Vitamin D deficiency may actually contribute to Crohn's disease because the hormone modulates the immune system. According to endocrinologists at McGill University, vitamin D appears to turn on genes to encode antimicrobial peptides that fight against intestinal invaders (1). The immune support may help avoid inflammation associated with an autoimmune response in Cronh's disease.
This may explain why Crohn's disease is more prevalent in Northern latitude countries. It also suggests that increased vitamin D could assist in avoiding Crohn's disease in the future.
How do these findings affect what we know about ulcerative colitis? I hope we find out soon.
Reference
1. McGill University Health Centre (2010, January 27). Vitamin D supplements could fight Crohn's disease. ScienceDaily. Retrieved March 31, 2010, from http://www.sciencedaily.com /releases/2010/01/100127104904.htm
31 March 2010
Managing Diverticulitis After Treatment
It is well documented that a diet low in insoluble fiber is considered the main etiological factor in leading to diverticulitis. The intake of insoluble fiber speeds up transit of food and increases bulk reducing pressure on the intestine (1). On the other hand, intake of red meat appears to increase risk (1).
Patients treated for diverticulits are often prescribed antibiotic therapy and recommended to stay on a low-fiber diet and reintroducing insoluble fiber gradually (2). In some cases, surgery is needed (2). Afterward, nutritionists would recommend gradual increases of fiber because a diet high in fiber can lead to high amounts of gas and forceful diarrhea (2-3).
Because of possible damage in the intestine, nutritionists should also evaluate patients are at higher risk of malnutrition. Malnutrition can lead to slow healing and recovery as well as deterioration of muscle, respiratory and immune function (4). To receive adequate nutrients, higher protein intake as well as supplements of certain vitamins such as B12 and minerals such as calcium may be needed (4).
A weight-management program may help to avoid diverticulitis in the future. According to a prospective cohort study, subjects with a BMI, waist circumference and waist-to-hip ratio that categorized them as obese had an increased risk of diverticulitis and diverticular bleeding (5).
Nutritionists may also recommend probiotics along with prebiotics to support growth of healthy intestinal flora after antibiotic therapy (4).
References
1. Korzenik JR. Case closed? Diverticulits: epedemiology and fiber. J Clin Gastroeneterol. 2006 Aug;40 Suppl 3:S1 12-6.
2. Kotzampassakis N, Pittet O, Schmidt S, Denys A, Demarines N, Calmes JM. Presentation and treatment outcome of diverticulitis in younger adults: a different disease than in older patients? Dis Colon Rectum. 2010 Mar;53(3):333-8.
4. Kohlstadt I. Food and Nutrients in Disease Management. Boca Raton, FL: CRC Press, 2009.
5. Strate LL, Liu YL, Aldoori WH, Syngal S, Giovannucci EL. Obesity increases the risks of diverticulitis and diverticular bleeding 2008;136(1):115-112.
Patients treated for diverticulits are often prescribed antibiotic therapy and recommended to stay on a low-fiber diet and reintroducing insoluble fiber gradually (2). In some cases, surgery is needed (2). Afterward, nutritionists would recommend gradual increases of fiber because a diet high in fiber can lead to high amounts of gas and forceful diarrhea (2-3).
Because of possible damage in the intestine, nutritionists should also evaluate patients are at higher risk of malnutrition. Malnutrition can lead to slow healing and recovery as well as deterioration of muscle, respiratory and immune function (4). To receive adequate nutrients, higher protein intake as well as supplements of certain vitamins such as B12 and minerals such as calcium may be needed (4).
A weight-management program may help to avoid diverticulitis in the future. According to a prospective cohort study, subjects with a BMI, waist circumference and waist-to-hip ratio that categorized them as obese had an increased risk of diverticulitis and diverticular bleeding (5).
Nutritionists may also recommend probiotics along with prebiotics to support growth of healthy intestinal flora after antibiotic therapy (4).
References
1. Korzenik JR. Case closed? Diverticulits: epedemiology and fiber. J Clin Gastroeneterol. 2006 Aug;40 Suppl 3:S1 12-6.
2. Kotzampassakis N, Pittet O, Schmidt S, Denys A, Demarines N, Calmes JM. Presentation and treatment outcome of diverticulitis in younger adults: a different disease than in older patients? Dis Colon Rectum. 2010 Mar;53(3):333-8.
4. Kohlstadt I. Food and Nutrients in Disease Management. Boca Raton, FL: CRC Press, 2009.
5. Strate LL, Liu YL, Aldoori WH, Syngal S, Giovannucci EL. Obesity increases the risks of diverticulitis and diverticular bleeding 2008;136(1):115-112.
Helping a Patient Manage IBS and Diarrhea
When IBS is diarrhea-predominant, a doctor may prescribe an antimotility agent to assist patients with symptoms (1). He or she may also prescribe an antibiotic if the IBS is a result of small intestinal bacterial overgrowth (1).
As a dietary aid for patients, a nutritionist may suggest soluble fiber such as from oats because it can help act against symptoms such as diarrhea by helping bind fat and slow emptying of food from the stomach into the small intestine (2).
The soluble fiber can include prebiotics such as fructo-oligosaccharides or resistant maltodextrin, which support growth of healthy intestinal bacteria. The prebiotics taken in conjunction with probiotics particularly after antibiotic therpay may help with promoting the growth of the good bacteria. This integrative therapy can help to alleviate symptoms by promoting competition against small intestinal bacterial growth (3).
Nutrionists should recommend suspending intake of insoluble fiber such as from wheat and cereal grains and limiting poorly-digested carbohydrates and sugar alcohols as these can worsen symptoms (4). Patients may find benefit from following an exclusion diet whereas trigger foods are eliminated and then, if thought advisable, reintroduced gradually (4).
References
1. Kohlstadt I. Food and Nutrients in Disease Management. Boca Raton, FL: CRC Press, 2009.
2. Bijkerk CJ, de Wit NJ, Muris JWM, Whorwell PJ, Knottnerus JA, Hoes AW. Soluble or insoluble fibre in irratble bowel syndrome in primary care? Randomized placebo controlled trial. Brit Med Jour 2009;339:b3154. Available at http://www.bmj.com/cgi/content/abstract/339/aug27_2/b3154. Accessed on March 31, 2010.
3. American College of Gastroenterology (2008, October 10). How Effective Are Probiotics In Irritable Bowel Syndrome?. ScienceDaily. Available at http://www.sciencedaily.com /releases/2008/10/081006092656.htm. Accessed on March 31, 2010.
4. Heizer WD, Southern S, McGovern S. The role of diet in symptoms of irritable bowel syndrome in adults: a narrative view. J Am Diet Assoc. 2009 Jul;109(7):1204-1.
As a dietary aid for patients, a nutritionist may suggest soluble fiber such as from oats because it can help act against symptoms such as diarrhea by helping bind fat and slow emptying of food from the stomach into the small intestine (2).
The soluble fiber can include prebiotics such as fructo-oligosaccharides or resistant maltodextrin, which support growth of healthy intestinal bacteria. The prebiotics taken in conjunction with probiotics particularly after antibiotic therpay may help with promoting the growth of the good bacteria. This integrative therapy can help to alleviate symptoms by promoting competition against small intestinal bacterial growth (3).
Nutrionists should recommend suspending intake of insoluble fiber such as from wheat and cereal grains and limiting poorly-digested carbohydrates and sugar alcohols as these can worsen symptoms (4). Patients may find benefit from following an exclusion diet whereas trigger foods are eliminated and then, if thought advisable, reintroduced gradually (4).
References
1. Kohlstadt I. Food and Nutrients in Disease Management. Boca Raton, FL: CRC Press, 2009.
2. Bijkerk CJ, de Wit NJ, Muris JWM, Whorwell PJ, Knottnerus JA, Hoes AW. Soluble or insoluble fibre in irratble bowel syndrome in primary care? Randomized placebo controlled trial. Brit Med Jour 2009;339:b3154. Available at http://www.bmj.com/cgi/content/abstract/339/aug27_2/b3154. Accessed on March 31, 2010.
3. American College of Gastroenterology (2008, October 10). How Effective Are Probiotics In Irritable Bowel Syndrome?. ScienceDaily. Available at http://www.sciencedaily.com /releases/2008/10/081006092656.htm. Accessed on March 31, 2010.
4. Heizer WD, Southern S, McGovern S. The role of diet in symptoms of irritable bowel syndrome in adults: a narrative view. J Am Diet Assoc. 2009 Jul;109(7):1204-1.
26 March 2010
Low-carb diets and dehydration
It is well known that dehydration is a potential adverse effect of a ketogenic diet, which is one higher in fat with adequate protein and lower in carbohydrates.
Nutritionists should be watchful, in particular, of those who use ketogenic diets as therapy for certain conditions such as epilepsy and type 2 diabetes.
A study in epileptic children on ketogenic diets, for example, found dehydration to be the "most common early-onset compllication"and higher in those who fasted (1-2). The dehydration could be partly blamed on the incidence of GI tract adverse effects (1).
When treating those with type 2 diabetes with a ketogenic diet, it is advisable to instruct drinking up to eight 8 oz. glasses of water daily. There may also be need for adjusting those recommendations if certain medications were used such as diuretics.
According to the researchers who performed an intervention trial on those with type 2 diabetes and a ketogenic diet that resulted in a few adverse effects, the following was concluded: "Until we learn more about using low carbohydrate diets, medical monitoring for hypoglycemia, dehydration, and electrolyte abnormalities is imperative in patients taking diabetes or diuretic medications" (1).
The lower carbs can have a diuretic effect on the body, which should lead clinicians to be aware and make recommendations for increased water intake as necessary.
References
2. Kang HC, Chung da E, Kim DW, Kim HD. Epilepsia 2004;45:1116-1123. Available at: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1198735/?tool=pmcentrez
Kidneys: Animal vs Veggie Protein
I was curious to know what it is about animal protein in general that would affect kidneys more than vegetable protein. So I went searching for a study.
There was a human intervention trial from the Dept of Internal Medicine in Texas that I found, which had evaluated animal protein-rich diet on kidney stones and calcium. The study took 15 subjects and fed them either vegetable protein, vegetable and egg protein or animal protein for 12 days in three different periods (1). What the study found was that the animal protein diet "conferred an increased risk for uric acid stones" but a lesser risk than the vegetarian diet for "calcium oxalate or calcium phosphate stones" (1).
Because my question really wasn't sufficiently answered by this study, I decided to pursue what National Kidney Foundation had to say. Finally, I found a publication they put out referencing nutrition and speaking to vegetarian diets in which they basically state that the veggie diets aren't "rich in higher quality protein" (2), but that also that the best sources of vegetarian protein may be ones lower in potassium and phosphorus depending on kidney dysfunction.
At best, the main focus on kidney health is a balance between protein and carbs because too few leads to more protein break down as well as protein with sodium (lower is better), phosphorus (lower is better), calcium, potassium (sometimes higher, sometimes low is better) and, of course, water amounts for keeping kidneys functioning well (2).
References
1. Breslau NA, Brinkley L, Hill KD, Pak, CY. J Clin Endocrinol Metab. 1988 Jan;66(1):140-6. Available at: http://www.ncbi.nlm.nih.gov/pubmed/2826524
2. National Kidney Foundation. Nutrition and Early Kidney Disease. Available at: http://www.kidney.org/atoz/pdf/NutriKidFail_Stage1-4.pdf
Why Evidence-based Nutrition
As a result of my profession in science communications, it is a fact of life that I come in to work to find 1-2 papers to read every morning on my desk. I must read an average of between 10 new scientific papers weekly. They can range from culture studies, animal studies, human clinical trials, epidemiological studies, meta-analyses or simply review articles.
As a writer who specializes in topics of nutrition, I am continually faced with the labor of assessing just how “big” the news coming from the study really is, whether or not it merits more attention by our research and sciences team, and whether or not we should communicate it to the public.
If I had any special talent for pointing out flaws or problems in studies, I would be thrilled. I don’t. Not at all. Lucky for me, however, I work with a few knowledgeable scientists with a keen awareness for what’s hot and what’s definitely not.
I doubt that many of my own colleagues share the same luxury that I have for being able to pass a study by an experienced nutritionist to help me place it in proper perspective for our audiences. This is simply evident by an Internet search for nutrition articles and a judgment of how other health writers handle their material.
Relying on experts to sift through the journals has been a unique experience, one that has been inspiring—which is why I now have hopes of ultimately gaining expertise of evidence-based nutrition (EBN) myself. EBN is simply true science and research, after all, and it informs decisions and practice.
It is my view that nutrition is a young science that is maturing quickly. I share a similar positive optimism for the field as Walter Willet, who has written of a merge of nutritional sciences with epidemiology to provide greater knowledge more quickly (1).
I follow with Willet’s assertion that nutritional research approaches are improving (that it won’t take us 100 years to discover flaws in dietary recommendations such as partially hydrogenated oils, for example(1)), and my interest is piqued in learning, as I would expect, that the study of genomics will further influence the future of nutrition.
While evidence-based nutrition and medicine may appear controversial to a few, I cannot see any other way for me, as I long to live in a world where science and statistics (even if we don’t “get” them) govern our understanding, not our often-flawed personal judgments.
I welcome the new process of nutritional epidemiology referenced by Willet that he expects will provide “vast and unprecedented information” (1). For that matter, I expect to be intensely studying as continual information appears over the next decade or so.
To achieve what Trisha Greenhalgh advises in her wonderful primer on evidence-based medicine, How to Read a Paper, it is my expectation to come away with the ability “not only to read papers, but also to read the right papers at the right time” (2) to best guide my decision making.
References
1. Willet WC. Nutritional epidemiology issues in chronic disease at the turn of the century. Epidemiol Rev. 2000;22(1):85-86. Available at: http://epirev.oxfordjournals.org/cgi/reprint/22/1/82.pdf
2. Greenhalgh T. How To Read A Paper: The Basics of Evidence Based Medicine. Malden, MA: Blackwell, 2006, p. 2.
As a writer who specializes in topics of nutrition, I am continually faced with the labor of assessing just how “big” the news coming from the study really is, whether or not it merits more attention by our research and sciences team, and whether or not we should communicate it to the public.
If I had any special talent for pointing out flaws or problems in studies, I would be thrilled. I don’t. Not at all. Lucky for me, however, I work with a few knowledgeable scientists with a keen awareness for what’s hot and what’s definitely not.
I doubt that many of my own colleagues share the same luxury that I have for being able to pass a study by an experienced nutritionist to help me place it in proper perspective for our audiences. This is simply evident by an Internet search for nutrition articles and a judgment of how other health writers handle their material.
Relying on experts to sift through the journals has been a unique experience, one that has been inspiring—which is why I now have hopes of ultimately gaining expertise of evidence-based nutrition (EBN) myself. EBN is simply true science and research, after all, and it informs decisions and practice.
It is my view that nutrition is a young science that is maturing quickly. I share a similar positive optimism for the field as Walter Willet, who has written of a merge of nutritional sciences with epidemiology to provide greater knowledge more quickly (1).
I follow with Willet’s assertion that nutritional research approaches are improving (that it won’t take us 100 years to discover flaws in dietary recommendations such as partially hydrogenated oils, for example(1)), and my interest is piqued in learning, as I would expect, that the study of genomics will further influence the future of nutrition.
While evidence-based nutrition and medicine may appear controversial to a few, I cannot see any other way for me, as I long to live in a world where science and statistics (even if we don’t “get” them) govern our understanding, not our often-flawed personal judgments.
I welcome the new process of nutritional epidemiology referenced by Willet that he expects will provide “vast and unprecedented information” (1). For that matter, I expect to be intensely studying as continual information appears over the next decade or so.
To achieve what Trisha Greenhalgh advises in her wonderful primer on evidence-based medicine, How to Read a Paper, it is my expectation to come away with the ability “not only to read papers, but also to read the right papers at the right time” (2) to best guide my decision making.
References
1. Willet WC. Nutritional epidemiology issues in chronic disease at the turn of the century. Epidemiol Rev. 2000;22(1):85-86. Available at: http://epirev.oxfordjournals.org/cgi/reprint/22/1/82.pdf
2. Greenhalgh T. How To Read A Paper: The Basics of Evidence Based Medicine. Malden, MA: Blackwell, 2006, p. 2.
25 March 2010
How much water do I drink?
I've been perusing through Dr. Batmanghelidj's book Your Body's Many Cries for Water. Yes, I'm well aware that it does not entirely scientific and does have a few claims that could be regarded as sensationalism for water (excess cholesterol is a result of too little water intake, really?).
I was intrigued, however, at some of the references to the possibility of chronic dehydration as an influence on disease and the beginnings of cellular aging, which can fuel chronic disease.
Plus, anyway, I needed to write a paper on water.
So, of course, I had to ask myself, "How much water do you drink?"
So here goes my diet for today:
8am: 1 cup of green tea (with 1 yogurt/protein shake/fruit)
10am: 1 cup of yerba maté (a habit passed from Argentine mom)
12pm: 1 cup iced tea (with chicken salad lunch)
2pm: 1 shot espresso
4pm: 1 cup yerba maté
6pm: 1 glass red wine (with 1 cup lentil-asparagus soup dinner)
9pm: 1 cup green tea
(Plenty of liquid, but no straight glasses of purified H2O.)
I suppose that from a nutritional standpoint, it appears I did pretty OK for the day and plenty of antioxidants from fruit, veggies, tea, maté, coffee, and red wine. I am simply trying to stick to a relatively decent DASH eating plan.
Although I didn't feel dehydrated (I drank about 7 cups of liquid), given what I have now read about water I'll probably have to reconsider what I'm doing.
I'm especially alarmed at the possible effects of chronic caffeine diminishing ATP and alcohol's influence on vasopressin causing dehydration. (And here I thought the regular tea, coffee and occasional red wine were pretty OK habits.)
It does make sense to me that cells would best function when well-hydrated. After all, as stated in the materials, life began in water, or an ancient primordial swamp.
No doubt in my mind that given our origins from the sea that it's water intake that is truly necessary for entire body's proper function (along with a bit of salt).
As the water-relationship makes common sense to me, I can see how I might recommend it as integrative therapy in certain situations, although I would hang back from calling it "prevention" or "cure" of disease without some considerable evidence-based research.
I admit I had no idea something like a low-grade "chronic dehydration" existed and could exist despite food and liquid intake and affected directly by caffeine and alcohol.
It seems to me that, since water represents pretty much the starting point of nutrition (at least from a cell's and ancient fishapod ancestor's standpoint), the topic of water intake definitely should be part of all nutrition programs.
My thoughts,
15 March 2010
What's the most dangerous item on a fast food menu?
When I first saw the movie Super Size MeI was first pretty shocked that someone would actually risk his own body this way. Then, I was shocked at how quickly this guy was able to gain weight. This may simply be because I don't tend to gain any weight even after stuffing myself day after day. Of course, I've never tried to stuff myself with McDonald's day after day. Maybe that would do it. It did for this guy. And it does for our children. Sure opened my eyes.
What's the most dangerous item on the fast food menu?
I remember a time when I was younger I would go off with my grandpa to Burger King. He'd say, "Let's get you a Whopper. They're only a buck." I'd gush with enthusiasm. He'd buy me one. He'd buy himself too.
My grandpa died of heart disease. I blame it on those Whoppers. I blame them because they're cheap and because the name itself, like the Big Mac, suggest that you're getting a lot of meat for your money. What you're really getting is a gimmick and a lot of saturated and trans fat. I have no doubt that Burger King Whoppers (they ate them all the time) are what killed both my grandfather and my grandmother.
What's the most dangerous item on the fast food menu?
I remember a time when I was younger I would go off with my grandpa to Burger King. He'd say, "Let's get you a Whopper. They're only a buck." I'd gush with enthusiasm. He'd buy me one. He'd buy himself too.
My grandpa died of heart disease. I blame it on those Whoppers. I blame them because they're cheap and because the name itself, like the Big Mac, suggest that you're getting a lot of meat for your money. What you're really getting is a gimmick and a lot of saturated and trans fat. I have no doubt that Burger King Whoppers (they ate them all the time) are what killed both my grandfather and my grandmother.
Why Statins May Require You Take Extra CoQ10 and Vitamin E
Statins are drugs used to lower cholesterol by blocking cholesterol synthesis in the liver (1). By lowering total and LDL cholesterol, in effect, they help lower risk of heart disease and death (1). The most commonly known statin drugs are simvastatin (Zocor), lovastatin (Mevacor), pravastatin (Pravachol), and rosuvastatin (Crestor).
Currently, it is theorized that as statins block cholesterol synthesis, they also block synthesis of coenzyme Q10 (2). This is unfortunate because coenzyme Q10 plays a key role in the mitochondria in the electron transport chain, as an antioxidant and as a regenerator of vitamin E (3).
Statin therapy, then, could potentially lead to deficiencies of both coenzyme Q10 and, possibly, increase the need for vitamin E in cells (4). It has been theorized that deficiencies in both coenzyme Q10 and vitamin E are why statins cause statin-related muscle pain and statin-related myopathy (3-4).
References
1. LaRosa JC, He J, Vupputuri S. Effect of statins on risk of coronary disease: a meta-analysis of randomized controlled trials. JAMA. 1999 Dec 22-29;282(24):2340-6. Available at: http://www.ncbi.nlm.nih.gov/pubmed/10612322
2. Schaars CF, Stalenhoef AF. Effects of ubiquinone (coenzyme Q10) on myopathy in statin users. Curr Opin Lipidol. 2008 Dec;19(6):553-7.
3. Gropper SS, Smith JL, Groff JL. Advanced Nutrition and Human Metabolism. Belmont, CA: Thomson Wadsworth, 2009.
4. Galli F, Iuliano L. Do statins cause myopathy by lowering vitamin E levels? Med Hypotheses. 2010 Apr;74(4):707-709. Epub 2009 Nov 6.
Currently, it is theorized that as statins block cholesterol synthesis, they also block synthesis of coenzyme Q10 (2). This is unfortunate because coenzyme Q10 plays a key role in the mitochondria in the electron transport chain, as an antioxidant and as a regenerator of vitamin E (3).
Statin therapy, then, could potentially lead to deficiencies of both coenzyme Q10 and, possibly, increase the need for vitamin E in cells (4). It has been theorized that deficiencies in both coenzyme Q10 and vitamin E are why statins cause statin-related muscle pain and statin-related myopathy (3-4).
References
1. LaRosa JC, He J, Vupputuri S. Effect of statins on risk of coronary disease: a meta-analysis of randomized controlled trials. JAMA. 1999 Dec 22-29;282(24):2340-6. Available at: http://www.ncbi.nlm.nih.gov/pubmed/10612322
2. Schaars CF, Stalenhoef AF. Effects of ubiquinone (coenzyme Q10) on myopathy in statin users. Curr Opin Lipidol. 2008 Dec;19(6):553-7.
3. Gropper SS, Smith JL, Groff JL. Advanced Nutrition and Human Metabolism. Belmont, CA: Thomson Wadsworth, 2009.
4. Galli F, Iuliano L. Do statins cause myopathy by lowering vitamin E levels? Med Hypotheses. 2010 Apr;74(4):707-709. Epub 2009 Nov 6.
What are blood thinners and how do they work?
Blood thinners, or anticoagulants and antiplatelet agents, are drugs to thwart blood clotting of which could block flow of blood to your heart causing a heart attack or your brain causing a stroke.
Common anticoagulants are Coumadin, Warfarin and Heparin. It controls the rate in which clotting can occur and prevents them from forming inside blood vessels and the heart. It can also help prevent existing clots from enlarging.
Common antiplatelet agents are Aspirin, Plavix (clopidogrel bisulfate) and Ticlid (ticlopidene hydrochloride). As the name suggests, they keep platelets from aggregation to prevent possible clotting, specifically where an injury to a blood vessel may have occurred.
Blood thinners aren't associated with any specific nutrient deficiency, but are contraindicated taken with foods and supplements high in vitamin K1 (a clotting factor) or large amounts of vitamins E and C. They are also contraindicated with alcohol, certain herbs and teas, and other dietary agents that cause thinning of blood.
Reference
http://www.nlm.nih.gov/medlineplus/bloodthinners.html
Common anticoagulants are Coumadin, Warfarin and Heparin. It controls the rate in which clotting can occur and prevents them from forming inside blood vessels and the heart. It can also help prevent existing clots from enlarging.
Common antiplatelet agents are Aspirin, Plavix (clopidogrel bisulfate) and Ticlid (ticlopidene hydrochloride). As the name suggests, they keep platelets from aggregation to prevent possible clotting, specifically where an injury to a blood vessel may have occurred.
Blood thinners aren't associated with any specific nutrient deficiency, but are contraindicated taken with foods and supplements high in vitamin K1 (a clotting factor) or large amounts of vitamins E and C. They are also contraindicated with alcohol, certain herbs and teas, and other dietary agents that cause thinning of blood.
Reference
http://www.nlm.nih.gov/medlineplus/bloodthinners.html
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