
“probably doing her as much, if not more good than the simvastatin.”
LG was taking the following supplements: Cholest-Off, fish oil
capsules, policosanol, CoEnzyme Q10, Organic Green Blend, Noni
Juice, Vitamin B complex plus folic acid, Pro-Biotic plus, cinnamon
capsules, and Grapeseed extract capsules. She admitted to spending
over 300 dollars per month on these products and was convinced they
were responsible for her improved lipids. It is likely that some of her
supplements (Cholest-Off, fiber and fish oil) are positively impacting
her lipid profile but the impact of the others is doubtful.
In 2005, Americans spent 21.3 billion dollars on over-the-counter
supplements.1 While some supplements have been proven beneficial
in rigorous, well-designed placebo controlled studies, others
have only media hype to back them up. The practicing physician
With contributing authors:
Suzanne Proulx, MS, RD, LD Cholesterol Treatment Center Concord Hospital Concord, NH was already taking a number of supplements and felt that they were
Donna Patch, MS, RD, LD
Cholesterol Treatment Center
Concord Hospital
Concord, NH
Mary Card, RD, MBA
Director of Clinical Trials
Cholesterol Treatment Center
Concord Hospital
Concord, NH
Last week, LG, a 56-year-old woman with familial combined
hyperlipidemia and a past medical/surgical history significant
for a myocardial infarction, congestive heart failure, implantable
defibrillator placement, and a coronary artery bypass procedure
presented complaining of muscle aches which she believed to be
the result of simvastatin. She wished to discontinue simvastatin
and was in favor of trying to lower her cholesterol “naturally.” She
in this issue . . .
• Clinical Insights...............................................1
• President’s Column...........................................2
• Practical Pearls............................................. 11
• Lipid Luminations........................................... 12
must be able to help his/her patients sort through a barrage of
media information and misinformation. This article will review
the scientific merits of supplements and a few nutraceuticals or
“functional foods” reported to influence lipid levels.
We conducted a Medline literature search of over-the-counter agents
reported to influence lipid levels. This article will evaluate the lipid
effects of the following supplements: plant stanols/sterols, red yeast
rice, fish oil, guggulipid, policosanol, and cinnamon. We will also
examine the following functional foods: nuts, water soluble fiber,
soy, and the “Profile Diet.” Other commonly used supplements will
be briefly noted including: garlic, lecithin, artichoke, and red wine
vinegar.
Plant Stanols/Sterols
Plant sterols are natural compounds present as minor components of
vegetable oils, nuts, seeds, legumes, fruits, vegetables and grains.
Continued on page 3
• 2007 NLA Scientific Sessions Preview.................. 13
• 2006 ABCL Diplomate Listing........................... 19
• Education Programs........................................ 20
• News & Notes............................................... 21
• Meetings & Events Calendar............................. 24
LIPID SPIN SPRING 2007
President’s Column
JAMES M. MCKENNEY, PharmD
NLA President
President and CEO, National Clinical Research
Professor Emeritus, Virginia Commonwealth
University
Richmond, Virginia
Big things are just around the corner for our Association. In March, we
are on track for the release of the first issue of the Journal of Clinical
Lipidology. Editor-in-Chief Virgil Brown, MD, has done a magnificent
job of collecting articles on HDL-C and overseeing the peer-review
process. The editorial board of the Journal is to be commended. Our
partner, Elsevier, has been of tremendous help and we are planning
to mail the first issue of the Journal to an expanded list of medical
professionals. We have every expectation that this publication will
management issues in their patient base.
Members who obtain ACCL certification will be able to effectively
demonstrate their professional commitment to lipid management and
the prevention of cardiovascular disease by validating their expertise to
patients, external organizations, and professional colleagues. While a
few details remain to be addressed, we have the basic foundation now
in place. Candidates for credentialing will need to meet basic eligibility
criteria, and also requirements for their particular professions, which
can be met by demonstrating a set number of credit hours or their
equivalent in a point system, much like the ABCL exam requirements.
Full details are posted at www.lipidspecialist.org and will be sent in
a brochure to NLA members soon. If you’re an MD, please pass the
brochure on to any of your colleagues you think may be interested.
draw more members to our Association and strengthen our efforts to
establish clinical lipidology as a medical subspecialty.
We’ve done our best to make the requirements rigorous, but fair, and
if a candidate has a degree in a related area of health science and
Our new journal will be published just in time for the American
College of Cardiology conference in New Orleans on March 24,
a substantial number of contact hours working with patients who
have lipid disorders, then that person may have already met a large
2007. NLA members should receive their copies in the mail at about
the same time. This is, in every way, your journal. If you have a paper
portion of the requirements needed to sit for the examination. We’ll
be offering the ACCL exam three times this year: June 1 and June 2 at
you’d like to see published, a case study you’d like to share, insights
from your research or clinical practice, we strongly encourage you
our Annual Scientific Sessions in Scottsdale, Arizona; on August 3 at
the SELA Scientific Forum in Savannah, Georgia; and on September
to submit your manuscript to www.lipidjournal.com. We want this
journal to be “must” reading for all of our members, and so a special
28 at the MWLA Scientific Forum in Minneapolis, Minnesota.
invitation is extended to our nurse, nurse practitioner, physician
assistant, pharmacist, dietitian, and exercise physiologist colleagues.
Give us ideas of what information you want and, better yet, submit
an article for publication consideration. We hope to quickly gain
approval from PubMed for indexing, such that all entries accepted to
the Journal will be indexed. Make us your first choice when looking
for journals in which to publish your work.
The NLA executive board will be meeting in New Orleans at the ACC
conference to continue our work on the NLA Five-Year Strategic
Plan, which we shared with you last year. We will be taking stock
of our progress on a range of issues and make adjustments where
needed, and form new goals where necessary. The results of this
meeting will be featured in the next Lipid Spin. I can say, however,
that our progress to date has been outstanding.
One recent major achievement has been the establishment of the
Accreditation Council for Clinical Lipidology. In my last column I
mentioned that we had formed the Council leadership and developed
an operating plan. Since then, we’ve created a curriculum and
examination for healthcare professionals who seek certification as
lipid specialists. This is a long-awaited milepost and one that will
directly support our pharmacist, dietician, physician assistant, nurse
practitioner, and exercise physiologist members who work with lipid
Speaking of our meetings, I hope to see many of you in Montreal,
Quebec, on April 13–15 at the NELA Third Annual Scientific Forum.
This marks our first regional meeting to be held outside the US and
we hope to reach out strongly to our Canadian colleagues. Then, in
Arizona at the Scientific Sessions, we’re going to try something new:
The NLA Live Challenge. We now have interactive technology and
will use it to hold a test of knowledge in a game-show format that
promises to be as entertaining as it will be educational.
As you can see, the NLA continues to grow and evolve to meet its
mission and you can take pride in being part of a thriving, successful
medical association. We welcome your input. Be sure to visit
www.lipid.org and select “Services” from the menu at left. There,
you’ll find a description of our various committees and volunteer
opportunities. This is a great way to get more involved in the NLA
and help direct its growth and activities. We appreciate the hard
work our members perform, and as you can see from the various
developments mentioned above, we all benefit from it as well.
Clinical Insights
Clinical Insights continued from page 1
The most abundant plant sterols include sitosterol, campesterol and
stigmasterol, with typical daily intakes ranging from 150 to 400 mg
per day.2 Plant stanols are the saturated counterparts of plant sterols
and occur more scarcely in nature. Average western diets provide
only 20 to 50 mg of plant stanols per day.3 These minor levels of
intake are of little significance but an enhanced daily consumption
of 800 to 3,000 mg of plant sterols or stanols per day has been found
to lower low-density lipoprotein cholesterol (LDL-C) by 6–20%
without changing high-density lipoprotein cholesterol (HDL-C) or
triglyceride levels.4–18 Optimal intakes are proposed to be around
2,000 mg per day and intakes above 2,500 mg appear to be of
little added benefit.2 Foods enriched with plant stanols or sterols
lower serum cholesterol levels by reducing intestinal absorption of
cholesterol.2
There are a wide variety of products available that have been
supplemented with plant sterols or stanols (Table 1). Some contain
plant sterol esters or plant stanol esters produced via esterification
with unsaturated fatty acids. This process increases solubility of the
plant compounds thereby improving distribution in the product and
enhancing dispersion in the intestine.3 Of note, 1,000 mgs of plant
sterols are equivalent to 1,600 mgs of plant sterol esters and 1,000
mgs of plant stanols are equivalent to 1,700 to 1,800 mgs of plant
stanol esters.3 Non-esterified and esterified forms of plant sterols
and stanols are both efficacious in reducing LDL-C.4–18
Most studies have distributed total daily intake of plant stanols and
sterols in 2 to 3 servings with meals, although one study did show
that 2,500 mg of plant stanols taken at lunch was as effective in
lowering LDL-C as 2,500 mg divided over three meals.20 It is also
of interest that plant sterols and stanols are effective in lowering
LDL-C even when added to a diet low in fat and cholesterol 2,11 or
if included in combination with statin therapy.5,7,8 Plant sterols and
stanols are generally well tolerated and few adverse effects have
been reported although a decrease in plasma beta carotene levels
has been observed.2,11,21 This decrease persisted even after correction
for lowered plasma lipid carriers. One study indicated that the
consumption of at least 5 servings of fruits and vegetables per day,
with inclusion of at least one carotenoid rich serving, can result
in maintenance of plasma carotenoid levels.22 The specific beta
carotene rich foods encouraged during this study included: carrots,
sweet potatoes, pumpkin, tomatoes, apricots, spinach and broccoli.
Table 1 provides a list of some of the currently available products
containing plant sterols, stanols and their respective esters. Choice
of a product is usually determined by availability, cost, calories and
taste preference.
Red Yeast Rice
Red yeast rice is the fermented product of rice on which red yeast
(Monascus pureus) has been grown. The active ingredient in red
yeast rice is believed to be Monacolin K, an agent reported to
be identical to lovastatin (a commonly prescribed statin). Like
statins, red yeast has been found to directly inhibit a 3-hydroxy-3methylglutaryl coenzyme A (HMG-CoA) reductase.23
There is little doubt that red yeast rice is an effective cholesterol
lowering agent. Two well designed studies of a no-longeravailable proprietary Chinese red yeast rice supplement found
significant LDL-C and triglyceride lowering effects. One of the
two studies also reported an HDL-C raising impact of red yeast rice
supplementation.
Heber and colleagues at the University of California at Los
Angeles enrolled 83 hyperlipidemic subjects in a double-blind,
placebo-controlled, prospectively randomized 12-week study.23 All
participants were instructed on the American Heart Association Step
I diet. There were no significant differences in lipids at baseline
between the treatment (n = 42) or the control (n = 41) groups.
Patients received 2.4 grams of Cholestin©, a proprietary red yeast
rice, or placebo for a period of 12 weeks. At study completion,
Table 1. Plant stanol/sterol content of various foods and supplements
Food Sources
Plant Stanol/
Sterol Content
Calories/
Serving
Take Control Margarine Light
1,700 mgs/tbsp
(plant sterol esters)
45
Benecol Margarine Light
850 mgs/tbsp
(plant stanol esters)
50
Smart Balance Omega Plus
Buttery Spread
450 mgs/tbsp
(plant sterols)
Smart Balance Omega Plus Light
Mayonnaise
100 mgs/tbsp
(plant sterols)
Minute Maid Heartwise Orange
Juice
1000 mgs/8 oz.
(plant sterols)
110
Nature Valley Healthy Heart
Chewy Granola Bars
400 mgs/bar
(plant sterols)
160
Health Valley Heartwise Cereal
400 mgs/1 cup
(plant sterols)
200
Right Direction Chocolate Chip
Cookie (4 grams of soluble fiber)
1,300 mgs/cookie
(plant sterols)
160
Cocoavia (snack bars)
1,500 mgs/bar
80
Nature Made Cholest-Off
450 mgs/capsule
(plant sterols and
plant stanols)
0.3
Basi Chol in Flax Oil
800 mgs/teaspoon
40
80
50
Supplements
Clinical Insights
LDL-C in the treated group had fallen by 21.9 % (39 + 19 mg/dL)
as compared to a 2.6% (5 + 22 mg/dL) reduction in the control
group (P = < 0.05). Triglycerides levels fell by 6.6% in the treated
group but remained unchanged in the control group. In this study,
HDL-C was not impacted by the red yeast rice.
Rippe and colleagues reported similar findings in a larger study
including 187 subjects treated at 12 medical centers.24 Participants
received either 2.4 grams of Cholestin© or matching placebo for
a period of 8 weeks. In this study, which was presented at the
American Heart Association’s (AHA) 39th Annual Conference
on Cardiovascular Disease Epidemiology and Prevention, active
treatment resulted in a reduction in LDL-C and triglycerides of 21%
and 24.5%, respectively. Unlike the aforementioned study, HDL-C
rose in by 14.6 % in the treated patients.
There is little doubt that the proprietary preparation of red yeast
rice known as Cholestin© favorably alters lipids. However, due to
legal issues, this preparation is no longer commercially available
in the United States. In 1998 the Food and Drug Administration
(FDA) determined that red yeast rice did not conform to the
definition of a dietary supplement under the 1994 Diet Supplement
and Health Education Act (DSHEA). This act states that marketed
dietary supplements cannot contain a compound already approved
as a drug (in this case lovastatin) unless the product was available
commercially before the drug’s approval. At present, Cholestin©
is still available as a red yeast rice dietary supplement in Canada,
Europe, and Asia. In the United States, Cholestin© has been
reformulated and no longer contains red yeast rice but rather
polymethoxylated flavones extracted from citrus fruits, geraniol
and marine fish oils.25 It is uncertain if this new preparation has any
impact on lipids.
Likewise it is unclear if other proprietary preparations of red
yeast extract will provide the same lipid effects as Cholestin©. At
least one study that evaluated the monocolin (believed to be the
active ingredient) content of 9 different preparations found wide
variation.26
Did the FDA do a disservice to patients by taking Cholestin©
off the market? There are many ways to look at this issue. It is,
however, clear that many patients as noted above are willing to take
supplements but unwilling to take prescription medications.
Fish oil
Dietary consumption of fatty fish and fish oil supplementation
has been shown to reduce sudden cardiac death and all causes of
mortality.27,28 Based on these findings, the AHA now recommends
that the general public consume oily fish at least twice a week.29
Furthermore, the AHA recommends persons with documented
CHD consume one gram of eicosapentaenoic acid (EPA) plus
docosahexaenoic acid (DHA) either in the form of fatty fish or via
supplementation.29 EPA and DHA are Omega-3 fatty acids present
in fish and are believed to be responsible for the cardiovascular
benefits of fish oil.
The AHA also recommends consideration of supplemental EPA +
DHA for patients requiring triglyceride reduction.29 Most over-thecounter 1-gram fish oil capsules contain, at most, 500 mg of EPA
+ DHA. Doses of between 2,000 and 4,000 mg of EPA + DHA are
required to significantly lower triglycerides. As such, persons with
hypertriglyceridemia will often require between 4 and 8 over-thecounter capsules to elicit a reduction in triglycerides.30 Omacor is
a newly available highly concentrated fish oil preparation available
by prescription, four capsules of which provide 3.36 grams of EPA
+ DHA. In patients with very high baseline triglyceride levels
(>500 mg/dL) reductions of up to 45% can be seen with Omacor
supplementation.31,32 Similar reductions can be achieved with overthe-counter products, although a greater number of capsules will be
required.
The mechanism by which EPA + DHA lower triglycerides is felt
to be via slowing the release of triglyceride rich very-low-density
lipioprotein (VLDL) particles into the plasma.33 Work by Harris
and colleagues suggests that omega-3 fatty acid supplementation
may accelerate the clearance of triglyceride rich lipoproteins via
enhanced lipolysis.34,35 As is frequently seen in the face of marked
triglyceride reduction, LDL-C may increase. The impact on HDL-C
is variable and can not easily be predicted.
Fish oil supplementation is not without potential side effects. Many
patients are troubled by slight gastrointestinal (GI) upset and fishy
aftertaste associated with consumption of high doses of EPA +
DHA.29 In our practice the GI upset often improves with time. The
fishy aftertaste is often minimized by storing fish oil either in the
refrigerator or freezer and taking fish oil with the largest meal of the
day. In diabetics or in persons with impaired glucose tolerance, it is
possible to observe worsening of glycemic control.29 Blood sugar
should be monitored in this population as fish oil is initiated. Large
doses of omega-3 fatty acids can inhibit platelet function mildly but
does not typically present a problem.36
Fish oil supplementation should be considered in patients with
significantly elevated triglycerides not responsive to dietary
measures. Supplementation may also be one way to avoid the
addition of a fibric acid derivative in persons with combined
dyslipidemia already on a statin.
Guggul (Guggulipid)
The stereoisomers E and Z guggulsterone (marketed in the United
States as guggulipid) are believed to be the active ingredients in
the resin of the Commiphora Mukul (guggul) tree found in arid
regions of India and Pakistan.37 The guggulsterones are extracted
from the resin using ethyl acetate. Studies performed by Urizar
and colleagues at Baylor College of Medicine have determined
that E and Z guggulsterones are antagonist ligands for the bile acid
receptor farnesoid X receptor (FXR) which is an important regulator
of cholesterol homeostasis.38
The gum resin of the guggul tree has been used in Ayurveda,
traditional Indian medicine, for more than 2,000 years and has been
reported to have many health benefits including treating obesity and
hyperlipidemia.39
The earliest studies evaluating the impact of guggul on lipids were
conducted by G.V. Satyavati, who in 1966 found treatment with
gum guggul lowered serum cholesterol and prevented diet induced
atherosclerosis in rabbits.40 Subsequently, many human trials have
been conducted.41–50 Although at least 10 studies have been reported,
only 2 have been placebo-controlled (1 each in Indian and Western
populations).49,50 The non placebo controlled trials of guggul have
been uniformly conducted in the Indian population.
Of the 2 placebo controlled trials, the study performed in the Indian
population found that guggulipid reduced total cholesterol by 11%,
LDL-C by 12% and triglycerides by 15%.49 In 1987, on the strength
of the Indian studies, guggulipid was approved for use as a lipidaltering drug in India. Guggulipid is widely available in the United
States where it is marketed as a dietary supplement.
The single study reported in the United States was a carefully
designed 8-week, double-blind randomized, placebo-controlled trial
using a parallel design.50 Of 103 persons enrolled, 85 completed the
three arm study. Participants received either placebo, standard-dose
guggulipid (SDG) 1,000 mg or high-dose guggulipid (HDG) 2,000
mg 3 times a day with meals for 8 weeks. Baseline characteristics
did not differ between the groups. Likewise, study dropouts were
not found to differ from study completers.
At the conclusion of the study, directly measured LDL-C levels
had fallen by 5 % in the placebo group but increased by 4% in the
SDG group (P = 0.01 vs placebo) and by 5% in the HDG group
(P = 0.006 vs placebo). Interestingly, participants randomized
to guggulipid whose baseline LDL-C was above 160 mg/dL
experienced a fall in triglycerides of 14% (p = 0.02 vs. placebo) in
the SDG group and 10% (P = 0.03 vs. placebo) in the HDG group.
Lipoprotein(a) was also noted to fall modestly in both actively
treated groups, but this did not reach statistical significance.
Of note, over the course of this study, highly sensitive C-reactive
protein fell by 29% in the HDG, remained unchanged in the SDG
group and rose by 25% in the placebo group.
A subgroup analysis was performed to determine whether there
were particular subgroups of participants who responded favorably
to guggulipid. Defined as a drop of 5% or greater in LDL-C from
baseline, only 18% of participants treated either with SDG or
HDG had a positive response and indeed 51 of actively treated
participants experienced a negative response (i.e., an increase in
LDL-C of 5 % or more. The responders did not differ from the nonresponders in terms of baseline characteristics.
Although most Indian studies reported significant lipid altering
effects of guggulipid, it should be noted that even in these studies
20–30% of Indian participants were also non responders.41–43 Of
some concern was the high rate of hypersensitivity rashes (9% of
participants) reported in the Western study.50
In summary, in a carefully controlled clinical trial conducted in the
US population, guggulipid did not lower LDL-C and in fact actually
increased LDL-C in the majority of treated patients. Interestingly,
in both Indian and Western studies there do appear to be some
patients who respond to guggulipid. The percentage of people
responding favorably in the Indian trials suggests that perhaps the
Indian population may differ in some basic way (genetically or
environmentally) from the primarily Caucasian population studied
in the aforementioned study. Larger, well designed, placebocontrolled studies should be considered in both the Indian and
Western populations.
Policosanol
Policosanol is a mixture of long-chain primary aliphatic alcohols
isolated from sugarcane wax.51 Other policosanol products can be
derived from wheat germ, rice bran and beeswax.52 Cuban sugarcane
policosanol is the most widely available policosanol product and is
sold as a lipid-lowering product in over 40 countries.51
Until recently, nearly all studies conducted on policosanol
were performed by a single Cuban research group.53–62 Funding
for virtually all the Cuban studies was provided by Dalmer
Laboratories, a commercial enterprise founded by the Center of
Natural Products, National Center for Scientific Research, La
Habana, Cuba, to market policosanol. The Cuban studies are
Clinical Insights
remarkably consistent and report a dose dependent cholesterol
for a total of 40 days followed by a 20 day wash out. After 40 days
lowering response to policosanol at doses ranging between 2–40
mg per day. LDL-C reductions over 15% have been reported for the
participants receiving cinnamon supplementation experienced a
reduction in their fasting glucose, triglyceride and LDL-C levels
2 mg dose. Average LDL-C reductions of 24% were consistently
reported in studies using 5–40 mg doses (average dose 12 mg/day).63
of (18–29%), (23–30%), and (7–27%) respectively. HDL-C was
not altered. The authors postulated that cinnamon might increase
In these studies virtually no response was seen in the placebo group.
Additionally, Cuban policosanol has been reported to raise HDL-C
phosphorylation of the insulin receptor leading to increased insulin
sensitivity which has been associated with both improved glucose
quite substantially.63
and lipid levels.68
It has been suggested that the mechanism of action of policosanol
involves down regulation of HMG-CoA reductase.64 However, with
Subsequently, studies performed in Germany and in the Netherlands
have been published.69,70 The results of these studies differ
the recent publication of a number of negative studies outside of
Cuba, the beneficial effects of policosanol have been called into
significantly from the initial Pakistani study.
question. In 2004, a Dutch study evaluated a 20 mg dose of wheat
germ derived policosanol and found no impact on either total
The German study randomized 79 type-2 diabetics to receive either
3 grams of aqueous cinnamon extract or placebo for a total of 4
cholesterol or LDL-C.65 In 2006, 3 groups (2 from the United States
and 1 from Germany) published placebo-controlled trials examining
the lipid altering effects of sugarcane-derived policosanol in doses
ranging from 10 to 80 mg per day.66,67,52 These studies failed to find
any significant lipid-altering effects of policosanol. It should be
noted that the German study examined doses of 10, 20, 40, and 80
mg of policosanol purchased from Dalmer Laboratories in Cuba.52
months.69 Baseline blood sugar in the treatment group was 167 + 41
mg/dL and 156 + 26 mg/dL in the control group. Hemoglobin A1c
was 6.86 + 1.00 in the treated group and 6.71 + 0.73 in the control
group. Patients were obese and were noted to have significantly
higher baseline LDL-C and lower triglycerides than the participants
in the Pakistani study. Study participants were on multiple
medications to treat their diabetes including: metformin (27.7%),
sulphonylureas (4.6%), thiazolidinediones (1.5%) and combination
therapies (30.8%). Additionally, 20% were on lipid altering
medications. At study conclusion, blood sugar was noted to have
fallen by 10.3% in the cinnamon treated group and by 3.4% in the
placebo group (p = 0.038). No significant changes were observed in
lipid levels.
While ethnic differences or variation in dietary habits of Latin
American participants as compared to European and American
participants cannot be ruled out as the cause for the marked
discrepancy between the earlier Cuban studies and the more recently
published data, this seems unlikely. At the present time policosanol
cannot be recommended for the treatment of hyperlipidemia.
Cinnamon
In 2003, Khan and colleagues published the first in vivo study
examining the impact of cinnamon supplementation on lipids and
blood sugar in a group of 60 poorly controlled (baseline fasting
blood sugars ranged from 140–400 mg/dL) Pakistani diabetic
subjects.68 Baseline LDL-C and triglyceride levels appeared to be
lower than would be expected in a Western population of diabetic
subjects and subject weight was not noted. Participants were all
taking sulfonylurea drugs. Because no mention was made of the
use of lipid lowering agents, it is not clear if study subjects were
taking lipid altering medications. This study received significant
media attention. Subsequently, the use of cinnamon as a dietary
supplement increased enormously in the United States and
elsewhere.
In brief, 30 men and 30 women were randomly enrolled into 6
groups. Groups 1, 2, and 3 consumed 1, 3, or 6 grams of cinnamon
(in capsules). Groups 4, 5, and 6 consumed corresponding placebo
capsules. Participants consumed cinnamon or matching placebo
The Dutch study enrolled 25 obese postmenopausal women with
type 2 diabetes to receive 1.5 grams of cinnamon (Cinnamomum
cassia—the same cinnamon used in the Pakastani study) or
matching placebo daily for 6 weeks.70 Baseline glucose, hemoglobin
A1c, and lipid values were similar to those noted at baseline in
the German study. Diabetes control was achieved utilizing the
same classes of medications as in the German study. No mention
was made of how many participants were on lipid altering agents.
At the conclusion of this study no changes were noted in any of
the metabolic parameters studied including: whole body insulin
sensitivity, oral glucose tolerance or lipid levels.
Based on the data from the latter 2 studies, it would appear that the
early enthusiasm for cinnamon supplementation (especially in terms
of lipids) might have been premature. The patients enrolled in the
German and Dutch studies appear to be more similar to American
patients (in terms of concomitant medications, lipids, and diabetes
control) than were those in the Paskistani study. Before we can
recommend cinnamon supplementation for our patients further
study is essential.
reductions, but also demonstrated a 11.2% increase in HDL-C.84
Nutraceuticals (Functional Foods)
Nuts
There is little doubt that diet influences lipid levels. Certain
foods—nuts for example—have been reported to lower lipid levels,
but which nuts, and how much should we be recommending?
The FDA has approved a qualified health claim for nuts.71 This
claim states that consumption of 1.5 ounces of nuts per day may
reduce cardiovascular risk. It is postulated that in addition to the
Barley has also been studied.86,87 Behall’s studies of moderately
hypercholesterolemic men and women found significant positive
results from the consumption of barley.86,87 A reduction of 20%
in total cholesterol and 24% in LDL-C was obtained in 1 study.87
Other recent studies have also demonstrated positive effects of flax,
psyllium, and other soluble fibers on LDL-C.88–90 Because of the
favorable effects of soluble fiber, particularly in lowering the
LDL-C risk factor, the Adult Treatment Panel (ATP) III recommends
fatty acid composition of nuts, other components of nuts (possibly
arginine, plant sterols, and phenolic components) may play a role
a minimum of 5–10 grams a day. Even higher intakes of 10–12
grams of soluble fiber per day can be beneficial.
in the favorable lipid effects seen in individuals who consume nuts
regularly.72
In contrast, insoluble fiber does not significantly affect LDL-C
Tree nuts include walnuts, almonds, pistachios, and macadamia
nuts. Peanuts are considered ground nuts or legumes. Walnuts and
almonds have been most comprehensively studied. Most clinical
trials evaluating the impact of nuts on lipid profiles have been small,
ranging from 10–49 participants.73-77 LDL-C reduction has been
consistently shown in these studies, typically in the range of 12–
13%. Triglyceride reductions have been less consistent and HDL-C
generally remains unchanged. The American Dietetics Association
evidence library concludes that “Consumption of 50–113 grams
(1/2 to 1 cup) of nuts daily with a diet low in saturated fat and
cholesterol decreased total cholesterol by 4–21% and LDL-C by
6–29% when weight was not gained.”78 Generally speaking, in our
clinic we only recommend consumption of 1/2 to 1 cup of nuts daily
as a cholesterol-lowering strategy in people who can afford this
significant caloric load. For most patients we recommend somewhat
smaller portions of nuts as part of a healthful diet.
Fiber
Dietary fiber is known to have a small but important impact
on LDL-C.79,80 Fiber is the edible part of a plant or analogous
carbohydrate that cannot be digested by the human digestive
system. There are two types of fiber: water-soluble (viscous fiber)
and water-insoluble. Recent reports indicate that the soluble forms
of fiber can reduce LDL-C levels.79,80 An approximate 5 percent
reduction in LDL-C levels is obtained from 5–10 grams of soluble
fiber per day except in individuals with normal LDL-C levels.81,82
Good sources of soluble fiber include oats, oat bran, barley, flax,
pectin (found in fruits), root vegetables, legumes, gums (e.g., guar
gum) and psyllium (found in some cereals and Metamucil).
Several recent studies have looked specifically at the effects of oats
or oat bran on LDL-C.80, 83–85 Both oats and oat bran demonstrated
favorable results in the lowering of LDL-C. Robitaille’s study
on overweight pre-menopausal women provided 28 grams
of oat bran daily over 4 weeks and not only obtained LDL-C
cholesterol levels.91 It does contribute, however, to the total dietary
fiber intake. In large prospective, epidemiological studies, total dietary fiber has been shown to protect against coronary heart
disease.92–96 The studies examined the relationship between whole
grain consumption and CHD. Researchers found a 20–40%
reduction in CHD risk for those who habitually consumed whole
grains as compared to those who rarely ate whole grains.79 Pereira’s
study found a 12% decrease in coronary events and 25% decrease in
death for every 10-gram increment of fiber consumed per day.96
There are several mechanisms by which it is believed dietary
fiber may protect against CHD. They include lowering serum
cholesterol and LDL-C, attenuating blood triglyceride levels and
decreasing hypertension.92,97 Fiber consumption also predicts
insulin levels and weight gain more strongly than a low total fat and
saturated fat diet.98 High fiber diets may protect against obesity and
cardiovascular disease (CVD) by lowering insulin levels. It has been
shown that the intake of dietary fiber is inversely correlated with
cardiovascular disease risk factors in both sexes.99
Most of the evidence shows that a mixture of both soluble and
insoluble forms of fiber is an important part of a diet that promotes
good cardiovascular health.100 Based upon this conclusion, the
National Academy of Science recommends 25 gr/day of fiber for
women 19–50 years of age and 21 gr/day for women over 50. For
men 19–50 years of age, 38 gr/day is recommended and 30 gr/day
for men over 50. This was set from an established 14 grams of fiber
per 1,000 calories.98
Portfolio Diet
In 2003, the first study evaluating the impact of an isocaloric diet
rich in a number of different functional foods was published.101
Jenkins and colleagues compared the LDL-C impact of a low-fat
diet rich in functional foods (portfolio diet group) versus either a
low-fat diet alone (control group) or in combination with a 20 mg
dose of lovastatin (an HMG CoA reductase inhibitor) (statin group).
Clinical Insights
postmenopausal women) were randomly assigned to one of the
aforementioned diets for 1 month. Participants received all of their
meals (with the exception of fresh fruits and vegetables) from a
central kitchen.
altering effects of the portfolio diet noted above were not the result
of the soy protein but rather the result of the almonds, plant sterols
and viscous fiber included in this diet.
Other Commonly Used Supplements:
The portfolio diet provided a number of supplements/functional
foods including plant sterols (1.0 gram/1,000 kcal), soy protein
(21.4 grams/1,000 kcal), viscous fibers (9.8 grams/1,000 kcal), and
almonds (14 grams/1,000 kcal). The low-fat diet was rich in whole
wheat cereals and breads and skim milk dairy products but did not
contain the functional foods found in the portfolio diet. In addition
to 20 mg of daily lovastatin, the statin group consumed the same
low-fat diet as the control group.
Baseline lipid levels did not differ significantly between the groups.
At the conclusion of the study control, statin, and portfolio groups
experienced mean (SE) reductions in LDL-C of 8.0% (2.1%)
(P=.002), 30.9 (3.6%) (P <.001), and 28.6% (3.2%) (P<.001)
respectively. The changes noted in both the statin and portfolio
groups were significantly different from those noted in the control
group. Of note, statin or portfolio groups did not differ in terms of
LDL-C reduction achieved.
Although the initial portfolio study enrolled free living individuals,
all foods with the exception of fresh fruits and vegetables were
prepackaged and provided to participants. Subsequently, the same
investigators invited 35 of the original cohort and 31 additional
participants to join the portfolio ad libitum study. A total of 55
individuals completed the 52-week study in which all participants
were asked to follow the portfolio diet as described earlier.102 At
3 and 12 months mean (+SE) LDL-C reductions were stable at
14.0 + 1.6 % (P < 0.001) and 12.8 + 2.0% (P < 0.001) respectively.
Although these reductions were considerably less marked than in the
1-month study, it should be noted that 31.8% of participants were
able to achieve an LDL-C reduction of > 20%. Not surprisingly,
degree of compliance correlated with LDL-C reduction.
Patients commonly use other supplements for their presumed
cholesterol-lowering impact. Among the most frequently used are
garlic, lecithin, artichoke, and apple cider vinegar. At least 3 welldesigned studies failed to document any influence of garlic (Allium
sativum) on serum lipoproteins.107–109 Lecithin is derived from soy
beans and is sold as a “fat emulsifier.” Many patients believe that
lecithin is capable of breaking down fat and cholesterol in their
intestines and bloodstream, thereby rendering it “harmless.” These
claims are totally unsubstantiated by the medical literature. In 2001,
Pittler and colleagues from the Department of Complementary
Medicine at the University of Exeter reviewed all published studies
evaluating the use of artichoke leaf extract for the treatment of
hypercholesterolemia.110 In short, although 2 studies found a
modest benefit on total cholesterol, overall the evidence was not
compelling. Clearly, further evidence is required before this therapy
can be recommended. Finally, although actress Shirley MacLaine
claims on her website that “research has shown that apple cider
vinegar can assist in lowering bad cholesterol,” she failed to provide
any clinical trial evidence in support of this statement. Likewise, we
were unable to find any (well-conducted or otherwise) studies on the
impact of apple cider vinegar on cholesterol.
In summary, of the available supplements touted for cholesterol
reduction, plant stanols/sterols appear to be the most effective.
Red yeast rice appears to be beneficial but Cholestin©, the only
well studied agent, is no longer available in the United States. The
portfolio diet provides evidence that combinations of supplements
and functional foods (plant sterols, nuts, and fiber) can significantly
improve lipid levels. For patients with mild hypercholesterolemia,
lifestyle changes combined with well-studied supplements and
functional foods may allow normalization of lipids without the use
of pharmaceutical agents.
Soy
Early research and a 1995 meta-analysis created a great deal of
interest in using soy protein as a means of lowering LDL-C.103 More
recent data has not supported the role of soy as a practical means
of lowering LDL-C.104 In order to achieve any meaningful LDL-C
reduction, large amounts of soy are required. Even when individuals
consume up to half of their daily protein with soy protein, only a
very small reduction (roughly 3%) in LDL-C is achieved.104 Soy
seems to be a more efficacious lipid lowering agent in persons with
marked hyperlipidemia.105,106 However, replacing high fat animal
protein with soy rich foods may indirectly result in lipid reduction
via a reduction in saturated fat intake. It would appear that the lipid
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Castano G, Fernandez L, Mas R, et al. Effects of addition of policosanol to omega-3 fatty
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with type II. hypercholesterolaemia. Asia Pac J Clin Nutr. 2004;13(suppl):S102.
30.
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studies. Lipids. 1996;31:243-252.
28.
Registration Is Still Open! Don’t Forget Your Passport
April 13–15, 2007
in
Montreal, Quebec!
Attend the first-ever
international meeting of the
Northeast Lipid Association,
being held in beautiful
Montreal, Quebec.
4HE4HIRD!NNUAL3CIENTIlC&ORUM
OFTHE
.ORTHEAST,IPID!SSOCIATION
Attend cutting-edge
presentations by today’s
leading experts on:
Current Clinical Trials and
Pharmacologic Control of Lipids
and Lipid Lipoproteins
From Basic Research to the
Clinic
New Approaches to Lipid
Management
Take part in workshops:
Secondary Hyperlipidemia
Therapeutic Lifestyle Changes
View entire
program &
register online
at
www.lipid.org
Passport Information
!PRILn
4HE&AIRMONT1UEEN%LIZABETH
-ONTREAL1UÏBEC
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A current Passport is now required to travel
from the US to Canada, and more pertinently,
to return to the US after ANY travel abroad.
Complete information on obtaining or renewing
a valid US passport is available at: http://travel.
state.gov/passport/passport_1738.html.
10
Hotel Reservations
The Fairmont Queen Elizabeth
900 René-Lévesque Ouest
Montreal, Quebec, Canada H3B 4A5
Call 1-800-441-1414 and ask for the Northeast
Lipid Association room rate of $138 per night.
Offer ends March 12, 2007.
Practical Pearls
Statins and Myopathy
PETER P. TOTH, MD, PhD, FAAFP, FACC,
FAHA, FICA
Visiting Clinical Associate Professor
University of Illinois School of Medicine
Peoria, Illinois
Director of Preventive Cardiology
Sterling Rock Falls Clinic
Sterling, Illinois
The statins are a safe and efficacious class of medication used for
the treatment of a variety of dyslipidemias.1,2 There is clear clinical
trial evidence supporting the use of high dose statin therapy to
achieve ever greater reduction of risk for atherosclerosis disease
progression and acute cardiovascular events.3,4 Among the most
important potential forms of toxicity attributable to statin therapy
are myalgia, myopathy, and rhabdomyolysis. This Practical Pearl
will provide some clinical and scientific perspectives on these
skeletal muscle-related side effects. It is important to emphasize
at the outset of this article that our understanding of how statins
induce these adverse events is rudimentary at best and considerable
work remains to be done on this important facet of statin therapy.
This article is by no means comprehensive.
When speaking with colleagues around the country, it is apparent
that myalgias are by far the most common reason for patient
noncompliance on stain therapy. Unfortunately, too often, when
a patient calls a healthcare provider’s office complaining of
musculoskeletal pain, they are advised as a matter of course to
discontinue their medication. While this may certainly be an
appropriate response in some situations, it should not be a “knee
jerk reflex.” Patients taking a statin should be asked to present for
further evaluation in order to more appropriately determine whether
these medications are in fact etiologic for the patient’s specific
complaints. Aches and pains are a fact of life. Frequently when
patients do call, further assessment indicates joint or tendinous
pain, rather than myalgia. If muscle pain has developed, often it
is a single muscle or a single group of muscles with a unilateral
distribution. This is usually not a sign of statin-induced myalgia.
The patient’s recent history may reveal muscle trauma or overuse as
the true cause of their discomfort.
Statin-induced myalgia is most commonly described as having
a symmetrical distribution and can involve the musculature of
the back and extremities. If muscle discomfort is intensifying or
accompanied by weakness, or if the patient reports sudden changes
in exercise or exertional tolerance, he or she warrants evaluation
for myopathy. To make matters even more complicated, a patient
may have myopathy even in the absence of an elevation in serum
creatine kinase (CK) levels.5 If CK is elevated, the threshold for
defining myopathy is currently set at 10 times the upper limit of
normal. When serum levels of CK elevate, it is a sign of skeletal
myocyte injury and lysis. Established risk factors for statin induced
myopathy include advanced age, renal or hepatic insufficiency,
polypharmacy (including fibrates) with potential for drug interactions,
excess alcohol intake, electrolyte disturbances, hypothyroidism,
hypertriglyceridemia, and dehydration, among others.6,7 In many
cases repleting electrolytes, identifying and correcting inappropriate
combinations of drugs, encouraging rehydration, providing thyroid
hormone supplementation, and reducing alcohol intake ameliorates
muscle symptoms. If myopathy is suspected, statin therapy should
be immediately discontinued and the patient monitored closely.
Rhabdomyolysis is a medical emergency and CK levels can increase
to > 50 times the upper limit of normal. Patients with rhabdomyolysis
should be admitted to hospital for supportive care and hydrated
aggressively to avoid renal failure secondary to myoglobinuria.
Patients with a history of statin-induced rhabdomyolysis should not
be rechallenged with a different statin. Patients with a history of
myopathy but who do not meet diagnostic criteria for rhabdomyolysis
can be rechallenged with either the same statin at a lower dose or,
more preferably, rechallenged with a different statin. Although there
is some conceptual argument for instituting a hydrophilic statin
in such patients, there is really no difference in the incidence of
myopathy when comparing lipophilic and hydrophilic statins.
What are some of the hypotheses for how statin therapy induces
skeletal muscle complications? Most theories invoke mitochondrial
dysfunction. Mitochondria are the nuclear power plants of cells as
they convert oxidizable substrates to ATP, the energy currency of
all eukaryotic cells. The mitochondrial inner membrane houses an
electron transport chain made up of a series of cytochromes and
other redox active centers that conduct electrons down a series of 4
oxidation-reduction complexes (complexes I-IV). As electrons pass
through these complexes, their energy is harnessed and converted
into a proton gradient (protonmotive force) across the mitochondrial
inner membrane. This protonmotive force is then used to induce a
series of conformational changes in the F1F0 ATP synthetase which
leads to the release of ATP. The terminal electron acceptor along the
electron transfer chain is cytochrome oxidase which uses oxygen as
a substrate to accept low energy electrons. The oxygen is reduced
to water. The reaction catalyzed by cytochrome oxidase forms the
very foundations of why we breathe and why we require a complex
cardiovascular system to deliver oxygen to every cell type comprising
our bodies.
Conenzyme Q or ubiquinone is an important component of complex
I. Statin therapy reduces farnesyl pyrophosphate biosynthesis,
an important precursor to ubiquinone formation. Some muscle
physiologists have hypothesized that statin therapy may impair rates
of electron transport and ATP biosynthesis because they reduce the
availability of ubiquinone. This would lead to an energy imbalance
in the myocyte and clinically could manifest as myalgia and easy
fatigability or weakness secondary to reduced availability of ATP.
Hence it has become fashionable to advise patients to take coenzyme
Q10 supplements. The NLA does not recommend that this be
done.8 There is wide variability in the bioavailability of CoQ10 in
commercially available preparations and to date there are no placebo
Continued on page 23
11
From the Journals
RONALD B. GOLDBERG, MD
Professor of Medicine, University of Miami School of Medicine
Director, Lipid Disorders Center
Associate Director, Diabetes Research Institute
Miami, Florida
CAD and High HDL
DeFaria Yeh D, Freeman MW, Meigs JB, Grant RW. Risk Factors
for Coronary Artery Disease in Patients with Elevated HighDensity Lipoprotein Cholesterol. Am J Cardiol. 2007;99:1-4.
Elevated high density lipoprotein cholesterol (HDL-C) levels are
associated with reduced risk of coronary artery disease (CAD).
However it has been noted that occasional subjects with CAD have
high HDL levels. To better understand CAD development in this
supposedly protected group of patients, the authors undertook a
cross-sectional analysis of patients with CAD from several large
internal medicine practices affiliated with a single academic center,
in order to evaluate the risk factor profiles in patients with versus
without elevated HDL-C. They hypothesized that patients with high
HDL-C values would have an excess of other CAD risk factors to
offset the protection from CAD associated with high HDL-C levels.
Of 41,982 patients with normal or elevated HDL-C levels, 1,610
were identified with CAD, of whom 98 had high HDL-C levels,
defined as >70 mg/dL in men and >80 mg/dL in women and the
remainder (n=1,512) were designated as having normal HDL-C
(40-60 mg/dL for men and 50-70 mg/dL for women). The average
age was ~70 years, and there was no difference in the proportion of
men to women (3:2), but there was a higher proportion of African
Americans to Caucasians in the high HDL-C group.
The frequency of alcohol use and of exercise was greater in the
high HDL-C group and mean weight and the prescription of beta
blockers and statins was lower. Although the mean total cholesterol
was higher in the elevated HDL-C group, low density lipoprotein
cholesterol and triglyceride levels were lower. Diabetes (28.6%
versus 38.4%) and obesity (10.2% versus 17.7%) were less common
in the high HDL-C group and chronic obstructive pulmonary
disease was more frequent (8.2% versus 3.9%), while hypertension
occurred with equal frequency in the two groups (78.6 versus
88.7%). Finally patients with high HDL-C levels had a mean of
2.5 of 4 CAD risk factors (age/gender, hypertension, diabetes and
12
dyslipidemia) as compared to 2.9 for the normal HDL-C group
(p<0.007). In multivariate analysis, including triglyceride and total
cholesterol in the model eliminated the association between diabetes
and obesity prevalence and high HDL-C, while African American
ethnicity continued to be independently associated.
These rather surprising findings do not support the notion that
subjects with high HDL-C and CAD have an excessive complement
of CAD risk factors to offset the protective effects of high HDL-C.
The findings of higher frequencies of alcohol intake, exercise, African
American ethnicity and chronic obstructive pulmonary disease in the
group with high HDL-C suggests that these factors, which are known
to be associated with higher HDL-C levels, may be contributing to
the elevated HDL-C values in these individuals.
Conversely the lower frequency of diabetes, obesity and
hypertriglyceridemia may indicate that selecting patients with high
HDL-C would tend to exclude subjects with insulin resistance, who
typically have low HDL-C levels. In any event, the absence of an
excess of CAD risk factors in subjects with CAD and high HDL-C
raises the possibility that these elevated HDL-C levels may not be
protective against risk for CAD. Although this is a cross-sectional
study and cause and effect cannot be determined, these findings
nevertheless add to the concern that HDL-C levels may not always be
independently associated with risk of CAD.
!MERICAN Certification in
"OARDOF
Clinical Lipidology
#LINICAL
,IPIDOLOGY The Pursuit of Excellence
2007 ABCL Summer Examination
Hyatt Scottsdale Resort at Gainey Ranch
Scottsdale, Arizona
Saturday, June 2, 2007
Application Deadline:
Postmarked by April 27, 2007
For eligibility requirements and an application visit:
www.lipidboard.org or call 904.674.0752
Register Today
Send in your registration or visit www.lipid.org
N L A
2007 Annual
Scientific Sessions
 P W 
S L A
N F  T
L  A
H R  G R
S, A
M –J , 
The 2007 NLA Scientific Sessions features an
expanded format offering 4 days of education
activities and diverse offerings designed to meet
the needs of our membership who focus on the
treatment of patients with lipid and related disorders.
Ancillary Courses and Symposia
• Updated - Masters in Lipidology Board Review
Course (meets criteria for both ABCL and ACCL
Examinations)
• Updated - Lipid Management Training Course
• New - Lipid Clinic Operation & Development
Course
• New - Nutrition Counseling Course
• Daily Satellite Breakfast and Dinner Symposia
Special Events
• Expanded Poster Sessions and Young
Investigator’s Award
• ABCL Certification Exam
• ACCL Certification Exam
• ABCL Convocation Ceremony
• President’s Gala Dinner and Reception
southwest
association
T S L A  
C   N L A
Conference Highlights
Scientific Session Offerings
• Treating Challenging patients
• Dietary, Therapy and Lifestyle Modification
• Diabetes Prevention and Treatment
• Early Detection of CAD
• Debating LDL Treatment Strategies
• Targeting HDL
• Developing a Comprehensive
Cardiometabolic Risk Reduction Program
• Workshops programs
Target Audience
This activity is designed to meet the needs of
physicians, physician assistants, pharmacists,
nurses, and registered dietitians interested in lipid
management.
CME Reviewers: Peter H. Jones, MD
2007 Scientific Sessions Program Co-Chairs:
Christie M. Ballantyne, MD and
Anne C. Goldberg, MD
Also featuring- The NLA-SAP Challenge:
An Interactive Competition
Accommodations
Hyatt Regency Scottsdale at Gainey Ranch
7500 E. Doubletree Ranch Road
Scottsdale, Arizona 85258
Tel: 480 444 1234
Reservations
Call the reservation hotline at 800-233-1234 and ask for the NLA
room rate of $185/night plus the resort fee of $6/night. Offer ends
April 30, 2007.
13
2007 Scientific Program
2007 NLA/SWLA Annual Scientific Sessions
Thursday, May 31
5:00–6:30 pm
Opening Session:
The NLA-SAP Challenge – An Interactive Competition
—Hosted by Michael Davidson, MD and
Alan Brown, MD
6:30 pm
Welcome Reception
7:30 pm
Satellite Dinner Symposium
Friday, June 1
14
6:30 am
Satellite Breakfast Symposium
8:00–9:00 am
Targeting HDL: What Have We Learned
and Where Are We Headed?
The Review of the Data of Recent Trials
—Ernst Schaefer, MD
Ongoing Approaches for New Therapies
—Benjamin Ansell, MD
9:00 am
10:00 am
Debate–LDL: Fixed Dose vs. Titration
to Target
—Michael Davidson, MD and
Christie Ballantyne, MD
Refreshment Break
10:30 am–Noon
Early Detection of Coronary Artery Disease
Non-invasive Imaging: Cardiac CT in 2007
—Matthew Budoff, MD
Non-invasive Imaging: Carotid Ultrasound —Edward Gill, MD
Current and Novel Biomarkers
—Vera Bittner, MD
Panel Discussion: Which Imaging/Blood
Tests Are Most Useful? Who Should Be Paying?
Noon
Lunch
1:00–3:00 pm
Elective Workshops – 50-minute workshops repeated one time
Imaging and Biomarkers–Applications for Practice
—Carl Rubenstein, MD and Vijay Nambi, MD
Management of Dyslipidemia, Metabolic Syndrome and Obesity in Children
—Piers Blackett, MD
Challenging Cases in Lipidology
—James Falko, MD, Jonathan Abrams, MD and
Thomas Blevins, MD
Who Is In Control? Enhancing Patient Adherence
—Beth Jackson, MSN and Kim Birtcher, PharmD
1:00–5:00 pm
NLA Nutrition Counseling Workshop (separate registration required)
7:00 pm
Satellite Dinner Symposium
Saturday, June 2
6:30 am
8:00–10:00 am
Satellite Breakfast Symposium
Diabetes Prevention and Treatment: What Can Be Done to Reduce CVD?
8:00 am
DREAM and PROACTIVE – Promise and Worries
—Steven Haffner, MD
8:30 am
Glucose Control in Diabetic Patients to Prevent CVD
—Darren McGuire, MD and
Kitty Wyne, MD, PhD
9:10 am
Treatment of Diabetic Dyslipidemia
—Anne Goldberg, MD
Panel Discussion and Q&A
10:00 am
Refreshment Break
New Frontiers in Treating Lipids and Atherosclerosis
Scientific Sessions: May 31–June 3, 2007 • Exhibits: May 31–June 2, 2007
10:30–Noon
10:30 am
Dietary Therapies and Lifestyle Modification
Nutritional Therapies and the Role of Extreme Diets in CVD Patients
—Rebecca Reeves, PhD, RD
11:00 am
How Do You Impact Lifestyle Modification and Sustain Weight Loss in Practice?
—John Foreyt, PhD
11:30 am
Cardiovascular Benefits of Omega-3
and -6 Fatty Acids
—Dariush Mozaffarian, MD, DrPH
Noon–12:15 pm
NLA/Baylor Virtual Lipid Preceptorship Program
12:15 pm
Lunch and Poster Session Presentations
1:30–3:50 pm
Treating the Challenging Patient: Management Strategies
1:30 pm
Managing the Statin Intolerant Patient
—Peter Jones, MD
1:55 pm
HIV-related Insulin-Resistance and Dyslipidemia
—Anthony Busti, PharmD
2:20 pm
Weighing the Risks and Benefits of Dyslipidemia Pharmacotherapy in Elderly Patients
—Joseph Saseen, PharmD
2:45 pm
Managing the Obese Adolescent Patient with Dyslipidemia
—Philip Zeitler, MD
3:10 pm
Ethnic Populations: Lipid Abnormalities and Treatment Strategies in South Asians and Native Americans
—Nicola Abate, MD and Beth Malasky, MD
4:00–4:15 pm
Young Investigator Award Presentation and Annual Business Meetings
5:30–7:00 pm
ABCL Convocation Ceremony
7:00–10:00 pm
President’s Dinner and Dance
Sunday, June 3
7:00–11:00 am
NLA Symposium:
Comprehensive Cardiometabolic Risk Reduction Program
—Christie Ballantyne, MD, Peter Jones, MD, and
Cathy Nonas, MS, RD
• Unmet Clinical Needs in Cardiometabolic Risk Management
• The Drivers of Cardiometabolic Risk • Patient Evaluation and Classification
• Treatment Options for Enhancing the Management of Cardiometabolic Risk
• Case Study Review
• Treatment Program
11:00 am
Adjourn
Scientific Posters and
Young Investigators Award
40 authors submitted scientific posters that will be
presented during a special session on Saturday, June 2 from
Noon–1:30pm. Submissions from fellows and other young
investigators will be judged. Further, the top ranked young
investigator will be chosen for an award, which will be
announced on June 2 at 4:00pm.
Poster categories include:
• Young Investigators (in-training residents,
fellows or < 5 years in practice)
• Academic Programs
• In-Practice
• Industry
All accepted abstracts submitted prior to the February 28,
2007 deadline will be printed in the May
Scientific Sessions edition of the Journal of Clinical Lipidology.
15
Satellite Symposia
Please note these are independent satellite CME/CE events held in conjunction with the 2007 NLA Scientific Sessions.
You may register onsite for these events.
Dinner Symposium
May 31, 2007 7:30–9:30 pm
Reducing Residual Cardiovascular Disease Risk in Patients with Type 2 Diabetes or the Metabolic Syndrome
Chair: W. Virgil Brown, MD, Emory University, Atlanta, GA
Supported by an educational grant from Abbott Laboratories, Inc.
Breakfast Symposium
June 1, 2007 6:30–8:00 am
Statins and Myotoxicity: What Do We Really Need to Know?
Chair: TBD
Supported by an educational grant from Novartis Pharmaceutical Corp.
Dinner Symposium
June 1, 2007 7:00–9:00 pm
Hypertriglyceridemia and Dyslipidemia: Targeting Treatment to Improve CVD Risk Reduction
Chair: Henry N. Ginsberg, MD, Columbia University, New York, NY
Supported by an educational grant from Reliant Pharmaceuticals.
Breakfast Symposium
June 2, 2007 6:30–8:00 am
Evaluation of HDL in Mixed Dyslipidemia
Chairman: Christie Ballantyne, MD, Baylor College of Medicine, Houston, TX
Supported by an educational grant from Merck & Co., Inc.
Commercial Support
NLA 2007 Industry Council
The National Lipid Association would like
to acknowledge the following companies
for their continued support of the
organization on an annual basis.
Diamond Supporter
Abbott Laboratories, Inc.
Platinum Supporter
AstraZeneca
Merck & Co., Inc
Sanofi-Aventis
Silver Supporter
Daiichi Sankyo, Inc.
Merck/Schering-Plough Pharmaceuticals
Pfizer, Inc.
Reliant Pharmaceuticals, Inc.
Bronze Supporter
Berkeley HeartLab, Inc.
16
SOUTHWEST
ASSOCIATION
2007 Commercial Support
The Southwest Lipid Association would
like to acknowledge the following
companies for their support of the 2007
Annual Scientific Sessions.
President’s Circle
Abbott Laboratories, Inc.
Merck & Co., Inc.
Pfizer, Inc.
Sanofi-Aventis
Patron
Daiichi Sankyo, Inc
Merck/Schering-Plough Pharmaceuticals
Reliant Pharmaceuticals, Inc.
Friend
AstraZeneca
Berkeley HeartLab, Inc.
2007 NLA Annual Scientific Sessions
Hyatt Gainey Ranch, Scottsdale, Arizona
Scientific Sessions: May 31–June 3, 2007
Pre-Conference Courses: May 30–31, 2007
1
Guest name(s), if attending meeting:
First Name
Middle Initial
Last Name
Mailing Address
Membership status:
City
State or Province
Phone
Emergency Contact/Phone
DO
PhD
RN
Email
Check all that apply: MD
2
3
Country
PA
RPH
PharmD RD
Member
Scientific Sessions May 31-June 3
Includes course syllabus and one admission badge to Exhibit
Hall for food functions. (Saturday Night Dinner NOT Included)
Join NLA and register for Scientific Sessions
$295
$345
$0
$0
$395
$0
Non-Member
Other
Trainee
Ancillary Courses
Please see Ancillary Events Pages for more info
$850
$1100
$850
Master’s Board Review Course
(Previously purchased NLA-SAP 3 vol. set) $100
$200
$100
Lipid Management Training Course
May 30-31
$195
$295
$195
$80
$180
$80
$75
$175
$75
$
$
$
Lipid Clinic Operations & Development Course
May 31 Nutrition Counseling Workshop June 1
Registration Fee Total
Social Events and Guest Fees
Please see Special Events Page for more info
Easy Ways To Register
Mail To:
NLA
8833 Perimeter Park Blvd #301
Jacksonville, FL 32216
Fax to:
NLA at 904-998-0855
Fax with credit card number
and signature
Online:
www.lipid.org
*Master’s Course
Additional discounts apply if
you have purchased individual
volumes of the NLA-SAP.
For those special discounts,
register online at www.lipid.
org/education
Registration: Registration and
payment must be received no
later then May 21, 2007. After
this date a syllabus and name
badge cannot be guaranteedso register TODAY!
Saturday Night Dinner-Registrant
$90 x 1
$______
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$90 x___ $______
Saturday Night Kids Party
$50 x ___ $______
Exhibit Hall Pass-Guest(s)
$60 x ___ $______
Cancellation: Telephone
cancellations will not be
accepted. A written notice of
cancellation must be received
no later then May 16, 2007.
*Includes Social Events and
Guest Fees.
CVD Dancing Lessons
Special Dietary needs:
$0 x ____ 0
$______
$0 x ____ 0
$______
Social Events and Guest Total
$______
Combined Total Sections 2,3 &4
$______
Credit Card #
Practical Pedometer Course and Walk
5
NP
Circle fee meeting category based on attendee type
Master’s Board Review Course*
May 30-31
(Includes NLA-SAP 3 vol. set) 4
Zip
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My application for membership has been submitted and confirmed.
I will apply at www.lipid.org
Please send me membership
information.
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ADA Compliance:
Attendees of the NLA Scientific
Sessions who need additional
reasonable accommodations or
who have special needs should
contact the NLA at 904-9980854.
Name on Card
17
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Castano G, Mas R, Fernandez JC, et al. Effects of policosanol on older patients with
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Castano G, Mas R, Fernandez L, et al. Effects of policosanol 20 versus 40 mg/day in the
treatment of patients with type II hypercholesterolaemia: a 6-month double-blind study. Int J
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Behall KM, et al. Lipids significantly reduced by diets containing barley in moderately
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Janikula M. Policosanol: a new treatment for cardiovascular disease? Altern Med Rev.
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Menendez R, amor AM, Rodeiro I, et al. Policosanol modulates HMG-CoA reductase
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Lin Y, Rudrum M, van der Wielen RP, et al. Wheat germ policosanol failed to lower
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policosanol and atorvastatin: A randomized, parallel, double-blind, placebo-controlled trial.
Am Heart J. 2006;152:982e1-982e5.
Lui S, et al. A prospective study of dietary fiber intake and risk of cardiovascular disease
among women. J Am Coll Cardiol. 2002;39:49-56.
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Merchant AT, et al. Dietary fiber reduces peripheral arterial disease risk in men. J Nutr.
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Khan A, Sefad M, Khan MMA, Khattak KN, Anderson RA. Cinnamon improves glucose and
lipids of people with type 2 diabetes. Diabetes Care. 2003;26:3215-3218.
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Pereira MA, et al. Dietary fiber and risk of coronary heart disease. Arch Intern Med.
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Mang B, Wolters M, Schmitt B, et al. Effects of cinnamon extract on plasma glucose, HbA1c,
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in normal men. N Engl J Med. 1993;328:603-607.
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Karmally W, et al. Cholesterol-lowering benefits of oat-containing cereal in Hispanic
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Chen J. et al. A randomized controlled trial of dietary fiber intake on serum lipids. Eur J Clin
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Darvy BM, et al. High-fiber oat cereal compared with wheat cereal consumption favorably
alters LDL-cholesterol subclass and particle numbers in middle-aged and older men. Am J
Clin Nutr. 2002 Aug;76(2):351-358.
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Robitaille J, et al. Effect of an oat bran-rich supplement on the metabolic profile of
overweight premenopausal women. Ann Nutr Metab. 2005 May-Jun; 49(3):141-148. Epub
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Saltzman E, et al. An oat-containing hypocaloric diet reduces systolic blood pressure
and improves lipid profile beyond effects of weight loss in men and women. J Nutr.
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100. Erkkila AT, Lichtenstein AH. Fiber and cardiovascular disease risk: how strong is the
evidence? Cardiovasc Nurs. 2006 Jan-Feb;21(1):3-8.
101. Jenkins DJA, Kendall CWC, Marchie A, et al. Effects of a dietary portfolio of cholesterollowering foods vs lovastatin on serum lipids and c-reactive protein. JAMA. 2003;290:502510.
102. Jenkins DJA, Kendall CWC, Faulkner DA, et al. Assessment of the longer-term effects of
a dietary portfolio of cholesterol-lowering foods in hypercholesterolemia. Am J Clin Nutr.
2006;83:582-91.
103. Anderson JW, Johnstone BM, Cook-Newell ME. Meta-analysis of the effects of soy protein
intake on serum lipids. N Engl J Med. 1995;333:276-282.
104. Sacks FM, Lichtenstein A, Van Horn L, Harris W, Kris-Etherton P, Winston M. Soy protein,
Isoflavones, and cardiovascular health. An American Heart Association science advisory for
professions from the nutrition committee. Circulation. 2006;113:1034-1044.
105. Crouse JR, Morgan T, Ellis J, Vitolins M, Burke GL. A randomized trial comparing the effect
of casein with that of soy protein containing varying amounts of isoflavones on plasma
concentrations of lipids and lipoproteins. Arch Intern Med. 1999;159:2070-2076.
106. Lichtenstein AH, Jalbert SM, Adlecreutz H, et al. Lipoprotein response to diets high in soy
or animal protein with and without isoflavones in moderately hypercholesterolemic subjects.
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107. Superko HR, Krauss RM. Garlic powder, effect on plasma lipids, postprandial lipemia,
low-density lipoprotein particle size, high-density lipoprotein subclass distribution and
lipoprotein (a). J Am Coll Cardiol. 2000;35:321-326.
108. Isaacsohn JL, Moser M, Stein EA, et al. Garlic powder and plasma lipids and lipoproteins: A
multicenter, randomized, placebo-controlled trial. Arch Intern Med. 1998;158:1189-1194.
109. Berthold HK, Sudhop T, von Bergmann K. Effect of a garlic oil preparation on serum
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110. Pittler MH, Thompson CO, Ernst E. Artichoke leaf extract for treating hypercholesterolemia.
Cochrane Database Syst Rev. 2002;(3):CD003335.
ABCL Recognizes Clinical Lipidology Diplomates
In 2006 the American Board of Clinical Lipidology officially awarded Diplomate status to the following physicians who qualified for this
distinction. The Diplomates will be honored at the ABCL Convocation Ceremony to be held at the NLA 2007 Annual Scientific Sessions at the Hyatt
Regency Scottsdale Resort at Gainey Ranch on Saturday, June 2, 2007. The National Lipid Association congratulates these dedicated professionals.
Nicola Abate, MD
Dallas, TX
John C. Dormois, MD
Tampa, FL
Walter D. Kohut, MD
Greensboro, NC
John R. Nelson, MD
Fresno, CA
Richard A. Sokol, MD
Norfolk, VA
Yoel R. Vivas, MD
Pittsburgh, PA
Rajaratnam Abraham, MD
Fall River, MA
George W. Douglass, MD
Charleston, SC
Jeffrey H. Kuch, MD
Largo, FL
Ahmed F. Okba, MD
Moline, IL
David B. Southren, MD
Valley Cottage, NY
Steven W. von Elten, MD
Warrenton, VA
C. David Akin, MD
Independence, MO
Ralph J. Duda, MD
Springfield, MO
Mariananda Kumar, MD
Lecanto, FL
Mark W. Oldendorf, MD
Rensselaer, NY
Andrew D. Sumner, MD
Hummelstown, PA
Karol Watson, MD
Los Angles, CA
Hisham A. Alrefai, MD
Scottsburg, IN
Honey East, MD
Jackson, MS
Dharamjit N. Kumar, MD
Jamaica, NY
Joseph Tannous, MD
Aurora, MN
Thomas R. White, MD
Cherryville, NC
Moutasim H. Al-Shaer, MD
Davenport, IA
Jeff L. Eggart, MD
Surfside Beach, SC
Richard L. Kunis, MD
Pittsford, NY
Trevor J. Orchard, MD,
M.Med.Sci.
Pittsburgh, PA
Kimberly Tibbs, MD
Colorado Springs, CO
Mary B. Wiles, MD
Blairsville, GA
Joseph R. Arulandu, MD
Laporte, IN
Scott Eisenberg, DO
Marlboro, NJ
Peter M. Lehmann, MD
Poulsbo, WA
Douglas L. Trenkle, DO
Ellsworth, ME
Robert D. Williams, MD
Franklin, NC
Christie Ballantyne, MD
Houston, TX
Andrea J. Frank, DO
Kenilworth, NJ
Ann M. Liebeskind, MD
Neenah, WI
Mohammad A. Tulimat, MD
Sterling Heights, MI
Gordon L. Wolfe, MD
Portland, OR
Sarang Baman, MD
Franklin, WI
Howard D. Frauwirth, MD
New York, NY
Bradford C. Lipman, MD
Atlanta, GA
Ernesto Ang Uy, MD
Lakeland, FL
John C. Wood, MD
Signal Mountain, TN
Mark A. Bartz, MD
Greenwood, SC
John G. Frownfelter, MD
Southfield, MI
Jonathan S. Lown, MD
Smithtown, NY
Michael P. Varveris, MD
Naples, FL
Hasan Zakariyya, MD, MBBS
Fulton, NY
Krishna R. Bhaghayath, MD
Nashua, NH
Joseph P. Giancaspro, MD
Westerly, RI
R. Clarke Maiocco, MD
Littleton, CO
Carmelo V. Venero, MD
North Haven, CT
Allan Zelinger, MD
Oak Lawn, IL
Thomas C. Blevins, MD
Austin, TX
Ronald Goldberg, MD
Miami, FL
Chadi H. Mansour, MD
Sterling Heights, MI
Jose V. Venero, MD
Palm Bay, FL
Paul E. Ziajka, MD, PhD
Winter Park, FL
Adolphus S. Bonar, MD
Waxhaw, NC
Edward M. Goldenberg, MD
Wilmington, DE
Sabyasachi Bose, MBBS, MRCP
(UK)
Saskatoon, Canada
Rob Greenfield, MD
Newport Beach, CA
B. Alan Bottenberg, DO
Carson City, NV
Howard A. Brand, MD
Stony Brook, NY
Clinton D. Brown, MD
Brooklyn, NY
Robert J. Buynak, MD
Valparaiso, IN
Brian Chesnie, MD
Newport Beach, CA
(D.H.) Dellie H. Clark, MD
West Monroe, LA
Michael E. Cobble, MD
Sandy, UT
Steven M. Curland, MD
Norwich, CT
Julio C. Delgado, MD
Selma, AL
Margo Denke, MD
Kerrville, TX
Martha D. Dickens, MD
Madison, MS
Avinash C. Gupta, MD
Lakewood, NJ
Rodolfo W. Guzman, MD
Bronx, NY
Alan Helmbold, DO
Senoia, GA
John A. Hoekstra, MD, PhD
Richmond, VA
Glenn R. Huth, MD
Appleton, WI
Ramakrishnan Iyer, MBBS
Charleston, WV
Frank J. Johnson, MD
Bluefield, VA
Steven R. Jones, MD
Virginia Beach, VA
Salman Khan, MD
Chester, VA
Amit Khera, MD
Dallas, TX
Jane E. Kienle, MD
Gulfport, FL
John A. Osborne, MD, PhD
Grapevine, TX
Robert L. Panther, MD
Oconomowoc, WI
Ramesh N. Patel, MD
Joliet, IL
Jane K. Pearson, MD
Madison, WI
Daniel F. Phillips, MD
Pensacola, FL
Stacey J. Porterfield, DO
Colorado Springs, CO
Maureen Rafferty, MD
Park Ridge, IL
William B. Martin, MD
Lawrenceville, GA
Khaled A. Reheem, MD
Munster, IN
Patrick F. Mathias, MD
Kissimmee, FL
Thomas B. Repas, DO
New Holstein, WI
Theodore Mazzone, MD
Chicago, IL
Nicholas P. Ricculli, DO
Chester, NJ
Donald L. McAlexander, MD James W. Roberts, MD
Concord, NC
Charlotte, NC
Patrick McBride, MD
Madison, WI
Robert Rosenson, MD
Chicago, IL
Patrick J. McCullough. MD
Cincinnati, OH
Gary E. Schaffel, MD
Lake Forest, IL
Chris S. McElroy, MD
Martinez, GA
Jeffrey C. Schultz, MD
Baltimore, MD
David G. Meyers, MD, MPH Simone M. Scumpia, MD
Fairway, KS
Austin, TX
Michael Miller, MD
Baltimore, MD
Barry Seidman, MD
Delray Beach, FL
Jeanette A. Moleski, DO
Hudson, OH
Charlie Shaeffer, MD
Rancho Mirage, CA
Terrance J. Moran, MD
Monterey, CA
Edward J. Shahady, MD
Fernandina Beach, FL
Richard L. Mueller, MD
New York, NY
Bridget P. Sinnott, MD
Chicago, IL
Vincent P. Murphy, MD
Beaumont, TX
Daniel E. Soffer, MD
Swarthmore, PA
American Board of Clinical Lipidology
2006 Honorary Diplomates
Elizabeth Barrett-Connor, MD
La Jolla, CA
John Brunzell, MD
Seattle, WA
William Castelli, MD
Framingham, MA
Jean Davignon, MD
Montreal, Quebec, Canada
William Hazzard, MD
Seattle, WA
Donald Hunninghake, MD
Carlsbad, CA
John Kane, MD
San Francisco, CA
Robert Knopp, MD
Seattle, WA
Ronald Krauss, MD
Oakland, CA
John LaRosa, MD
Brooklyn, NY
19
Education Programs
2007
New Starting May 2007 – Updated curriculum
2007 Course Dates
Held prior to NLA Regional Scientific Meetings
May 30–31 • Scottsdale, AZ August 2–3 • Savannah, GA September 27–28 • Minneapolis, MN
www.lipid.org/education
JANUARY
This intermediate level course will present a comprehensive indoctrination to clinical lipidology and will provide essential information and resource materials for the systematic management of dyslipidemia in a lipid clinic program.
January 19–21, 2007
APRIL
JANUARY
Lipid Management Training Course
January 19–21, 2007
April 13–15, 2007
Pacific Lipid Association
3rd
AnnualMeeting
Scientific Forum
Inaugural
of the Northeast Lipid AsSheraton San Diego Hotel
sociation
and Marina
Fairmont Queen Elizabeth
—San Diego
— Montreal
MAY
APRIL
Upcoming Meetings
LEVEL I–II
April 13–15, 2007
May 31–June 3, 2007
3rd Annual Scientific Forum
National
Lipid Association
of the Northeast
Lipid AsAnnual
Scientific
Sessions
sociation
Hyatt
Regency
Scottsdale
Fairmont
Queen
Elizabeth
at Gainey Ranch
— Montreal
—Scottsdale
NLA Nutrition Counseling Workshop – New Course
This half-day workshop is designed to assist all levels of healthcare practitioners in improving their nutrition counseling
skills. It will include discussions on building rapport and listening skills, application of principles and techniques
involved in interviewing, assessing and providing nutrition counseling, and developing goals/outcomes and therapeutic
relationships with patients/clients. Small group role-playing will focus on case-study evaluation and simulated nutrition
counseling with patients.
2007 Course Dates
Held at NLA Regional Scientific Meetings
June • Scottsdale, AZ August 5 • Savannah, GA September 30 • Minneapolis, MN
For complete information and to register, visit www.lipid.org/education
LEVEL IV
National Lipid Association Self-Assessment Program
The Metabolic Syndrome
Volume III: Vascular Biology & Advanced Lipid Metabolism
Each module provides up to 60 hours of AMA PRA Category 1 Credit™. Credit hours earned by completing the NLA-SAP
series can be applied toward meeting the credentialing requirements for the ABCL and ACCL certifying examinations.
Order online at www.lipid.org/sap
Masters in Lipidology – Advanced Training and Board Review Course
This intensive 2-day board review course is offered by the NLA to members seeking an in-depth, advanced review of
the specialty and/or certification by the American Board of Clinical Lipidology or the Accreditation Council for Clinical
Lipidology. The 3-volume NLA Self-Assessment Program (NLA-SAP) is included in the course fee.
New starting May 2007 – Expanded curriculum and individual tracks for physicians and mid-level providers
preparing for certification
2007 Course Dates
Held prior to NLA Regional Scientific Meetings
April 12–13 • Montreal May 30–31 • Scottsdale, AZ August 2–3 • Savannah, GA September 27–28 • Minneapolis, MN
nual Scientific Sessions
ented with the
nnual Scientific Forum
For complete information and to register, visit www.lipid.org/education
2007
Gainey RangeONLINE
in Scottsdale,
AZ
PROGRAMS
An all-inclusive online education resource for
NLA members that provides access to:• Online
CME/CE activities
• Live and enduring webcasts
• NLA presentation highlights
• Interactive newsletters
20
NLACME.COMmunity
LIPID EDUCATION ONLINE
• Professional development tracking tools
• Auto log-in for NLA members
• And much more to come.
—San Diego
2007
California
Québec
Québec
Arizona
May 31–June 3, 2007
National Lipid Association
August 3–5, 2007
Annual Scientific Sessions
10th Annual Scientific
Hyatt Regency Scottsdale
Forum of the Southeast
at Gainey Ranch
Lipid Association
—Scottsdale
The Westin Savannah
— Savannah
Arizona
Georgia
SEPTEMBER SEPTEMBER
AUGUST
Volume II:
MAY
AUGUST
The NLA-SAP series is a comprehensive, interactive clinical problem-solving program that objectively validates, strengthens
and reinforces your knowledge of clinical lipidology.
Diagnosis & Management of Dyslipidemia
Sheraton San Diego Hotel
and Marina
Upcoming
Meetings
California
LEVEL II–III
Volume I: Pacific Lipid Association
Inaugural Meeting
August 3–5, 2007
September 28–30, 2007
4th
Annual
Forum
of theScientific
Southeast
Forum
of
the Midwest
Lipid Association
Lipid Association
The Westin Savannah
The Millennium Hotel
— Savannah
— Minneapolis
Georgia
Minnesota
September 28–30, 2007
Forum of the Midwest
NLA 2006 Scientific Meeting
LipidHighlights
Association
Now Online – CME/CE certified
— Minneapolis
Visit nlacme.com to learn more
Minnesota
News & Notes from the National Office
Launch of the Journal of Clinical Lipidology
On March 15th members wil be mailed their first edition of the
Journal of Clinical Lipidlogy. This is a milestone achievement for
our organization due to the efforts of the Board of Directors and our
Editor in Chief Dr. Virgil Brown. Members current in thier dues will
receive a regular subscription.
The Journal is always interested in content, to submit for publication
visit the Elsevier website at www.lipidjournal.com or contact Dan
Sosnoski ([email protected]), Commnications Director in the
NLA office.
Non-Physician Exam Ready: Apply Now
The highest priority established by the NLA Board of Directors
was to create and implement the exam for the non-physician
membership of the organization.The first exam will be held in
Scottdsale, Arizona on June 1st and a second exam will be offered
on June 2nd. Download your application for examination at www.
lipidspecialist.org applications must be received no later than April
30th. Remember the Accreditation Council for Clinical Lipidology
(ACCL) recommends the NLA-SAP program and the Masters to
prepare for this examination. Special arrangements have been made
to the Montreal Masters program for interested ACCL candidates.
Information on the Masters program or NLA-SAP program can
be found in this edition or at www.lipid.org . Contact Nicole
Woodsmall, RD ([email protected]), Assistant Education
Director, at the NLA office for questions and information.
Ongoing Committee and Board Nominations
The NLA website lists all our committees and opportunities to serve
on chapter and national Boards. Each committee is listed with its
specific charge, point of contact and availability. Members willing to
serve should apply through this process. Remember that the NLA is
a non-profit organization and all activity is conducted on a voluntary
basis. Expenses are reimbursed when conducted on behalf on the
NLA. Need more information? Contact Adam Beamer (abeamer@
lipid.org), Assistant Director of Programs and Membership in the
NLA office.
Strategic Planning II
The NLA Executive Committee, Committee Chairs, Chapter
Presidents and Presidents-Elect will be meeting on March 23, 2007
in New Orleans to review and update our strategic plan adopted
just last April. We have achieved many of our goals stated and the
leadership group is to reconvene to update our progress and redefine
our goals and assign new priorities. Two examples have been the
Journal of Clinical Lipidology and the new credentialing exam
offered by the ACCL. A full report will be presented at the Annual
Business meeting in Arizona on June 2, 2007.
Digestive Tract Masters Summit
The HDL Summit held at the American Heart Association meeting
last November drew an attendance of over 500 and launched a
new level of educational programing designed to debate topics at
the highest level of science and clinical application. In this vein,
the NLA is pleased to offer a Summit program at the 2007 AHA
meeting in Chicago on the topic of Digestive Tract Therapies. Dr.
Peter Jones is the Program Chairman and details regarding faculty
and agenda will be available this summer.
VLP Program to be Launched at NLA Meeting
The NLA has been working with the Center for Collaborative
and Interactive Technologies at Baylor University to develop an
interactive online preceptorship program that will be previewed
during the NLA Scientific Sessions in Arizona. The program is
unique in that participants can not only educate but will be able to
participate in a continuous quality improvement approach related
to their practice’s patient-care strategies. A key element with be
a self-audit tool that presents a snapshot of patient outcomes and
gives each practice an assessment with respect to all participating
facilities.
Counseling and Nutrition Workshop
The NLA has been awarded a grant from Unilever Inc. to develop
a stand-alone course on Nutrition and Behavioral Counseling. The
first course will be offered at the NLA Scientific Sessions this May
and is offered in the annual meeting registration package. For more
information contact, Nicole Woodsmall, RD (nwoodsmall@lipid.
org) at the NLA office.
CLM-SAPs and New SSM Programs
Approved for 2007
Four Complex Lipid Management Programs (CLM) are being
developed for release in 2007. Each program offers 5 CME
credit hours to participants. There are two variants, including the
traditional “Self-Assessment” Module and the new “Self-Study”
Module, that will include syllabus materials prior to presenting
the question section. All current members of the NLA will receive
a complimentary copies of all programs as they are released. The
estimated release dates are as follows:
21
The NLA Board of Directors
CLM-SAP: Management of Low HDL (September 2007)
PRESIDENT
James McKenney, PharmD
Richmond, VA
CLM-SAP: Clinical Applications of Lipoprotein
Subfractionation Testing, Inflammatory Markers and Noninvasive Assessments of Atherosclerosis (September 2007)
CLM-SAP: Primary Care Optimal Management of NCEP
LDL and Non-HDL Goals: Focus on Combination Therapies
(September 2007)
NLA-SSM: Lipid Altering Drug Pharmacology and Safety
(August 2007)
Back issues of the CLM-SAP programs can be found on a website
established by the developer, Professional Evaluation Inc. (www.
proevalinc.com). Back issues are currently not in print but can
downloaded electronically to NLA members for $35 each. Nonmembers pay $150.
NLA Forms GME Committee
The NLA Board recently formed a Graduate Medical Education
(GME) Committee, chaired by Dr. James Howard, to encourage
fellow involvement in the NLA and to encourage specialization in
IMMEDIATE PAST-PRESIDENT
Peter Jones, MD
Houston, TX
PRESIDENT-ELECT
Anne Goldberg, MD
St. Louis, MO
TREASURER
Neil Stone, MD
Chicago, IL
SECRETARY
Tom Bersot, MD
San Francisco, CA
TERM EXPIRING IN 2009
Roger S. Blumenthal, MD, FACC
Baltimore, MD
John R. Crouse, MD
Winston-Salem, NC
Mark J. Cziraky, PharmD, FAHA
Wilmington, DE
Penny Kris-Etherton, PhD, RD
University Park, PA
John Guyton, MD
Durham, NC
Janet Long, MS, ANCP
Providence, RI
Peter P. Toth, MD, PhD, FACC
Sterling, IL
Karol Watson, MD
Los Angeles, CA
Continued on page 23
AC C L
The Accreditation Council
for Clinical Lipidology
Eliot A. Brinton, MD
Salt Lake City, UT
W. Virgil Brown, MD
Decatur, GA
Vera A. Bittner, MD, MSPH
Birmingham, AL
David M.Capuzzi, MD, PhD
Philadelphia, PA
Michael H. Davidson, MD
Chicago, IL
Scott M. Grundy, MD, PhD
Dallas, TX
D. Roger Illingworth, MD, PhD
Portland, OR
H. Bryan Brewer, Jr., MD
Washington, DC
Mary Anne Champagne, RN, MSN
Palo Alto, CA
Luther T. Clark, MD
Brooklyn, NY
Jerome D. Cohen, MD
St. Louis, MO
Carlos A. Dujovne, MD
Overland Park, KS
Barbara J. Fletcher, RN, MN
Jacksonville Beach, FL
Robert H. Knopp, MD
Seattle, WA
Maria F. Lopes-Virella, MD, PhD
Charleston, SC
Mary P. McGowan, MD
Concord, NH
EXECUTIVE DIRECTOR
Christopher R. Seymour, MBA
Certification as a Clinical Lipid Specialist
The Accreditation Council for Clinical Lipidology (ACCL) is an independent
certifying organization that has developed standards and an examination in the field
of Clinical Lipidology for the growing number of mid- and advanced-level healthcare
practitioners who manage and treat patients with lipid or other related disorders.
The examination is designed to comprehensively evaluate the knowledge and experience of a wide range of medical
professionals. As a prerequisite, candidates must successfully credential to sit for the examination. The specific criteria
and the associated fees can be found at www.lipidspecialist.org. Those who successfully complete this examination
will be awarded the designation of “Clinical Lipid Specialist.”
2007 ACCL Examination Dates
First National Examination Day
Hyatt Scottsdale Resort at Gainey Ranch
Scottsdale, Arizona
Friday, June 1 or Saturday, June 2, 2007
Application Deadline: April 27, 2007
Summer Examination
The Westin Hotel
Savannah, GA
Friday, August 3, 2007
Application Deadline: July 5, 2007
Fall Examination
Minneapolis, MN
Friday, September 28, 2007
Application Deadline: August 30, 2007
For eligibility requirements and an application, go to www.lipidspecialist.org or call 904.674.0752
22
News and Notes continued from page 22
Practical Pearls continued from page 11
the field of clinical lipidology. To this end, the GME committee is
currently working on their first project, which is to develop a core
curriculum in clinical lipidology and a teaching module for program
directors/educators. Additionally, as part of this program, the
NLA will provide a limited quantity of the NLA Self-Assessment
Program to program directors and fellows free of charge.
controlled trials with this substance demonstrating any subjective or
objectively defined benefit in preventing myalgia or myopathy.
If you are a program director and would like to participate in this
training initiative, or you work closely with program directors or
fellows who might be interested in receiving a complimentary set
of the 3-volume NLA Self-Assessment Program, please contact
Nicole Woodsmall at [email protected] or 904-998-0854. We
look forward to your assistance in enhancing the level and quality
of dyslipidemia education that fellows and residents receive in their
training programs.
THE
Lipid Spin
Editors
Ronald B. Goldberg, MD
Professor of Medicine,
University of Miami School of Medicine
Director, Lipid Disorders Center
Associate Director, Diabetes Research Institute
Miami, FL
Maria F. Lopes-Virella, MD, PhD
Professor of Medicine and Pathology
Medical University of South Carolina
Ralph H. Johnson Medical Center
Charleston, SC
Co-editors
Lynn Cofer, MSN, RN, FAHA
Clinical Director,
Midwest Heart Specialists Lipid Clinic
Naperville, IL
Peter P. Toth, MD, PhD, FAAFP, FICA, FAHA, FACC
Director of Preventive Cardiology
Sterling Rock Falls Clinic, Ltd
Sterling, IL
Clinical Associate Professor
Southern Illinois University School of Medicine
Springfield, IL
NLA Staff Editor
Daniel Sosnoski
NLA Executive Director
Christopher R. Seymour, MBA
The Lipid Spin is published quarterly by the National Lipid Association
8833 Perimeter Park Blvd. #301 • Jacksonville, FL 32216
Phone: 904-998-0854 • Fax: 904-998-0855
Copyright © 2007 by the National Lipid Association. All rights reserved.
Visit us on the web at: www.lipid.org
Other effects have also been identified. Statin therapy is associated
with reduced intramyocellular mitochondrial number and volume,9
which would also be expected to adversely impact muscle cell
energy metabolism. It has also been shown that in some patients
statin induced myalgia/myopathy can be accompanied by increased
intramyocellular lipid deposition secondary to impaired beta-oxidation
of fatty acids by mitochondria and reduced cytochrome oxidase
activity.7 A particularly intriguing recent finding is that when patients
exercise after being given a statin, relative to patients not on a statin,
the activity of the ubiquitin-proteasome pathway increases, thereby
leading to increased catabolism of actin and myosin.10 It is possible
that patients who develop true persistent myalgia or go on to develop
myopathy may activate this pathway to a greater degree than those
who do not. To what extent any or all of these mechanisms are
operative in a given patient is still a matter of investigation. Clearly,
however, progress is being made in unraveling the etiologies of why
statins can induce myalgia and myopathy.
Unfortunately, there is a great deal of misinformation about statins
propagated in the media, the internet, and “patient advocacy groups.”
There is no question that it is of utmost importance that we protect
our patients’ health and do everything possible to identify true adverse
events. However, it is also important that these life-saving drugs
that also reduce risk for devastating complications of atherosclerotic
disease such as myocardial infarction and stroke not be discontinued
prematurely. The majority of patients will need reassurance about
continuing their therapy. For the ones who cannot tolerate a statin
and truly experience debilitating myalgia or myopathy, then
discontinuation and institution of appropriate alternative therapy is
clearly in their best interest.
REFERENCES
1.
Baigent C, Keech A, Kearney PM, et al. Cholesterol Treatment Trialists’ (CTT) Collaborators.
Efficacy and safety of cholesterol-lowering treatment: prospective meta-analysis of data from
90,056 participants in 14 randomised trials of statins. Lancet. 2005; 366: 1267–1278.
2.
Pasternak RC, Smith SC Jr, Bairey-Merz CN, Grundy SM, Cleeman JI, Lenfant C; American
College of Cardiology; American Heart Association; National Heart, Lung and Blood Institute.
ACC/AHA/NHLBI clinical advisory on the use and safety of statins. J Am Coll Cardiol. 2002; 40:
567–572.
3.
Cannon CP, Braunwald E, McCabe CH, et al. For the Pravastatin or Atorvastatin Evaluation
and Infection Therapy-Thrombolysis in Myocardial Infarction Investigators. Intensive versus
moderate lipid lowering with statins after acute coronary syndromes. N Engl J Med. 2004; 350:
1495–1504.
4.
Nissen SE, Tuzcu EM, Schoenhagen P, et al. For the REVERSAL Investigators. Effect
of intensive compared with moderate lipid-lowering therapy on progression of coronary
atherosclerosis: a randomized controlled trial. J Am Med Assoc. 2004; 291: 1071–1080.
5.
Phillips PS, Haas RH, Bannykh S, et al. Statin-associated myopathy with normal creatine
kinase levels. Ann Intern Med. 2002; 137: 581–585.
6.
Ballantyne CM, Corsini A, Davidson MH, et al. Risk for myopathy with statin therapy in high-risk
patients. Arch Intern Med. 2003; 163: 553–564.
7.
Antons KA, Williams CD, Baker SK, Phillips PS. Clinical perspectives of statin-induced
rhabdomyolysis. Am J Med. 2006; 119: 400-409.
8.
Thompson PD, Clarkson PM, Rosenson RS. An assessment of statin safety by muscle experts.
Am J Cardiol. 2006; 97: 69C-76C.
9.
Chapman MJ, Carrie A. Mechanisms of Statin-Induced Myopathy: A Role for the Ubiquitin–
Proteasome pathway. Arterioscler Thromb Vasc Biol. 2005;25:2441-2444
10.
Urso ML, Clarkson PM, Hittel D, Hoffman EP, Thompson PD. Changes in ubiquitin proteasome
pathway gene expression in skeletal muscle with exercise and statins. Arterioscler Thromb
Vasc Biol. 2005;25:2560–2566. 23
National Lipid Association Educational Activities & Meetings Calendar
Name and Time of Activity
Online: September 2006 – September 2007
CME Newsletter: Statin Safety – NLA Recommendations for the Primary Care Community
CME Newsletter: Diabetes & Dyslipidemia: Reports from the ADA Scientific Sessions
Sponsored by Albert Einstein College of Medicine
Webcast: New Perspectives on Real World Management of Dyslipidemia in Diabetes :
Cases and Controversies
NLA Sponsored/
Endorsed/Other
Contact and Registration
Information
Sponsored – CME
Online Activity
www.nlacme.com/statinsafety
Endorsed – CME, CE
Online Activity
www.NLACME.com
Endorsed – CME, CE
Online activity
www.NLACME.com
Sponsored – CME, CE
Online activity
Online Activity
www.nlacme.com/lipidmanagementtoday
Endorsed – AOA, CME
Online Activity
www.NLACME.com
Sponsored – CME
Live Meeting
www.lipid.org/education/masters
Sponsored by Albert Einstein College of Medicine
Online: November 2006 – November 2007
CME Newsletter: Lipid Management Today
Online: January 2007 – January 2008
Meeting Highlights: Presentations from the 2006 NLA Scientific Meetings
Online: January 2007 – January 2008
Webcast: Why Your Patients Are Not Getting to Goal – Steps You Can Use to Improve
Dyslipidemia Treatment Outcomes
www.NLACME.com
Sponsored by American Osteopathic Association
April 12-13, 2007
NLA Masters in Lipidology Board Review Course
Queen Elizabeth Fairmont Hotel, Montreal, Canada
April 13-15, 2007
Northeast Lipid Association 3rd Annual Scientific Forum
Queen Elizabeth Fairmont Hotel, Montreal, Canada
April 26-28, 2007
Preventive Cardiovascular Nurses Association 13th Annual Symposium
Hyatt Regency, Minneapolis, MN
May 4-5, 2007
Managing the Metabolic Syndrome & Reducing the Risk of Coronary Disease
The Westin Chicago River North, Chicago, IL
Live Meeting
Other
E-mail: [email protected]
Ph:904.998.0854
www.lipid.org
www.pcna.net/education/symposium/
index.php
Other
Live Meeting
www.blackwellfuturacourses.com
Live Meeting
www.lipid.org/education/lmtc
Sponsored – CME
Live Meeting
Live Meeting
www.lipid.org
Live Meeting
Ph:904.998.0854
www.lipid.org
Examination
www.lipidboard.org
Sponsored by Blackwell Futura Media Service
May 30-31, 2007
NLA Lipid Management Training Course
Hyatt Scottsdale Resort at Gainey Ranch, Scottsdale, AZ
May 30-31, 2007
June 1, 2007
NLA Nutrition Counseling Workshop
May 31 – June 3, 2007
National Lipid Association & Southwest Lipid Association
2007 Annual Scientific Sessions
June 1 or June 2, 2007
ABCL Physician Certification Exam
June 1 or June 2, 2007
ACCL Non-Physician Certification Exam
August 2-3, 2007
NLA Lipid Management Training Course
The Westin Hotel, Savannah, GA
August 2-3, 2007
The Westin Hotel, Savannah,GA
August 3, 2007
ACCL Non-Physician Certification Exam
August 5, 2007
NLA Nutrition Counseling Workshop
The Westin Hotel, Savannah
August 3-5, 2007
Southeast Lipid Association Annual Scientific Forum
24
Examination
www.lipidspecialist.org
Live Meeting
www.lipid.org/education/lmtc
Sponsored – CME
Live Meeting
Examination
www.lipidspecialist.org
Live Meeting
www.lipid.org
Live Meeting
Ph:904.998.0854
www.lipid.org

the Lipid Spin (Spring 2007)

Transcription

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