Maintaining a healthy weight is especially challenging for obese persons with chronic spinal cord injury, requiring nutritional interventions tailored to each individual’s needs.

T

he ability to attain and maintain a healthy weight eludes many able-bodied individuals, despite their independence with feeding, food shopping, meal preparation, and ability to ambulate and exercise. For obese individuals with chronic spinal cord injury (SCI), achieving safe weight loss may be beyond both their physical and mental grasp. It is not uncommon for patients to present to our SCI wound clinic with pressure ulcers after several months of “dieting.” Studies indicate that measured resting metabolic rate is 14–27% lower for those with SCI as compared to able-bodied individuals due to loss of lean body mass, decreased sympathetic nervous system activity, and decrease in physical activity.¹ At the same time, protein and micronutrient needs may be the same or higher than they were before the injury.
       So, for an individual with SCI, a small serving of fast-food french fries containing 210 cal and 10 g of fat can provide 15% of the person’s daily calorie requirements. Add an 8-oz glass of cranberry juice cocktail (150 cal) or a 12-oz cola (160 cal) and the individual has already consumed 25% of his or her total caloric needs but fewer than 5 g of protein and minimal micronutrients. For those with SCI and pressure ulcers, nutritional supplements are often recommended in addition to regular meals to augment dietary protein intake. Standard oral supplements provide 9 g of protein and 250 cal, about the same amount of protein as an 8-oz serving of skim milk but at close to 3 times the number of calories. Obese or not, it is difficult to justify the use of these supplements with SCI.

Prevention'

       Given this scenario, the first step in the management of obesity in SCI is prevention. It seems logical that nutritional interventions at the time of acute injury as well as subsequent treatments should be aimed at preserving and restoring as much lean body mass as possible without incurring unwanted weight gain. During physiologic stress, the provision of aggressive early nutritional support can decrease net catabolic losses by about 50%.^2,3 For a variety of reasons, however, early nutritional intervention is not always possible. Unfortunately, the net effect of the stress response to injury or infection is significant loss of lean tissue, which correlates with increased risk of morbidity and mortality.^4,5 Current research by Zaloga et al⁶ suggests that during critical illness, modulation of the inflammatory process is required before nutritional repletion can impact lean body mass.
       The inflammatory response is associated with lower anabolic and higher catabolic hormone production. Cortisol, a glucocorticoid hormone, mobilizes protein from body cells, making them available to enter the Krebs cycle for oxidation. Oxidative stress increases, causing cellular damage and death from free radicals. Insulin resistance increases, blocking access to fat stores for energy. Under these altered nutrient-utilization circumstances, protein is rapidly depleted as it is used to meet increased energy requirements to a degree counter to normal nutrient-partitioning principles. In particular, the demand for the amino acids glutamine and arginine markedly increases; both are classified as conditionally essential amino acids.^2,4,7,8 Supplementing with these amino acids can help preserve lean body tissue and support the part they play in bodily functions.
       Arginine is a substrate for protein synthesis and has a pivotal role in many metabolic processes. Arginine can be metabolized to various bioactive compounds and, among other functions, can perform cell signaling through the production of nitric oxide and cell proliferation through its metabolism to ornithine and polyamines. In the step to polyamines, arginine acts as a modulator of inflammation and immune function.^7,9 A recent analysis⁷ of clinical studies using enteral formulas with supplemental arginine “suggests benefits upon outcome, with no evidence of significant detrimental effects.”
       During periods of critical illness, glutamine is utilized by rapidly proliferating cells at a rate faster than it can be synthesized or released by skeletal muscle, resulting in decreased plasma and muscle glutamine concentrations. Depressed stores may limit the rate of glutamine uptake by cells of the immune system, gastrointestinal (GI) tract, and endothelium.^8,10,11 Animal studies indicate that intestinal uptake of glutamine exceeds any other amino acid and serves as a fuel source for both enterocytes and colonocytes; it is considered a “gut-essential nutrient.”¹² Within these cells, metabolism of glutamine via the Krebs cycle yields 30 moles of adenosine triphosphate (ATP) per mole of glutamine.¹³ Approximately 50% of enterally administered glutamine is metabolized in humans by the intestinal mucosa.^10,14 Loss of gut integrity with associated malabsorption of nutrients during periods of increased nutrient utilization would limit the body’s ability to prevent malnutrition and preserve lean tissue.

Inflammation and Immune Function

       When considering essential nutrients, one cannot discuss inflammation and immune function without mentioning omega-3 polyunsaturated fatty acids (PUFAs). The omega-3 PUFAs of nutritional interest are alpha-linolenic acid (ALA) and its derivatives, eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). These fatty acids act as precursors of eiconsanoids (eg, prostaglandins, thromboxanes, and leukotrienes), hormone-like compounds that help regulate blood pressure, heart rate, vascular dilation, blood clotting, lipolysis, and immune response. A deficiency of omega-3 PUFAs is associated with neurological changes, learning deficits, abnormal electroretinograms, and impaired visual acuity.¹⁵
       Clinical assessment of dietary supplementation with omega-3 PUFAs indicate their beneficial impact in certain human diseases, particularly those in which inflammation is suspected as a significant component in pathogenesis. Their molecular bases of action in reducing disease and inflammation are an important interest of study given the heightened awareness that inflammation can be directly associated with many disease states, such as cardiovascular disease, asthma, arthritis, psoriasis, Alzheimer’s disease, and periodontitis.^15,16,17 A recent study by Makoto et al¹⁵ identified a new class of aspirin-triggered bioactive lipids in humans, called resolvins, which could partly explain the anti-inflammatory effects of fish oils.
       In addition to the acute injury phase and episodes of skin breakdown or infection, inflammation can be problematic in otherwise healthy individuals with chronic SCI. In a review of the literature, Bauman and Spungen found, “When compared with the able-bodied population, people with SCI are more likely to have oral carbohydrate intolerance, insulin resistance, elevated low-density lipoprotein cholesterol, and reduced high-density lipoprotein cholesterol, associated with increased prevalence of diabetes mellitus and cardiovascular disease.”¹⁶ These findings are characteristic of metabolic syndrome, which is a pro-inflammatory state as evident by elevated C-reactive protein levels. In a study by Lee et al¹⁸ involving 93 individuals with chronic SCI, metabolic syndrome and insulin resistance were present in 22.6% of subjects.

Approaches to Manage Obesity

       The issue remains in how to translate the literature into everyday clinical practice in the management of obesity in SCI. What is the appropriate enteral feeding in acute SCI for those with chronic injury or pressure ulcers? Are there oral supplement options to promote wound healing without exceeding the calorie requirements? Which dietary guidelines can be used to provide nutritional counseling for individuals with new and chronic SCI?
       In recent years, there has been increasing interest in using specific nutrients to modulate the inflammatory response, resulting in the development of several “immune-enhancing” enteral formulas. Immune-enhancing

Table 1

formulas contain immune-modulating nutrients, such as arginine, glutamine, and omega-3 fatty acids (see Table 1).^20,21 But the protein and fat content and composition can vary, affecting tolerance. In order to realize benefit, the enteral product has to be well tolerated as measured by normal stooling, rapid recovery of visceral proteins, normal

Table 2

liver function tests, and glycemic control, to name a few.^22-25 The GI tract is one of the largest immune systems in the body, and restoration of gut integrity is critical in modulating immune function (see Table 2).¹⁰
       Oral supplements containing arginine and glutamine are also available (see Table 3). Most of these products do not contain omega-3 fatty acids or a source of complete protein.

Table 3

For individuals with high protein needs and/or poor protein intake, whey protein powder can be mixed with any moist food or low-calorie beverage. Currently available are low-carbohydrate liquid protein supplements that contain hydrolyzed collagen-casein protein that can be taken as is or mixed in any food or beverage. In some cases, a standard oral supplement is needed, often for feasibility issues. A comparison of all available products should be made to find a product that is high in protein and low in calories.
       A sample “one-size-fits-all” diet does not exist for the

Table 4

management of obesity in any population. However, there are general dietary guidelines (see Table 4) that can be used during nutrition counseling sessions that are similar to dietary recommendations for those with cardiovascular disease and/or diabetes. As part of a prevention model, each person should receive diet education by a registered dietitian during rehabilitation for acute spinal injury. Nutritional counseling should be conducted as indicated or, at a minimum, as part of the person’s annual physical, with the inclusion of appropriate monitors (eg, actual weight, abdominal circumference, lipid profile, fasting and postprandial blood glucose, and C-reactive protein).