contents functional foods · each back issue order of 1–4 issues. for orders of 5 or more back...

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Andrea M. Hutchins, Donna M. Winham,PhD, RD DrPh, CHES

Introduction

The role of functional foods in chronic disease risk reduction has been given increasing attention

over the past 10 years by researchers. Functional foods are generally considered to be foods that provide health benefits beyond those associated with basic nutri-tion.1 Media promotions have heightened consumer awareness about the cardiovas-cular benefits of some functional foods such as whole grains, nuts, fish, and flaxseed. While legumes or dry beans have yet to receive as much publicity, a recent review of the literature has highlighted their positive effects on improving serum lipid profiles in patients with coronary heart disease (CHD),2 and a growing body of evidence supports the positive effect that dietary legume consumption confers on health, particularly in relation to CHD risk.

The current recommendations from the National Cholesterol Education Pro-gram (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III) include the use of functional foods such as legumes, oats, and marga-rines containing plant stanols/sterols in the Therapeutic Lifestyles Diet recommenda-tions.3 The NCEP Adult Treatment Panel III (ATP III) guidelines identify legumes as a good, low saturated fat protein source and also recognize their contribution to viscous fiber intake in the diet. One-half cup of legumes supplies 5.5 - 8 grams of total fiber, including 1 - 3.5 grams of viscous fiber or 10-35% of the 5 - 10 grams of daily viscous fiber intake recommended by the NCEP ATP III.

Research Trials

Few randomized, crossover research studies have examined the effects of legumes on cholesterol concentrations, and most of these have included legumes as only one part of a high-plant, low- cholesterol-type diet; however, a few studies have focused on the hypocholes-terolemic effects of legumes as part of a controlled or normal diet.

In a recent randomized, crossover re-search study, serum total cholesterol (TC) and low-density lipoprotein cholesterol

ContentsFunctional Foods The Hypocholesterolemic Effects of Legumes ...................1

Chair’s Corner ............2

Editor’s Notes .............3

Members in the News.... ............................3

Personal Approach to Weight Regulation ......6

TherapiesLipid Management in Type 2 Diabetes ...............................13

Have You Read? ......17

Resource Review ....19

Upcoming Issues

• Winter 2008 Editor’s Deadline, November 1• Spring 2008 Editor’s Deadline, February 1, 2008• Summer 2008 Editor’s Deadline, April 15, 2008• Fall 2008 Editor’s Deadline, July 1, 2008

Summer 2007 Volume 9, Issue 1

Functional FoodsThe Hypocholesterolemic Effects of Legumes

continued on page 4Spring 2007 Volume 9, Issue 4

Summer 2007 Volume 9, Issue 1www.complementarynutrition.org

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Chair’s Corner:Gretchen Forsell MPH, RD, LMNT

NCC EDITORIAL STAFFEditor

Sarah Harding Laidlaw, MS, RD, CDECopy Editor

Rebecca Schauer, RDPublications Chair

Laura W. Lagano, MS, RDEditors

Christian Calaguas, MPH, RDDanielle Torisky, PhD, RD

CPE EditorKatherine Stephens-Bogard, RD

EML CoordinatorGretchen Forsell, MPH, RD, LMN

The views expressed in this newsletter are those of the authors and do not necessarily reflect the policies and/or official positions of the American Dietetic Association. We invite you to submit articles, news and comments. Contact us for author guidelines. Send change-of-address notification to the American Dietetic Association, 120 South Riverside Plaza, Ste. 2000, Chicago, IL 60606-6995. Copyright © 2007 Nutrition in Complementary Care, a Dietetic Practice Group of the American Dietetic Association. All material appearing in this newsletter is covered by copyright law and may be photocopied or other-wise reproduced for noncommercial scientific or educational purposes only, provided the source is acknowledged. For all other purposes, the written consent of the editor is required.

Annual Subscription Rates (in U.S. dollars, payable in U.S. funds)Individuals who are ineligible for ADA membership ...................................................................... $35/yearBack issues ............................................................... $10 each, 4 for $35For international orders, add $5 shipping and handling per annual subscription and for each back issue order of 1–4 issues. For orders of 5 or more back issues, shipping is $6.50 and $1.50 for each additional issue. Make checks payable to NCC DPG#18 and mail to the Treasurer. See back cover for address. ISSN 1524-5209

Welcome to a new year for NCC-DPG. Let me start by saying THANK YOU to each and every current and new member. This is your DPG

and everyone on the Executive Committree (EC) is looking forward to serving the needs of our members.

I would like to thank Doug Kalman for his leadership during the last year. A special thank you to outgoing EC members and the many volunteers of NCC. It is with their committment that NCC continues to be one of the premier DPGs offered to ADA members.

Mark your calendar for Monday, October 1st for the NCC priority session at ADA’s Food and Nutrition Conference & Expo (FNCE) in Philadelphia where EC member Kathy Swift, MS, RD, LDN and Dr. Mark Hyman will be conducting a session on “Ultrametabolism: The Causes of Obesity - An Integrative Approach to Weight Loss.” On Friday and Saturday prior to the start of FNCE the EC will be meeting and looking at ways to streamline the business of the DPG, improve the structure of the DPG, enhance educational opportunities and improve the financial status of NCC. While at FNCE be sure to drop by and say hello at the NCC booth in the DPG Showcase and Product Market-place. Check the NCC Web site www.complementarynu-trition.org additional information.

2007 ADA Awards and HonorsIn recognition of outstanding service and contributions to the dietetics profession, twenty individuals and two programs have been selected by the Honors Committee and the Board of Directors to receive top American Dietetic Association awards and honors. The awards and honors will be presented at various times during the 2007 Food & Nutrition Conference & Expo in Philadelphia, PA.

Congratulations to the following NCC members who are recipients for outstanding leadership achievements and contributions to the profession and practice of dietetics!

Marjorie Hulsizer Copher AwardPenny M. Kris-Etherton, PhD, RD

Medallion AwardsGeorgia G. Kostas, MPH, RDMarilyn Laskowski-Sachnoff, MA, RD Vivan B. Pilant, PhD, RD

Late this summer the new redesign for the Web site will be unveiled. We hope it makes navigating the site easier.

Finally, NCC is always looking for volunteers! Feel free to contact me if you are interested. Welcome to an exciting year!


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Editor’s Notes:Sarah Harding Laidlaw, MS, RD, MPA, CDE

Another year is well upon us — welcome back to renewing members and welcome to those

who are joining us for the first time. I sincerely hope that you enjoy your member benefits in NCC as much as I have over the past nine years. It is hard to fathom that NCC is approaching its first

decade as a DPG. I can still remember the meetings held in Boston to get the group organized and our first, what I would call real presence at FNCE in Kansas City in 1998. We have come a long way and we will continue to strive for excellence as the practice group continues to move forward in what are exciting times for complementary nutrition and alternative and integrative therapies.

For some reason, this seems to be the hottest summer ever. No rain, below average precipitation and raging wild-fires do not help. Everyone stays in because of the heat, the smoke, or both. For those of us who are very active, these are challenges that must be met with conservatism that means plenty of fluids and electrolyte replacement beverages! And, getting out only in the early morning hours. For those clients and patients we work with, fluid replacement is equally important, especially for the elderly who have a blunted thirst response in the first place and the very young who rely on us for knowing when and how much they need to drink. So, drink to your health and remind others to do the same.

This issue provides several different approaches to health issues we are seeing all too often – diabetes, heart disease, and obesity. Each topic is related and I am certain that reading these articles will provide you with some of the most recent information to enhance your practice.

Save time and avoid missing important NCC and ADA news!

ADA makes it easy for you to update your contact information. Visit the online Business Center at http://www.eatright.org/obc to access your profile; e-mail [email protected]; fax changes to 312/899-4812; or call the Member Service Center at 800/877-1600, ext. 5000, from 8 a.m. to 5 p.m. Central time, Monday through Friday.

Stephanie Richards, RD, MPA in conjunction with Cleveland Heights, University Heights School District received a $10,000 General Mills Champions

for Healthy Kids Youth Nutrition and Fitness grant for nutrition and wellness programming and physical fitness equipment in 2006. The SMART! (Students Making a Realistic Transformation!) program was designed to help 6th through 8th grade students assess their current fitness and nutrition levels, and help them develop individual goals. Students learned interesting facts about food and diet. In addition, a circuit-training method was incorpo-rated into physical activities. Students were able to use the fitness equipment as they completed the program, which is designed to help create a preventive health culture within the school and community. For more on Stephanie’s work, see the Resource Review on page 19 and the General Mills Youth Nutrition and fitness Web site at http://www.gen-eralmills.com/corporate/commitment/champions.aspx.

Let your fellow NCC members know about your accomplishments. Email Sarah Harding Laidlaw, at [email protected] with information about YOU and YOUR business, innovative approaches to CAM, and achieve-ments.

Members in the News….

Those of you who would like to contribute an

article or have topics that you would like to see

in future issues, please feel free to drop me an

email or give me a call – peaknut@cascadeac-

cess.com or 702-346-7968 – or contact anyone

of the capable NCC leaders listed on the back of

the newsletter.


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(LDL-C) concentrations decreased in a moderate risk popu-lation by over 8%, following pinto bean consumption (1/2 cup daily) for 8 weeks4 as part of the participants’ normal diets. Cholesterol concentrations were lowered regardless of the starting concentration point of the participants. The mean percent reductions in serum TC and LDL-C of 8.4% and 8.6%, respectively, observed in this trial are in accord-ance with the reductions observed in most other trials that investigated pinto beans either individually or as part of a component of mixed legumes.

Jenkins et al.5 also observed mean percent reductions of 7% and 5% in serum TC and LDL-C, respectively, in a free-living, hypercholesterolemic population fed a mixed legume diet. Greater reductions were observed in serum TC and LDL-C of 19% to 23% and 23% to 24%, respec-tively, in two similar, but separate trials that examined the effects of greater than ½ cup of pinto beans and navy beans6, 7

by Anderson et al. These researchers7 also reported a significant 20% reduction in mean serum HDL-C, in addition to a 23% reduction in mean serum TC. In con-trast, Mackay and Ball8 noted almost no change in serum TC and LDL-C when a legume mixture (80 grams or about 1/3 cup) was consumed by free-living, hypercholesterolemic participants.

Furthermore, legume powders were used in two studies. Frühbeck et al.9 asked participants with either borderline high, or high, serum cholesterol concentrations to consume 90 grams of cooked or raw field bean flour in addition to a controlled diet. Consumption of the cooked field bean flour significantly lowered TC by 2% and 7% and LDL-C by 5% and 7% in the borderline high and high cholesterol groups, respectively. The groups also experienced increases in serum high-density lipoprotein cholesterol (HDL-C) concentrations of 18% and 15% (borderline high and high cholesterol groups, respectively). Consumption of the raw field bean flour also lowered TC and LDL-C and raised HDL-C by 8%, 8%, and 15%, respectively, in the high cholesterol group. In contrast, a whole grains and legume powder (22% legumes) significantly increased HDL-C by 16%, but did not significantly change TC or LDL-C10 in adults with coronary artery disease.

Two studies have examined the effects of consuming canned baked beans versus canned spaghetti for two weeks on cholesterol levels in either healthy participants11 or mildly hypercholesterolemic participants12 with contrasting results. Shutler et al.11 reported that baked bean consumption (one 450 gram can per day) reduced TC by 12%, but there was no reduction in TC associated with the canned spaghetti consumption. However, Cobiac et al12 noted almost no

change in serum TC and LDL-C with either baked bean (approximately 377 grams per day) or canned spaghetti consumption.

Trials have also found reductions in serum triglycerides (TG), although larger amounts of legumes were fed, and often the legumes replaced carbohydrate sources that may have been composed of simple rather than complex carbohydrates. For instance, Jenkins et al.5 observed a significant reduction in mean serum TG of 25% after feed-ing 335 grams of mixed legumes, including pinto beans that replaced 25% of calories from other carbohydrate sources in the diet. Anderson et al.6 also observed similar results, as mean serum TG levels were reduced significantly by 20% after feeding 240 grams (about 1 cup) of navy and pinto beans combined. The simple and complex carbohydrate sources were controlled for in this diet, and were equivalent to amounts in the control diet.

A number of studies have also included legumes as part of carbohydrate-rich, protein-rich, low-fat, or plant-based diets that have been used to examine effects on cholester-ol concentrations. Most of these studies reported that the diets containing legumes as a component lowered TC and/or LDL-C concentrations in the participants.13-16 However, two studies did not find any differences in TC or LDL-C concentrations when the participants consumed modest (greater than 25 grams per day) or intense (greater than 35 grams per day) dietary fiber diets17 compared to a control diet, or a high-fiber diet compared to a low-fiber diet.18

Several possible mechanisms of action exist that may explain the hypocholesterolemic effects of legumes. These mechanisms include fat displacement from the diet, direct binding of dietary cholesterol by viscous fiber in the intestine, interruption of bile acid enterohepatic circulation, and inhibition of endogenous cholesterol synthesis by short chain fatty acids (SCFA). However, it has yet to be deter-mined which mechanism or combination of mechanisms is responsible for the hypocholesteremic effects of legumes.

Take Home Message

Overall, research studies support the hypocholestero-lemic effects of legumes. Due to the fact that many legume types are inexpensive, readily available, and widely accepted among the US population, implementation of dietary changes that include increased legume consumption to improve the risk for CHD appears realistic in comparison to other more traditional interventions, namely conventional drug therapy. Although it cannot be argued that some in-dividuals, particularly those with excessively elevated serum lipoprotein profiles and genetic predisposal to lipid abnor-

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Functional Foods – Legumes


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malities, require the help of medications such as statins to achieve normal, healthy serum lipoprotein profiles, this type of therapy does not appear to be optimal for everyone due to safety concerns and cost constraints.3 Therefore, individuals who do not require the use of such medications should be encouraged to make reasonable diet and physical activity behavior modifications that are generally safer, offer fewer side effects, are more affordable, and provide more wide-spread health benefits. Thus, it is essential that the current recommendations established by governmental agencies for increased, frequent legume consumption be conveyed to the public, who can use this simple dietary modification to improve their health.

Andrea Hutchins, PhD, RD is an assistant professor in the Department of Health Sciences at the University of Colorado at Colorado Springs. Her research focuses on the role of func-tional foods in the prevention and treatment of cardiovascular disease and diabetes. Contact Andrea at: [email protected]; 719-262-4467.

Donna Winham, DrPH, CHES assistant professor in the Department of Nutrition at Arizona State University-Poly-technic focuses her research on the biological, environmental, and sociocultural factors that shape food practices and influ-ence chronic disease risk across the lifespan. Contact Donna at: [email protected]; 480-727-1722.

References

1. Tapsell LC. Herbs and spices as functional foods. Med J Aust. 2006;185:S6.

2. Anderson JW, Major AW. Pulses and lipaemia, short- and long-term effect: Potential in the prevention of cardiovascular disease. Br J Nutr. 2002;88(Suppl 3): S263-S271.

3. National Cholesterol Education Program Expert Panel on Detection E, and Treatment of High Blood Choles- terol in Adults (Adult Treatment Panel III). Third Report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III), Final Report. Washington, D.C.: National Heart, Lung and Blood Institute of the National Institutes of Health; September 2002. NIH Publication No. 02-5215.

4. Winham DM, Hutchins AM, Johnston CJ. Pinto bean consumption reduces biomarkers for heart disease risk. J Am Coll Nutr. In press.

5. Jenkins DJ, Wong GS, Patten R, et al. Leguminous seeds in the dietary management of hyperlipidemia. Am J Clin Nutr. 1983;38:567-573.

6. Anderson JW, Gustafson NJ, Spencer DB, Tietyen J, Bryant CA. Serum lipid response of hypercholestero-

lemic men to single and divided doses of canned beans. Am J Clin Nutr. 1990;51:1013-1019.

7. Anderson JW, Story L, Sieling B, Chen W-JL, Petro MS, Story J. Hypocholesterolemic effects of oat-bran or bean intake for hypercholesterolemic men. Am J Clin Nutr. 1984;40:1146-1155.

8. Mackay S, Ball MJ. Do beans and oat bran add to the effectiveness of a low-fat diet? Eur J Clin Nutr. 1992;46:641-648.

9. Frubeck G, Monreal I, Santidrian S. Hormonal implications of the hypocholesterolemic effect of intake of field beans (Vicia faba L.) by young men with hyperc- holesterolemia. Am J Clin Nutr. 1997;66:1452-1460.

10. Jang Y, Lee JH, Kim OY, Park HY, Lee SY. Consump- tion of whole grain and legume powder reduces insulin demand, lipid peroxidation, and plasma homocysteine concentrations in patients with coronary artery disease: randomized controlled clinical trial. Arterioscler Thromb Vasc Biol. 2001;21:2065-2071.

11. Shutler SM, Bircher GM, Tredger JA, Morgan LM, Walker AF, Low AG. The effect of daily baked bean (Phaseolus vulgaris) consumption on the plasma lipid levels of young, normo-cholesterolemic men. Br J Nutr. 1989;61:257-265.

12. Cobiac L, McArthur R, Nestel PJ. Can eating baked beans lower plasma cholesterol? Eur J Clin Nutr. 1990;44:819-822.

13. Anderson JW, Ward K. High-carbohydrate, high-fiber diets for insulin-treated men with diabetes mellitus. Am J Clin Nutr. 1979;32:2312-2321.

14. Appel LJ, Sacks FM, Carey VJ, et al. Effects of protein, monounsaturated fat, and carbohydrate intake on blood pressure and serum lipids: results of the OmniHeart randomized trial. JAMA. 2005;294:2455-2464.

15. Gardner CD, Coulston A, Chatterjee L, Rigby A, Spiller G, Farquhar JW. The effect of a plant-based diet on plasma lipids in hypercholesterolemic adults: a randomized trial. Ann Intern Med. 2005;142:725-733.

16. O’Dea K, Traianedes K, Ireland P, et al. The effects of diet differing in fat, carbohydrate, and fiber on carbo hydrate and lipid metabolism in type 2 diabetes. J Am Diet Assoc. 1989;89:1076-1086.

17. McAuley KA, Williams SM, Mann JI, et al. Intensive lifestyle changes are necessary to improve insulin sensitivity: a randomized controlled trial. Diabetes Care. 2002;25:445-452.

18. Giacco R, Parillo M, Rivellese AA, Giacco A, D’Episcopo L, Riccardi G. Long-term dietary treatment with increased amount of fiber-rich low-glycemic index natural foods improves blood glucose control and reduces the number of hypoglycemic event in type 1 diabetic patients. Diabetes Care. 2000;23:1461-1466.

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Obesity Overview

With approximately two-thirds of adults in the United States characterized as over-

weight or obese, the condition of obes-ity is widely considered a public health epidemic. Obesity increases the risk of

the development of conditions such as hypertension, type 2 diabetes, osteoarthritis, coronary artery disease, stroke, and respiratory complications, as well as cancers of the breast, prostate, and colon.1

The etiology of obesity is multifactorial, but can be abridged to accommodate two dominant categories: physi-ological and environmental elements. The physiological aspects of obesity include body metabolism, hormones, and the neurological components of appetite regulation. Environmental causes include the abundance of high calorie foods in the Western diet, as well as the prevalence of increas-ingly sedentary lifestyles due to technological advances.

Neurological Aspects of Weight Regulation

The significance of appetite control in weight regula-tion, especially in cases of obesity, cannot be overempha-sized. Appetite control plays a vital role in the competition between energy consumption and energy expenditure. Food consumption behavior is administered by various hormonal, psychological, and neural signals, each characterized as short-term, and each derived from the gastrointestinal tract.2

Hormones involved in the brain-gut axis of eating behavior come from various sources. Some hormones, such as leptin, arise from fat stores; others, including cholecysto-kinin (CCK), glucagon-like peptide (GLP), ghrelin, peptide YY, and neuropeptide Y, arise from the brain or gastrointesti-nal tract. Some of these hormones suppress eating behavior, while others stimulate it.

Recent research has concentrated on the neurological aspects of weight regulation, with a primary focus on the neuro-gut interaction. The discovery of neuropeptides, in-cluding neuropeptide Y (NPY) and cholecystokinin (CCK),

has contributed to our understanding of the neurological components of weight control. These neuropeptides play significant roles in the manner in which brain, gut, and fat stores interact to control food intake. Multiple feedback loops regulate hunger and satiety.

Appetite Regulation and the Hypothalamus

According to a classic model of the role of the brain-gut axis, eating behavior remains under the control of a satiety center located in the ventromedial hypothalamic area, as well as under a feeding or appetite center located in the lateral hypothalamic area. The satiety center inhibits the feeding center, which is always active but can be suppressed by gastric distention or by hormones, such as CCK.3

Still, a more sophisticated model of the role of the brain-gut axis has emerged. The Arcuate (infundibular) Nucleus is situated at the base of the hypothalamus.4 The two main populations of Arcuate Nucleus neurons that control food intake are appetite-inhibiting neurons and appetite-stimu-lating neurons. Pro-opiomelanocortin (POMC) neurons inhibit food intake, whereas neuropeptide Y (NPY) and agouti-related peptides (AGRP) stimulate appetite.5

POMC is the precursor of melanocyte-stimulating hormone, which inhibits eating behavior. AGRP antago-nizes the melanocortin receptors, thereby increasing food intake. NPY is one of the most potent appetite-stimulating peptides. Both the AGRP and NPY are inhibited by leptin and insulin, whereas ghrelin activates them.4

Neuropeptide YThe most impressive effect NPY has on behavior and

assorted functions is its post-central administration arousal of feeding. Chronic administration of NPY encourages hyperphagia and obesity.2

Y5 receptors, responsible for the mediation of the stim-ulating effects of NPY, are exhibited at comparatively high levels in the LHA (a hypothalamus site) in close proximity to the location of heightened NPY stimulative activity. When starvation occurs, NPY receptor density dwindles in this location; the release of NPY is enhanced when the body is deprived of food.2

Ghrelin and NPYGhrelin, which tends to increase appetite, is secreted

primarily by the stomach.6 Grehlin accomplishes appetite stimulation by encouraging the production of NPY.2 Ghrelin decreases after food consumption, but returns to its baseline before the next meal.6 Moreover, grehlin remains a vital component in acute and long-term control of energy stability.2

Subjects characterized as healthy and lean have gener-ally higher levels of ghrelin in their bodies. Additionally,

Personal Approach to Weight Regulation — Are Hormones the Key?Karon R. LoCicero, MD


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patients diagnosed with bulimia nervosa have higher levels of ghrelin than control subjects with identical weights. A substantial decrease in ghrelin levels has been noted in patients diagnosed with anorexia nervosa, surprisingly before any substantial changes to their body mass indices have occurred.2

Cholecystokinin and SatietyCholecystokinin has been one of the most widely

studied hormones involved in the control of satiety. It is secreted by the mucosal cells in the duodenum, as well as by neurons in the brain. CCK stimulates contraction of the gallbladder to release bile.This response occurs primarily in the presence of fat, such as long chain free fatty acids or protein (amino acids). CCK also stimulates the release of pancreatic enzymes, which along with bile promote diges-tion within the small intestine.7

CCK plays an active role in the stimulation of the vagus nerve; the vagus nerve sends a signal to the brainstem, and then to the satiety center of the brain. Studies have demon-strated that this effect is reduced by vagotomy. CCK also acts on the dorsomedial nucleus in the hypothalamus by reducing neuropeptide Y, a potent orexigenic peptide.7

Additionally, CCK remains a vital component of meal size control processes; CCK endocrine actions in the intes-tine, as well as its neurocrine actions elsewhere in the body are instrumental in this control. This effect is amplified by gastric distension.2

While the effects of CCK on food consumption are swift, they fail to endure at length. The half-life of CCK is one to two minutes. Moreover, its effects are mitigated if administered fifteen minutes prior to food intake. It has been suggested however, that CCK is able to positively affect long-term control of meal size and body weight when leptin levels are demonstrably elevated.2

Leptin and CCKLeptin, discovered in 1994, is synthesized by adipose

tissue. It has been shown to reduce food intake and body weight in certain animal studies.6 The amount of leptin in the body is proportional to the amount of fat in the body. Leptin inhibits NPY/AGRP neurons and stimulates POMR neurons, thereby decreasing appetite.5 Low caloric intake causes a decrease in leptin levels and an increase in appe-tite, whereas high caloric intake causes an increase in leptin levels; it would be reasonable to expect a decrease in appe-tite. While this has proven true in certain animal studies, it does not hold true for obese humans who already have high circulating leptin levels. It is postulated that leptin resistance plays a significant role in obese individuals, but the etiology remains unclear.4

When leptin levels rise a signal that excess energy is being stored is sent to the brain; in turn, appetite decreases and energy expenditure increases. It has also been demonstrated that food intake restrictions – over the course of several days – suppresses levels of leptin in the body. These effects can be reversed by re-feeding.2

Approximately one-twentieth of obese populations may be regarded as comparatively leptin deficient. This group may benefit from exogenous administration of lepitin.2 Interestingly, a study by Matson, et al has demonstrated that the administration of leptin, along with CCK, significantly decreases daily total caloric intake compared to the adminis-tration of leptin alone. More research, however, needs to be completed regarding the use of leptin as a weight loss drug in light of the limited results in human studies.8

Recent Studies of CCK CCK inhibits gastric emptying, resulting in appetite

reduction. A study by Straathof et al. demonstrates that CCK, at postprandial plasma concentrations, decreases basal gastric tone, thereby slowing gastric emptying. It has been hypothesized that fatty foods, which relax the stomach, exert this effect through stimulation of endogenous CCK.9 Another study by Matzinger et al. demonstrates that inhibition of food intake in response to intestinal lipid is medicated by CCK.10

A study by Burton-Freeman et al. demonstrates that the feeling of satiety produced by CCK is enhanced by increasing the fat or fiber content of the diet. Whereas fat increases the release of CCK, fiber prolongs its release, perhaps by slowing the rate of fat absorption.11 Loxiglumide, a CCK receptor antagonist, stimulates hunger in humans.12 Other studies have shown that the inhibition of CCK metabolism decreases caloric intake.

Administration of butabindide, which inhibits the CCK-inactivating peptidase, called tripeptidyl peptidase, has been shown to elicit CCK-like satiation in rats. Another study illustrates that the oral administration of a proteinase inhibitor extracted from potatoes (POT II), which binds to both trypsin and chymotrypsin, thereby preventing the degradation of endogenous CCK, has been shown to stimulate CCK release and reduce caloric intake by 20% following a fat or protein preload.13 Additionally, supple-mentation with a potato protein extract in humans has been shown to modify the glycemic response to a meal.14

Kissileff et al. demonstrates that the administration of IV CCK in humans reduced food intake by 19%. An ad-ditional study by Kissileff et al. demonstrates that gastric distension enhances the effect of CCK on the reduction of food intake.15

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Peptide YY, another protein secreted by the distal ileum and colon, stimulates the Y2 receptor in the hypothalamus; this inhibits the release of neuropeptide Y, the strongest cen-tral nervous system stimulant of appetite.6 It also slows gas-tric emptying.7

Chronic administration of PYY to rodents resulted in reduced weight gain. Obese patients have suppressed PYY levels. Gastric bypass patients have a greater PYY response to food intake than patients who have not undergone bypass. This response may contribute to the weight loss associated with the surgery.7 Interestingly, CCK stimulates the release of PYY.10

GLP-1 (glucagon-like peptide-1) is secreted by the ileum in response to fat and carbohydrate intake. GLP-1 stim-ulates the pancreas to secrete insulin and inhibits glucagon release. It also diminishes gut motility, thus suppressing appetite.6,7 Studies have demonstrated that a dose-dependent reduction in food intake and increase in satiety occur after an IV infusion of GLP-1.3 Another study demon-strates that intravenous infusion of physiological doses of CCK and GLP-1 produce an additive reduction in food intake.10

Exenatide, the first in a new class of diabetes medica-tions known as incretin mimetics, shares many of the same characteristics as GLP-1 with the exception of half-life. GLP-1 is metabolized rapidly (from 1.5 to five minutes), whereas exenatide has a half-life of several hours. Weight loss tends to occur with exenatide.

Norepinephrine and SerotoninOther more commonly recognized discoveries in this

area are the neurotransmitters norepinephrine and serot-onin, both present within the hypothalamus. The prescrip-tion drug phentermine causes the release of norepinephrine, which in turn reduces food intake. Another prescription drug, sibutramine, increases both norepinephrine and sero-tonin by blocking their reuptake; it also stimulates certain 5-HT receptors, which in turn reduces food intake.

Indeed, many prescription weight control drugs aid weight loss by decreasing appetite, increasing metabolic rate, or decreasing fat absorption. Each has potential side effects, and each remains only somewhat effective, however. Both phentermine and sibutramine can increase blood pressure and cause dry mouth, insomnia, and constipation. Neither should be used in patients with uncontrolled hypertension, cardiac disease, or a history of stroke.

Recent Advances in Weight Management

Exciting research continues in the field of obesity man-agement. The presently available drugs, such as sibutramine, phentermine, and orlistat, have potentially significant adverse effects. Gut hormones, if able to be used as drugs for appetite control, would be expected to have potential for low side effects, as they would act only on the specific appetite center in the brain.5

Unfortunately, gut hormones must be given parenter-ally as they have an exceedingly short half-life. Other forms of administration (e.g., intranasal), or the development of an analogue that is resistant to breakdown, would need to be developed.5 Drugs that mimic or enhance productions of appetite-regulating proteins or neuropeptides are stud-ied extensively at present. For example, trypsin inhibitors, which block the inactivation for CCK, have been shown to suppress food intake in animals and humans.5

Exenatide, as mentioned earlier, is an incretin mimetic which is now being used for the treatment of type 2 diabetes mellitus. This drug is an excellent example of one that mimics natural hormones, the incretins, such as GLP-1. Because exenatide promotes weight loss, it is anticipated that a similar drug, specifically for weight loss, will be available in the near future.

Endocannabinoid System

Another exciting area of interest is the endocannabinoid system; this system plays a vital role in control over appe-tite and satiety. Stimulation of the endocannabinoid system leads to increased food intake, whereas inhibition of that system decreases food intake.16

Endocannabinoid receptors (called CB1 and CB2) are located on cell membranes in the brain, gastrointestinal tract, white adipose tissue, and skeletal muscle. Endocan-nabinoids are fatty acids that are synthesized from phosphol-ipids that are a part of cell membranes. In the brain, they inhibit the release of GABA, which is a neurotransmitter that diminishes food intake.16

Endocannabinoid receptors in fat cells (adipocytes) increase the activity of lipoprotein lipase, which leads to fat accumulation.16 They also enhance the production of adiponectin from adipocytes.17 Adiponectin improves insulin sensitivity and fatty acid oxidation in muscle thereby improving blood sugar and decreasing triglycerides.18

Endocannabinoids within the small intestine have an appetite-stimulating effect. CCK diminishes this effect by suppressing the cannabinoid receptors on the vagal nerves which transmit to the brain.

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In skeletal muscle, endocannabinoids reduce energy expenditure. Blockade of the endocannabinoid receptors in skeletal muscle increases glucose uptake and basal oxygen consumption.16

Rimonabant which is awaiting FDA approval is an endocannabinoid receptor blocker that has been shown, in the RIO (Rimonabant in Obesity) studies, to produce weight loss and improve blood sugar and lipids,16 which tend to be elevated in patients with metabolic syndrome (abdominal obesity, elevated triglycerides, hyper-glycemia or diabetes, and low HDL cholesterol).

Presently, I am anticipating approval of this drug in the United States as many of my patients have some or all the features of the metabolic syndrome, including hyper-tension, excessive intraabdominal fat, hyperlipidemia, and diabetes mellitus or glucose intolerance. I expect that the use of rimonabant in conjunction with a low glycemic diet and the use of “healthful” fats, such as monounsaturated or polyunsaturated fats, would produce significant health benefits in terms of weight loss and metabolic parameters.

A Personal Approach to Weight Loss

With a new fad diet for every season, the selection of and commitment to a weight management plan often proves difficult for patients. Frequently, fad diets fail to provide adequate nutrition; once the diet is complete, many patients experience weight gain. Moreover, weight lost under a nutritionally unbalanced scheme is not necessarily fat lost.19

It is advisable for bariatric patients to take an inventory of their weight loss desires, motivations, physi-cal activities, daily food intake, emotional attachments to eating, and outside sources of support.19 After careful consideration of these factors, patients are often better equipped to design a weight management program tailored to their individual lifestyles.

These programs which may include prescription weight loss drugs, prove most successful when they maintain cultural sensitivity. A patient accustomed to meals of black beans and yellow rice, or another whose dietary habits include steak and potatoes, will do best with weight management plans that incorporate their tastes, but are adjusted for portion and calorie control.

Additionally, patients should balance calories through-out the day; skipping meals and starvation should be avoided. Successful weight loss begins with healthy eating, and more frequent meals. Divide daily caloric intake into quarters; allot one-fourth each to the three traditional meal-times, saving the remaining quarter for snacks.19

It is also advisable to focus on simple, unprocessed foods. These foods contain more vitamins, minerals, and

fiber, and have less undesirable additives such as sodium and sugar. Exchange sugary sodas and fruit drinks for water, consume whole grains with significant amounts of fiber, and choose high-protein beans and other legumes to stave off cravings.19

Still, patients are advised to remain mindful of their caloric intake. To more easily manage this task, watch portion sizes and always eat meals on a plate or out of a bowl. Eating out of containers or other packages makes it difficult to gauge serving sizes. Because precisely measuring foods can prove cumbersome, patients often find shortcuts such as adjusting plate or cup size easier methods to control portions.19

A personally tailored food plan should be coupled with a personally tailored physical activity plan. No two bodies are the same. Most patients are able to walk at a moderate pace for at least thirty minutes; increasing steps walked per day remains a straightforward and easily adhered to physical activity plan.19

Formulate an aerobic exercise plan for a greater impact on cardiovascular health, strength, and flexibility. Consider the health benefits, risks, total calories burned, frequency, and convenience of each activity prescribed before adopting a plan. Patients should slot new exercise plans around their current daily routines. A major readjustment of an oft-fol-lowed schedule is more consistently followed if the change is not drastic.19

Resistance training is also advised to build strength, boost metabolism, and increase bone density.20 Patients are advised to develop plans that accommodate their weight-lifting abilities at present, gradually building up the ability to lift more weight. In addition to the visible physical benefits, resistance training also reduces overall levels of body pain, relieves stress, balances moods, and provides en-ergy spikes.19

In the field of weight management, emphasis must be placed on the development of new, healthful food and activity habits. Patients will find success in balance.

Hopefully, newer developments in the field of neuro-physiology, such as CCK research, incretin-mimetics and the endocannabinoid system, will help promote further weight loss beyond that expected from diet alone.

Karon R. LoCicero, MD graduated summa cum laude and Phi Beta Kappa from Duke University, and received her medical degree from the University of South Florida College of Medicine. She is Board Certified in Internal Medicine, Diplo-mate American Board of Bariatric Medicine. She may be con-tacted at LoCicero Medical Group, 2605 West Swann Avenue,

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Tampa, FL 33609; (813) 876-7073 Fax (813) 879-3737 www.Internal-Medicine.com.

References

1. National Institutes of Health. The Practical Guide: Identification, Evaluation, and Treatment of Overweight and Obesity in Adults 2000; 00-4084.º2. Arora, S. Role of neuropeptides in appetite regulation and obesity. Neuropeptides 2006;40:375-401.

3. Bray G. Afferent signals regulating food intake. Proc Nutr Soc. 2000;59:373-384.

4. Neary NM, Goldstone AP, Bloom SR. Appetite regulation: from the gut to the hypothalamus. Clin Endocrin. 2003;60:153-160.

5. Murphy KG, Bloom SR. Gut hormones in the control of appetite. Exp Physiol. 2004;89:507-516.

6. de Graaf C, Blom W, Smeets P, et al. Biomarkers of satiation and satiety. Am J Clin Nutr. 2004;79:946-961.

7. Bloom S, Wynne K, Chaudhri O. Gut feeling – the secret of satiety? Clin Med 2005;5:147-152.

8. Matson C, Wiater M, Kuijper J, Weigle D, 1997. Synergy between Leptin and Cholecystokinin (CCK) to control daily caloric intake. Peptides. 1997;8:275-1278.

9. Straathof JWA, Mearadji ., Lamers C, Mascle, A. Effect of CCK on proximal gastric motor function in humans. Am J Gastrointestinal and Liver Phys.1998;274:939-944.

10. Matzinger D, Gutzwiller ., Drewe J, et al. Inhibition of food intake in response to intestinal lipid is mediated by cholecystokinin in humans. Am J Reulatory, Integrative and Comparative Physiology. 1999;R1718-R1724.

11. Burton-Freeman B, Davis PA, Schneeman BO. Plasma cholecystokinin is associated with subjective measures of satiety in women. Am J Clin Nutr.2002;76:659-667.

12. Beglinger C, Degen L, Matzinger Det al. CCK-A receptor antagonist, stimulates calorie intake and hunger feelings in humans. Am J Regulatory, Integrative and Comparative Physiology 2001;280:R1149-R1154.

13. Little TJ, Horowitz ., Feinle-Bisset C. Role of cholecystokinin in appetite control and body weight regulation. Obesity Rev. 2005;6:297-306.

14. Spreadbury D, Shao AE, Essman EK, et al. A proteinase extract inhibitor from potatoes reduces post prandial blood glucose in human subjects. JANA 2003;6; 29-38.

15. Kissileff H, Carretta J, Geliebter A, Pi-Sunyer FX. Cholecystokinin and stomach distension combine to reduce food intake in humans. Am J Regulatory, Integrative and Comparative Physiology 2003;285:R992-R998.

16. Woods S, Sakai R. The Endocannabinoid System: What is it? Baylor College of Medicine 2006;1:1-10.

17. Van Gaal L, Rissanen A, Scheen A, et al. Effects of the cannabinoid-1 receptor blocker rimonabant on weight reduction and cardiovascular risk factors in overweight patients: 1-year experience from the RIO-Europe study. Lancet 2005;365:1389-1397.

18. Greenway F, Greenway S, Raum W. The Physiology of the Brain, the Gut, and the Fat Cells in the Morbidly Obese. In: Louis F. Martin, ed. Obesity Surg. Columbus, OH: McGraw-Hill; 2004.

19. Kozak D., Springer-Riddle J. Foolproof Weight Loss, Emmaus, PA: Rodale; 2000.

20. Johnson, J., Maleskey, G. Total Body Toning, Emmaus, PA: Rodale; 2000.

Reprinted with permission from NutriNews, a publication of Douglas Labs, Pittsburg, PA March 2007

Web site: www.ComplementaryNutrition.orgMember Electronic Mailing List:

Contact Gretchen Forsell to get connected([email protected]).

Weight Regulation

Join NCC for FNCE 2007 in Philadelphia, Penn-sylvania on September 29 – October 2, 2007! As always, your DPG will be very busy with a myriad of activities for members. For more information on FNCE and to register, visit www.eatright.org/fnce.

NCC-Sponsored Educational Session: Ultrametabolism: The Causes of Obesity—An Integrative Approach to Weight Loss Monday, October 1, 8:00 – 9:30 amPennsylvania Convention Center

See us at Product Market Place Booth #7 – Sunday, September 30, 8:00 am – 4:00 pm

Visit us at DPG Showcase Booth #12 – Monday, October 1, 10:30 am – 1:00 pm

Member BreakfastTuesday, October 2, 6:15 – 7:45 amPhiladelphia Marriott Downtown, Room 407-409

Food & Nutrition Conference & ExpoSeptember 29 to October 2, 2007

The Natural Medicines Comprehensive Database website gives instant answers on herbal and dietary supplements, complete with brand name searches and Patient Handouts. The Database saves your time by offering highly researched information like...

• Patients on Coumadin could have their levels thrown off when they take ginger or garlic, or any of more than 65 different herbs.

• Women on oral contraceptives risk unwanted pregnancy when taking St. John’s wort. • Patients on omeprazole can have levels decreased 40% when they take ginkgo. • Soy might decrease the effectiveness of tamoxifen for breast cancer. • Echinacea might interact with lovastatin and other cholesterol drugs.

The Natural Database website is updated daily. Access to the Natural Database lets you search natural meds and learn more detailed, scientifi c information about:

– Safety and effectiveness ratings – Brand names and product ingredients – Interactions with drugs, foods, lab tests, and diseases – Dosages and mechanism of action, and much more

This information is especially important considering many people use, or have used, natural products...whether they say so or not. With the Natural Database you can easily provide helpful, scientifi c info on natural medicines.

U.S. News & World Report calls the Database “the scientifi c gold standard.” Other terrifi c reviews in JAMA, American Journal of Pharmaceutical Education, and others make it clear this is the best resource to use.

P.S. See reverse for access info and tips on how to use the Natural Database.

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NCC has purchased access rights for you to useNatural Medicines Comprehensive Database

Natural Medicines Comprehensive Database • 3120 W. March Ln., P.O. Box 8190, Stockton CA 95208Tel: 209-472-2244 • Fax: 209-472-2249 • [email protected]

Dear NCC Members,

I am overjoyed and pleased to share with you that we, the Nutrition in Complementary Care Dietetic Practice Group (NCC DPG), have just secured advanced online access to the Natural Medicines Comprehensive Database (“NMCDB”) for all of NCC. This member benefi t is exclusive to the NCC community. You can use this database to research dietary supplements, nutraceuticals, herbals and other items that your clients, patients, family or friends may ask you about. The database, which is updated daily, provides instant answers along with brand name searches and consumer handouts. The NCMDB is the premier database that is easy to navigate, modern in its knowledge and thus we now have a wonderful opportunity to expand our knowledge while helping others. Please use this member benefi t to your advantage and enjoy the great resource!

The reverse side of this letter provides access information and tips on how to use the Natural Medicines Comprehensive Database.

Sincerely,

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To Use the Natural Database Online:

1. From your computer, go to the NCC - Nutrition in Complementary Care website:

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2. Login with your ADA # and password.

3. Click on the link to Natural Medicines Comprehensive Database from the menu on the left (under Member Resources). You’ll now be logged into www.naturaldatabase.com, where you should see a box in the top-right corner asking for your User ID#.

4. Click the I Need a User ID# link (circled in red).

5. Follow the instructions on the resulting pages, and fi ll out the required information as needed. Be sure to make note of your User ID#.

If you forget your User ID#, it will be NCC-, 1st 6 letters of your last name, 1st letter of fi rst name, and the last 4 numbers of

your Social Security Number. Example: NCC-SMITHJ1234

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To Use the Special Features on Natural Database:

Find info on safety, interactions, dosage, effectiveness, Patient Handouts, and more. You can also read the Clinical Management Series, covering natural meds usage in such areas as depression, PMS, and insomnia.

Click the Search button (circled in red). Then use any of these searches...

Search – By name of product, ingredient, drug, disease, etc.

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To Get the Natural Database CE:

Using your User ID#, you can take Natural Medicines CE courses. Just click on the Continuing Education button to select the course you’d like to take from your CE homepage.

Jenna A. Bell-Wilson, PhD, RD, LD

It is not uncommon to face a patient with type 2 diabetes who has elevated lipid levels or dyslipidemia. Nutrition profes-

sionals consider this of grave concern as type 2 diabetes is associated with a marked increased

risk of cardiovascular disease (CVD). Cardiovascular mortality from diabetes continues to grow despite constant progress in our ability to normalize blood glucose through new oral and injectable medication regimens.1 The exact link between CVD and diabetes is not completely under-stood, partly because the relationship is multi-faceted, including the deleterious effects of hyperglycemia, resulting in endothelial dysfunction, hypercoagulability, increased oxidative stress, and protein glycosylation.2 Adults with type 2 diabetes without coronary heart disease (CHD) have a similar 10-year risk for cardiac events as do non-diabetic adults with CHD. Aggressive management of CVD risk factors, including lipid control, is crucial to reduce the incidence of cardiovascular events among this population.

Diabetic dyslipidemia, or atherogenic dyslipidemia, are terms used interchangeably in persons with type 2 diabetes.2 Atherogenic or diabetic dyslipidemia typically presents with hypertriglyceridemia, low high-density lipoprotein choles-terol (HDL-C) levels, and a preponderance of small, dense low-density lipoprotein (LDL) particles. Dyslipidemia is well-recognized as a modifiable risk factor that should be identified early to institute strict cardiovascular prevention and management. The American Heart Association, the American Diabetes Association (ADA), and the National Cholesterol Education Program (NCEP) Adult Treatment Panel III (ATP III) currently recommend that first priority should be given to lowering LDL cholesterol (LDL-C), followed by increasing HDL-C and lowering triglycerides.3, 4 Clinical trial results support the identification of LDL-C as the primary target of therapy for people with type 2 diabetes and elevated blood cholesterol, similar to the treatment of patients without diabetes.4

Treatment Goals and Research

In NCEP ATP III, diabetes is designated a CHD risk equivalent, meaning it confers a high risk of new CHD within 10 years.4 This high risk is partly due to the frequent association of diabetes with multiple risk factors such as obesity, hypertension, dyslipidemia, insulin resist-ance, and other abnormalities in fibrinolysis and endothelial function. Furthermore, persons with diabetes who experi-ence a myocardial infarction have an unusually high death

rate either immediately or in the long term.3 To decrease this risk, an intensive prevention strategy is warranted; people with CHD risk equivalents, such as diabetes, have the lowest LDL-C goal of <100 mg/dL.5 To achieve this goal, two major strategies of lipid-modification among persons with type 2 diabetes have emerged - therapeutic lifestyle changes (TLC) and drug therapies, which include bile acid sequestrants, ezetimibe, fibrates, HMG Co-A reductase inhibitors or statins, and/or niacin.3, 6

Therapeutic Lifestyle Changes

Diet modification, exercise, and weight reduction in overweight individuals are essential in the management of lipid disorders in diabetes. NCEP ATP III and ADA agree that reducing the intake of saturated and trans-fatty acids is the first step to lowering LDL-C levels.4, 7 NCEP ATP III recommends limiting the intake of saturated fat to less than 7% of daily calories, while limiting cholesterol intake to less than 200 mg/day. Other dietary options include increasing soluble fiber intake to 10-25 mg/day, adding 2-3 g of plant stanols/sterols, and including soy protein in the diet. For individuals with elevated triglycerides and low HDL-C levels, the ATP III also recommends limiting the intake of carbohydrates to less than 60% of calories. Lastly, monoun-saturated fatty acid (MUFA) and polyunsaturated fatty acid (PUFA) enriched diets appear to be a reasonable dietary alternatives for most individuals with diabetes. Replacing saturated fat with carbohydrates, PUFA, or MUFA is rec-ommended by ADA.7

Drug Trials

Statins are often considered to be first line therapy for the treatment of dyslipidemia. The NCEP ATP III guide-lines recommend pharmacological therapy when LDL-C is greater than 100 mg/dL in individuals with established CHD, or when LDL is greater than 130 mg/dL in those without CHD. However, the 2005 guidelines suggest that statin therapy may be appropriate to achieve an LDL-C reduction of approximately 30%, regardless of baseline LDL-C.7

Many clinical trials have shown that statins provide significant benefits to patients with diabetes in lowering LDL-C. A meta-analysis of lipid treatment for patients both with and without diabetes showed that the reduction in major coronary events was similar in primary and secondary settings: a 21% decrease in patients with diabetes and a 23%

Therapies Lipid Management in Type 2 Diabetes

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decrease in patients without diabetes.6 It is important to note, although the relative risk reduction was similar, the absolute risk reduction for patients with diabetes was nearly three times higher in secondary prevention.

Most of our knowledge in assessing the effects of improving lipid levels in patients with diabetes comes from subgroup analyses of large coronary artery disease (CAD) prevention trials. These include both primary [Helsinki Heart Study (HHS) and Heart Protection Study (HPS)] and secondary prevention trials [Scandinavian Simvastatin Survival Study (4S), Cholesterol and Recurrent Events Trial (CARE), and Veteran Affairs High Density Lipoprotein Cholesterol Intervention Trial (VA-HIT)].8-12 The HPS, 4S, and CARE involved statin therapy, while HHS and VA-HIT utilized fibrates. In all analyses, the subgroup with diabetes enjoyed the same, or better, relative risk reduction with active treatment as compared to the non-diabetic group. It is believed that the absolute benefit of aggressive lipid management in patients with diabetes is significantly greater, due to an overall increase in mortality from CVD.8-12

The first statin trial to assess the benefit of lowering LDL-C in patients with type 2 diabetes without CVD was the Collaborative Atorvastatin Diabetes Study (CARDS).13, 14

In 2,838 study participants with type 2 diabetes, and who had a mean baseline LDL level of 118 mg/dL and a mean baseline HDL level of 55 mg/dL, atorvastatin 10 mg and placebo were compared over four years. The primary endpoint of time to the first major cardiovascular event was reduced by 37%, fatal and nonfatal strokes were reduced by 48%, and total mortality was reduced by 27% with atorvastatin.

Fibrates are a class of amphipathic carboxylic acids used for a range of metabolic disorders. Although less effective in lowering LDL, fibrates improve HDL and triglyceride levels. In the Diabetes Atherosclerosis Intervention Study, fibrates have been shown to reduce the progression of microabulinu-ria, a marker for diabetic nephropathy, as well as CVD in patients with type 2 diabetes.15

Despite growing recognition that people with type 2 diabetes are at increased risk for CVD and are designated CHD risk equivalents, this population is 30% less likely to have a lipid profile, and 20% less likely to receive lipid-low-ering therapy, than their non-diabetic counterparts.16 TLC and drug-therapy have been clinically proven to reduce the primary LDL-C target to within recommended levels. Diabetes is a complex disease with a myriad of vascular risk factors and complications. Finding viable options for care is essential to the health and wellness of the individual with diabetes. Delving deeper into dietary modifications

can help nutrition professionals find suitable treatments for their patients.

Plant Sterols for Lipid Management with Type 2 Diabetes

Maximizing the dietary management of cholesterol for individuals with type 2 diabetes is a focal point of care. As discussed in the Nutrition in Complementary Care spring is-sue Volume 9, Number 4, plant sterols are recommended as an adjunct to a cardioprotective diet by the American Dietetic Association, the National Cholesterol Education Program, and the American Heart Association to enhance cholesterol lowering (see sidebar, Plant Sterols for Choles-terol Management).4, 17 More than 140 studies have been published showing that plant sterols can significantly lower LDL-C. In addition, a meta-analysis concluded that 2 grams of plant sterols daily can provide a 6-15% reduction.18 The question is: are they an appropriate option for persons with type 2 diabetes? In short, the evidence points to yes.

In case you missed it… Plant Sterols for Cholesterol Management

The National Cholesterol Education Program Adult Treatment Panel III (NCEP ATP III) Report, released in 2001 with an update in 2004, emphasized the value of maximizing the diet and lifestyle to manage cholesterol, specifying low density lipoprotein-cholesterol (LDL-C)-raising nutrients as well as therapeutic options for lowering LDL-C.4 Included in those guidelines was the addition of 2-3 grams per day of plant sterols. Small quantities of plant sterols can be found in vegetable oils, nuts, grain products, fruits, and vegetables. In recent years manufacturers have fortified food products, including soft margarines (vegetable oil spreads), orange juice, yogurt, and snack bars.

In plants, sterols are involved in cell membrane perme-ability, structure, and function, similar to that of cholesterol in humans. Unlike cholesterol, the absorption of plant sterols in the body is very low and plant sterols are not metabolized to bile acids. Although the details remain elusive, plant sterols appear to block the absorption of cholesterol in the body, leading to a reduction in blood cholesterol levels.19, 20

According to the American Dietetic Association Evidence Based Library, 2-3 g of plant sterols daily may pro-vide a 4-10% reduction in total cholesterol and a 7-15% reduction in LDL-cholesterol. To put in perspective the

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potential positive impact, epidemiological studies estimate that on average a 10% lowering of LDL-C will reduce the risk of CHD by up to 10%.4

In the Research

Because of the serious health implications of elevated lipid levels in individuals with type 2 diabetes, the efficacy of plant sterols for cholesterol lowering has been investigated. Of equal importance to the healthcare professional working with diabetes is whether plant sterols threaten glycemic control. Lee et al. sought to address these concerns in a 2003 study.21 Researchers enlisted 85 eligible subjects with the following inclusion parameters: type 2 diabetes for greater than 1 year, stable medication, LDL greater than 3.60 mmol/L (140 mg/dL), and no hypolipidemic or hypocaloric treatment. A 12-week randomized, double-blind, placebo-controlled dietary intervention provided subjects with 10 gram portions (1 tablespoon) of soft margarine of either a low-fat spread or a phytosterol-enriched low-fat spread. The subjects were asked to consume 2 table-spoons per day with meals, providing 1.6 g of phytosterols per day for those receiving the plant sterol-containing soft margarine. The subjects remained “free living” throughout the study. Although they did not receive dietary counseling, their intake was assessed by a questionnaire to ensure that no drastic changes were made. Blood samples were taken at weeks 0, 4, 8, and 12 to determine serum total cholesterol, HDL-cholesterol, triglycerides, LDL-cholesterol, and whole blood glucose concentrations.

Summary of research findings: • At baseline…total cholesterol, HDL, LDL, and

triglycerides were similar among the groups. • At week 4…total cholesterol and LDL were reduced

by 5.2% and 6.8%, respectively, from baseline in the plant sterol group.

• At weeks 8 and 12…no difference from baseline, but significant differences between the groups, with the plant sterols group showing lower total and LDL-cholesterol levels. HDL was elevated in the plant sterol group compared with baseline.

• The glycemic control of all participants over time was not influenced by the type of soft margarine they consumed.

The researchers speculate that the modest decline

in cholesterol may be attributed to the low level of plant sterols administered (1.6 g/day vs. 2-3 g/day recommended), noting that previous research points to a dose response with

plant sterol administration. They also pondered the com-plexities of diabetes and lipid management, emphasizing that this is only speculative. Despite the modest changes, the results show that plant sterols do not interfere with glycemic control in individuals with type 2 diabetes, and also provide an option for cholesterol management.

A similar, but smaller investigation observed the effects of plant sterols on LDL and non-HDL cholesterol in hypercholesterolemic individuals with and without type 2 diabetes.22 The researchers provided 15 subjects without diabetes, and 14 subjects with diabetes, 1.8 g/day of plant sterols or a corn starch placebo in a double blinded, crossover study. After the 21 day trial, the results showed signifi-cant decreases in LDL-cholesterol from baseline (15.1% in subjects without diabetes, 26.8% in subjects with diabetes) without alterations in glycemic control. Lau et al. concluded that the study results supported the efficacy of plant sterols as a dietary option for hypercholesterolemic diabetics.22

Take Home Message: Caring for Patients with Type 2 Diabetes and Elevated Lipids

Despite growing recognition that people with type 2 diabetes are at increased risk of CVD and are designated CHD risk equivalents, this population is 30% less likely to have a lipid profile, and 20% less likely to receive lipid-low-ering therapy, than people without diabetes.16 The multiple lifestyle and pharmaceutical interventions for management of diabetes, obesity, hypertension, and dyslipidemia can be overwhelming to patients, resulting in inadequate control of CVD risk factors. Implementing healthy lifestyle and dietary modifications is paramount to managing not only blood glucose, but also serious CVD risk factors such as elevated lipids. For people with diabetes, modifying their diet can be a manageable and realistic first step to control-ling cholesterol, and subsequently, risk of CVD or CHD.

Jenna A. Bell-Wilson, PhD, RD, LD is a free lance

nutrition writer, consultant, and nutrition advisor for Training Peaks, LLC. Contact Jenna at [email protected].

References

1. Gu K, Cowie CC, Harris M. Diabetes and decline in heart disease mortality in US adults. JAMA. 1999;281:1291-1297.

2. Insucchi S, Amatruda J. Lipid management in patients with diabetes: Translating guidelines into action. Diabetes Care. 2003;26:1309-1311.

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Therapies: Have You Read... ?

3. Buse JB, Ginsberg HN, Bakris GL et al. Primary prevention of cardiovascular diseases in people with diabetes mellitus: a scientific statement from the American Heart Association and the American Diabetes Association. Circulation. 2007; 115:114-26.

4 . National Cholesterol Education Program. Executive summary of the third report of the National Cholesterol Education Program (NCEP) expert panel on detection, evaluation and treatment of high blood cholesterol in adults (adult treatment panel III). JAMA. 2001;285:2486-2497.

5. Brown DJ. New guidelines for low-density lipoprotein levels from the National Cholesterol Education Program (NCEP): a 2004 update. Prog Cardiovasc Nurs. 2004;19:165.

6. Costa J, Borges M, David C, Vaz CA. Efficacy of lipid lowering drug treatment for diabetic and non-diabetic patients: meta-analysis of randomised controlled trials. BMJ. 2006;332:1115-24.

7. Kulkarni K, Boucher JL, Daly A et al. American Dietetic Association: Standards of practice and standards of professional performance for registered dietitians (generalist, specialty, and advanced) in diabetes care. J Am Diet Assoc. 2005;105:819-24.

8. Koskinen P, Manttari M, Manninen V, Huttunen JK, Heinonen OP, Frick MH. Coronary heart disease incidence in NIDDM patients in the Helsinki Heart Study. Diabetes Care. 1992;15:820-5.

9. MRC/BHF Heart Protection Study of cholesterol lowering with simvastatin in 20,536 high-risk individuals: a randomised placebo- controlled trial. Lancet. 2002;360:7-22.

10. Haffner SM, Alexander CM, Cook TJ et al. Reduced coronary events in simvastatin-treated patients with coronary heart disease and diabetes or impaired fasting glucose levels: subgroup analyses in the Scandinavian Simvastatin Survival Study. Arch Intern Med. 1999;159:2661-7.

11. Goldberg RB, Mellies MJ, Sacks FM et al. Cardiovascular events and their reduction with pravastatin in diabetic and glucose- intolerant myocardial infarction survivors with average cholesterol levels: subgroup analyses in the cholesterol and recurrent events (CARE) trial. The Care Investigators. Circulation. 1998;98:2513-9.

12. Rubins HB, Robins SJ, Collins D et al. Gemfibrozil for the secondary prevention of coronary heart disease in men with low levels of high-density lipoprotein cholesterol. Veterans Affairs High- Density Lipoprotein Cholesterol Intervention Trial Study Group. N Engl J Med. 1999;341:410-8.

13. Colhoun HM, Betteridge DJ, Durrington PN et al. Primary prevention of cardiovascular disease with atorvastatin in type 2 diabetes in the Collaborative Atorvastatin Diabetes Study (CARDS): multicentre randomised placebo-controlled trial. Lancet. 2004;364:685-96.

14. Colhoun HM, Betteridge DJ, Durrington PN et al. Rapid emergence of effect of atorvastatin on cardiovascular outcomes in the Collaborative Atorvastatin Diabetes Study (CARDS). Diabetologia. 2005;48:2482-5.

15. Ansquer JC, Foucher C, Rattier S, Taskinen MR, Steiner G. Fenofibrate reduces progression to microalbuminuria over 3 years in a placebo-controlled study in type 2 diabetes: results from the Diabetes Atherosclerosis Intervention Study (DAIS). Am J Kidney Dis. 2005;45:485-93.

16. Rubins HB, Robins SJ, Collins D et al. Gemfibrozil for the secondary prevention of coronary heart disease in men with low levels of high-density lipoprotein cholesterol. Veterans Affairs High- Density Lipoprotein Cholesterol Intervention Trial Study Group. N Engl J Med. 1999;341:410-8.

17. Lichtenstein AH, Appel LJ, Brands M et al. Diet and lifestyle recommendations revision 2006: a scientific statement from the American Heart Association Nutrition Committee. Circulation. 2006;114:82-96.

18. Katan MB, Grundy SM, Jones P, Law M, Miettinen T, Paoletti R. Efficacy and safety of plant stanols and sterols in the management of blood cholesterol levels. Mayo Clin Proc. 2003;78:965-78.

19. Normen L, Dutta P, Lia A, Andersson H. Soy sterol esters and beta-sitostanol ester as inhibitors of cholesterol absorption in human small bowel. Am J Clin Nutr. 2000;71:908-13.

20. Mensink RP, Ebbing S, Lindhout M, Plat J, van Heugten MM. Effects of plant stanol esters supplied in low-fat yoghurt on serum lipids and lipoproteins, non-cholesterol sterols and fat soluble antioxidant concentrations. Atherosclerosis. 2002;160:205-13.

21. Lee YM, Haastert B, Scherbaum W, Hauner H. A phytosterol- enriched spread improves the lipid profile of subjects with type 2 diabetes mellitus--a randomized controlled trial under free-living conditions. Eur J Nutr. 2003;42:111-7.

22. Lau VW, Journoud M, Jones PJ. Plant sterols are efficacious in lowering plasma LDL and non-HDL cholesterol in hypercholesterolemic type 2 diabetic and nondiabetic persons. Am J Clin Nutr. 2005;81:1351-8.

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Background Information and Final Rule for Current Good Manufacturing Practices (CGMPs) for Dietary Supplements

Overview

Under the Dietary Supplement Health and Education Act of 1994 (DSHEA), dietary supplement manufacturers have the essential responsibility to substantiate the safety of the dietary ingredients used in manufacturing a product. Manufacturers are also responsible for determining that any representations or claims made about their products are substantiated by adequate evidence to show that they are not false or misleading. FDA is responsible for taking action against any unsafe dietary supplement product after it reaches the market. FDA accomplishes its responsibilities through monitoring safety literature; dietary supplement adverse event reports; and product information, such as labeling, claims, package inserts, and accompanying literature.

As part of DSHEA, Congress gave the Secretary of Health and Human Services and the FDA by delegation, the express authority to issue regulations establishing current good manufacturing practice requirements (CGMPs) for dietary supplements. The FDA has issued a final rule establishing requirements for the production of dietary supplements.

Specifically this rule:• Requires certain activities in manufacturing,

packaging, labeling and holding of dietary supplements to ensure that a dietary supplement contains what it is labeled to contain and is not contaminated with harmful or undesirable substances such as pesti- cides, heavy metals, or other impurities.

• Requires certain activities that will ensure the identity, purity, quality, strength, and composition of dietary supplements, which is a significant step in assuring consumers thay are purchasing the type and amount of ingredients declared.

History

• 1994 - Dietary Supplement Health and Education Act is passed by Congress.

• 1997 - The FDA issued an advance notice of proposed rulemaking that contained CGMPs submitted by representatives of the dietary supplement industry as well as nine specific questions from FDA. Approximately 100 comments were received

• 1999 - FDA conducted numerous outreach activities

to include public meetings to ascertain the best approach to rulemaking for dietary supplements.

• 2003 - The FDA issued a proposed rule to establish CGMPs for dietary supplements and dietary supplement ingredients. There were approximately 400 comments submitted in response to the proposal. The comments came from trade associations, govern- ment organizations and officials, health care professionals, consumer groups, manufacturers of dietary supplement and dietary ingredients, and individuals. The dietary supplement CGMP final rule and interim final rule (IFR), issued today are based on the comments received and FDA’s expertise.

• 2007 - Today the FDA took action to help Americans get accurately labeled and properly manufactured dietary supplements, through its final rule establishing dietary supplement CGMPs. An IFR has also been issued to allow the manufacturer to petition the FDA for an exemption to the 100 percent testing requirement for the identity of dietary ingredients to be used in dietary supplements. The manufacturer would have to provide data demonstrating that less than 100 percent identity testing does not materially diminish assurance that the dietary ingredient is the correct dietary ingredient.

Science-Based Consumer Protection

• FDA has found that manufacturing problems have been associated with dietary supplements. Products have been recalled because of microbiological, pesticide, and heavy metal contamination and because they do not contain the dietary ingredients they are represented to contain or they contain more or less than the amount of the dietary ingredient claimed on the label.

• In the past, several private sector laboratory analyses found that a substantial number of dietary supplement products analyzed did not contain the amount of dietary ingredients claimed in their product labels.

• FDA has taken enforcement actions against dietary supplements due to undeclared ingredients, subpo- tency and contamination. Some examples include:

o 2006 - FDA warned several firms after FDA analysis of dietary supplements found undeclared active ingredients used in prescription drugs for erectile dysfunction and their analogs in several dietary supplement products.

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o 2005 - FDA issued a warning letter to a firm after FDA analysis of two of the firm’s products were found to be significantly subpotent in several components, such as Vitamin A, Folic Acid, and Vitamin C.

o 2004 - FDA issued a Warning Letter to a firm after FDA analysis found the firm’s tablets to be underweight, such that the weight of the tablets could not contain the amount of nutrients declared on the label. Also, FDA initiated a seizure action against ginseng because analysis found the product to contain illegal pesticide residues.

CGMP Final Rule:

• The U.S. Food and Drug Administration issued the final rule establishing regulations to require current good manufacturing practices (CGMPs) for dietary supplements.

• The current good manufacturing practices (CGMPs) final rule will require that proper controls are in place for dietary supplements so that they are processed in a consistent manner, and meet quality standards.

• The CGMPs apply to all domestic and foreign companies that manufacture, package, label or hold dietary supplements, including those involved with the activities of testing, quality control, packaging and labeling, and distributing them in the U.S.

• The rule establishes CGMPs for industry-wide use that are necessary to require that dietary supplements are manufactured consistently as to identity, purity, strength, and composition.

• The requirements include provisions related to: o the design and construction of physical plants

that facilitate maintenance o cleaning o proper manufacturing operations o quality control procedures o testing final product or incoming and in process

materials o handling consumer complaints o maintaining records.

• To limit any disruption for dietary supplements produced by small businesses, the rule has a staggered three-year phase-in for small businesses. The final CGMPs is effective in June 2008 for large companies. Companies with less than 500 employees have until June 2009 and companies with fewer than 20

employees have until June 2010 to comply with the regulations.

Interim Final Rule:

• The interim final rule (IFR) establishes a petition process for a manufacturer to apply for exemption from the 100 percent identity testing requirements for dietary ingredients used in manufacturing dietary supplements.

• If a manufacturer is granted an exemption, the manufacturer would still be responsible for ensuring the quality of the final dietary supplement product.

• The manufacturer would have to provide data in its petition demonstrating that less than 100% identity testing does not materially diminish assurance that the dietary ingredient is the correct dietary ingredient. • The IFR is effective in June 2008 when the CGMP final rule becomes effective. However, there is a 90-day comment period. Based on the comments received, the IFR may be revised.

Consumer Benefits:

• Consumers should have access to dietary supplements that meet quality standards and that are free from contamination and are accurately labeled.

• The rule will give consumers greater confidence that the dietary supplement they use has been manufactured to ensure its identity, purity, strength, and composition.

• The rule addresses the quality of manufacturing processes for dietary supplements and the accurate listing of supplement ingredients. It does not limit consumers’ access to dietary supplements, or address the safety of their ingredients, or their effects on health when proper manufacturing techniques are used.

Manufacturers:

• Under the Dietary Supplement Health and Educa- tion Act (DSHEA), manufacturers have an essential responsibility to substantiate the safety of their products and for determining that any representations or claims made about their products are substantiated by adequate evidence to show that they are not false or misleading.

• The CGMPs will help to ensure manufacturers produce unadulterated and properly labeled dietary supplements.

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• Under the CGMP rule, manufacturers are required to:

o Employ qualified employees and supervisors. o Design and construct their physical plant in a

manner to protect dietary ingredients and dietary supplements from becoming adulterated during manufacturing, packaging, labeling and holding.

o Use equipment and utensils that are of appropriate design, construction, and workmanship for the intended use.

o Establish and use master manufacturing and batch production records.

o Establish procedures for quality control operations.

o Hold and distribute dietary supplements and materials used to manufacture dietary supplements under appropriate conditions of tempera- ture, humidity, light, and sanitation so that the quality of the dietary supplement is not affected. o Keep a written record of each product complaint related to CGMPs.

o Retain records for 1 year past the shelf life date, if shelf life dating is used, or 2 years beyond the date of distribution of the last batch of dietary supplements associated with those records.

• Examples of product quality problems that the rule will help prevent are:

o dietary supplements that contain ingredients in amounts that are greater than those listed on the label dietary supplements that contain ingredients in amounts that are less than those listed on the label

o wrong ingredient o other contaminant (e.g., bacteria, pesticide, glass, lead) o foreign material in a dietary supplement container, o improper packaging, and

o mislabeled • The interim final rule allows manufacturers to

petition FDA for an exemption from the requirement of 100 percent identity testing of one or more dietary ingredients used in manufacturing the dietary supplement. The manufacturer would provide data to demonstrate that its proposed reduced frequency of identity testing does not materially diminish assurance that the dietary ingredient is the correct dietary ingredient. Each petition will be considered on a case by case basis.

From: US FDA/CFSAN website available at: http://www.cfsan.fda.gov/~dms/dscgmps6.html . Accessed 7/31/2007

Holistic Living Guide and Journal: 180 Days of Healthy Living

Stephanie Richards, RD, MPAPepper Pike, OH: Wellness Solutions; 2007.Soft cover, spiral bound:233 p.p. $19.95Available from the author: email: [email protected], Phone: 216-324-2073 Fax: 216-464-9291

NCC member, Stepahnie Richards developed the Holistic Living Guide and Journal: 180 Days of Healthy Living to meet a need that other food or

exercise journals were not able to fill – guiding the reader through change by setting lifestyle goals and journaling not only what the reader eats, but also mood, quite time, sleep, water, exercise, and supplement intake. There are 13 chapters, followed by the Personal Vital Statistics, Food and Activity Diary, and Monthly Log tracking sheets.

Each chapter briefly, but succinctly address issues that are critical to wellness beginning with the importance of positive attitude and self affirmations, followed by choosing whole foods, the role of supplements in a healthy diet, carbohydrate intolerance, and the ever important eating consciously. Stephanie has included recommended meal ideas beginning with breakfast, the oft missed but impor-tant snacks, and main meals. For those that have little time for planning or preparation, a three day sample menu and five day menu with quick to fix meals shows readers how they can eat healthy with less effort. All suggested food items and recipes focus on whole grains including beans, high biological protein -- fish and chicken, and healthy fats, including nuts.

The only limitation in the journal information is the lack of references to support natural remedies and detoxification. She does provide suggested sources for more information and products where some additional information can be found. Stephanie relies on her experience with the natural remedies that she recommends. The detoxification diet that is proposed for one to three days should be under-taken only under the guidance of a nutrition professional or healthcare provider and may not be advised for certain acute or chronic conditions.

Overall, the Holistic Living Guide and Journal: 180 Days of Healthy Living provides an alternative guide for those individuals interested in a more holistic approach to lifestyle change. It is worth adding to your library to refer to for yourself or to recommend to those you counsel.

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