COMPOSITIONS CONTAINING FATTY ACIDS FOR IMPROVING DIGESTION AND ABSORPTION IN THE SMALL INTESTINE

Abstract: The present invention provides methods and compositions for slowing gastrointestinal transit and prolonging residence time, thereby optimizing presentation and absorption of ingested nutrients and/or pharmacologically active agents in the small intestine. The present invention further provides methods and compositions for enhancing the bioavailability and therapeutic effectiveness of pharmacologically active agents.

Description: COMPOSITIONS CONTAINING FATTY ACIDS FOR IMPROVING DIGESTION AND ABSORPTION IN THE SMALL INTESTINE FIELD OF THE INVENTION The present invention relates to methods and pharmaceutical compositions for controlling the presentation of luminal content to the gastrointestinal tract. BACKGROUND OF THE INVENTION A principal function of the gastrointestinal tract is to process and absorb food. The stomach, which is both a storage and digestive organ, works to optimize the conditions for digestion and absorption of food in the small intestine. Following the stomach and preceding the large bowel (colon) is the small intestine, which comprises three regions: the duodenum, jejunum, and ileum. A major function of the small intestine is one of absorption of digested nutrients. The passage of a meal through the gastrointestinal tract, which leads to digestion and absorption of nutrients, is controlled by a complex system of inhibitory and stimulatory motility mechanisms which are influenced by the composition of the meal ingested. Specific sensors in the small intestine respond to fats, proteins, carbohydrates, osmolality, acidity, and the size of the meal. These sensors activate propulsive and inhibitory motor activities, which modulate transit and thereby shorten or lengthen the amount of time a substance resides in the small intestine. Since digestion and absorption are both time-demanding processes, the rate of passage through the small intestine is of great significance to the rate, extent and location (duodenum, jejunum, ileum, or colon) of digestion and absorption within the gastrointestinal tract. The period of time during which substances are in contact with the mucosa of the small intestine is crucial for the efficacy of digestion and absorption. Therefore, modulation of gut motility and transit time of substances through the gastrointestinal tract will ensure optimal digestion and utilization of the absorptive surface, as well as prevent absorptive mechanisms from being overloaded, resulting in the spilling of luminal content into the colon (which could occur if substrates were passed on too rapidly and exceeded the absorptive capacity of already maximally loaded surfaces in the small intestine) . Important steps in dietary lipid absorption begin in the stomach with regulated gastric emptying, whereby the system of inhibitory and stimulatory mechanisms for the control of gut motility are set in motion. Once food enters the small intestine to trigger nutrient-sensitive inhibitory sensors, these mechanisms prevent premature emptying of gastric contents into the duodenum, which would overwhelm its capacity for lipid absorption. However, early in the meal, before nutrient-triggered inhibitory mechanisms are fully activated, and depending on the load, fat may surge uncontrollably out of the stomach. Thus, after a meal with a large amount of fat, fat may be dumped into the small intestine, overwhelming the proximal small intestine and spilling distally into the jejunum and ileum. The proper operation of gastric emptying control mechanisms prevents this occurrence, and ensures a maximum interface of the water-insoluble lipid with the aqueous contents of the intestinal tract. Depending on the extent of this surge of fat into the small intestine, e.g., after a small meal of fat, only the proximal small intestine (duodenum and proximal jejunum) is presented with fat. In the duodenum, jejunum, and/or ileum, the fats which have been released from the stomach encounter bile acids and pancreatic enzymes. The function of the bile acids is to act as surfactants which bring the insoluble triglyceride molecules into solution, and thereby render them amenable to digestion by pancreatic enzymes and absorption by cells in the intestinal mucosa. Due to the control of the speed of transit (more residence time in the small intestine to complete digestion and absorption of a meal having more fat) , intestinal absorption of lipid is normally very efficient over wide ranges of dietary fat intake. A normal person generally absorbs approximately 95-98% of dietary lipid. However, when the normal digestive and absorptive processes, or the control of transit, are impaired, malabsorption syndromes frequently ensue. For example, it usually takes 2 to 4 hours for food to reach the colon. This allows sufficient time to complete digestion and absorption. However, when gastrointestinal transit becomes abnormally accelerated, there is not enough time to complete digestion and absorption. In addition to nutrients, water, vitamins, minerals and electrolytes, the small intestine is also an important site for the absorption of pharmacological agents, or drugs. The proximal part of the small intestine has the greatest capacity for absorption of drugs. Intestinal absorption of drugs is influenced to a great extent by many of the same basic factors that affect the digestion and absorption of nutrients, water and electrolytes. For drug absorption to proceed efficiently, the drug must first arrive at a normal absorbing surface in a form suitable for absorption; it must remain there long enough in a form and in a concentration that promotes absorption; and it must be absorbed by a normal epithelial cell without being metabolized by that cell. Additionally, if a drug is delivered in a solid form, it must dissolve before it can be absorbed. Therefore, sufficient gastrointestinal residence time must be available to allow complete dissolution and absorption of a drug. Accordingly, considerable advantage would be obtained if a pharmaceutical dosage form could be retained for a longer period of time within the stomach and/or the small intestine for proper absorption to occur. Absorption of a drug in the gastrointestinal tract is a function of characteristics of the drug, such as its molecular structure, as well as attributes of the gastrointestinal tract. The rate of absorption of certain drugs, which are absorbed slowly and usually incompletely, varies according to the small intestinal transit time. Although the normally short (2 to 4 hour) intestinal transit time is an important and limiting factor in drug absorption, transit times are especially important when the optimal absorption site of a drug is located in only a particular segment of the gastrointestinal tract, most commonly the proximal small intestine (duodenum and proximal jejunum) . This phenomenon is referred to as an "absorption window" (see Davis, "Small Intestine Transit", Ch. 4, pp. 57-58, in "Drug Delivery to the Gastrointestinal Tract", Hardy et al. (Eds.), Ellis Horwood Ltd. (1989)). Passage through this area is usually too rapid for complete drug dissolution and absorption to take place therein. Current methods used to increase the contact time of a drug with the absorptive surface of the small intestine have not been very successful. These methods have included formulations that slow the release of the active drug (e.g., sustained-release formulations), the use of bioadhesives that adhere to the intestinal mucosa (e.g., polycarbophil) , and strategies directed at retention of the dosage form in the stomach (e.g., flotation on top of gastric contents with alginate and hydroxypropylmethyl cellulose based tablets or swelling devices that expand to form large drug-containing boluses in the stomach) . See "The Stomach: Its Role in Oral Drug Delivery" and "Small Intestine: Transit and Absorption of Drugs", Ch. 4 and 5 in "Physiological Pharmaceutics: Biological Barriers to Drug Absorption", Wilson and Worthington (Eds.), Ellis Horwood Ltd. (1989) . A tremendous amount of research has been undertaken in efforts to elucidate the role of adverse effects on nutrition and absorption in gastrointestinal disorders (Cerda, Med. Clin . N. Am. , 77:881-87 (1993); Meyer, Gastro . Clin . N. Am. , 23:227-60 (1994); Thompson, Gastro. Clin . N. Am. , 23:403-20 (1994); Farrugia et al. , Gastro . Clin . N. Am. , 25:225-46 (1996)). Despite this research, few standards of care presently exist to correct abnormal nutrition and enhance digestion and absorption in most of these disorders. The rate at which food passes through the gastrointestinal tract is an important factor that affects absorptive efficiency (how completely nutrients are absorbed) and the outcome following gastric surgery and/or intestinal resection. The resection of extensive sections of bowel as well as loss of absorptive surface secondary to diseased small bowel mucosa can lead to the loss of absorptive capacity as well as specific malabsorption syndromes. Extensive loss of small intestine may prevent successful feeding via the gut. Resection or disease of large amounts of terminal ileum is also known to cause vitamin B12 and bile acid deficiencies, which, in turn, can lead to fat and other fat-soluble substances, such as vitamins, being less well absorbed. Strictures or bypassed loops of bowel, created by either surgery or fistula formation, can result in blind loop syndromes with bacterial overgrowth and subsequent malabsorption. Even after antibiotic correction of bacterial overgrowth, the severity of fat malabsorption is often greater than expected from the loss of absorptive surfaces. Abnormally rapid transit resulting from loss of transit control mechanisms provides another explanation for maldigestion and malabsorption seen in this setting. By reducing the time available for digestion and absorption, contact between nutrients and the already reduced absorptive surfaces is further limited. After surgical procedures of the bowel, the most important therapeutic objective is to resume nutritional intake so as to maintain the patient's nutritional status. By necessity, this is often achieved by parenteral nutrition support in the early postoperative period. Enteral nutrition support may be started early after the operation. Maximization of enteral absorption of nutrients is important for successful enteral feeding. Generally, such maximization in the postoperative patients who may have impaired digestive and absorptive capacities requires that the enteral intake greatly exceed the usual nutritional needs in an effort to ensure that the nutritional requirements are met. Disruption of normal digestive and absorptive processes frequently manifests as a variety of syndromes, such as, for example, weight loss, malnutrition, diarrhea, thirst, steatorrhea, vitamin deficiencies, electrolyte imbalance, and the like. Malabsorption syndromes are associated with a large heterogeneous group of gastrointestinal disorders with the common characteristic of failure to assimilate ingested substances normally. The defect is characterized by decreased or impaired function of almost any organ of the gut, including the liver, biliary tract, pancreas, and lymphatic system, as well as the stomach and intestine. The clinical manifestations may vary from a severe symptom complex of rapid intestinal transit, dumping syndrome, diarrhea, thirst, weight loss, distention, steatorrhea, and asthenia, to symptoms of specific nutrient deficiencies (i.e., malnutrition and vitamin deficiencies) . Examples of gastrointestinal disorders that frequently manifest as one or more maldigestion or malabsorption syndromes are inflammatory bowel disease, postgastrectomy syndrome, dumping syndrome, AIDS-associated chronic diarrhea, diabetes-associated diarrhea, postvagotomy diarrhea, bariatric surgery-associated diarrhea (including obesity surgeries: gastric bypass, gastroplasties and intestinal bypass) , short bowel syndrome (including resection of the small intestine after trauma, radiation induced complications, Crohn's disease, and infarction of the intestine from vascular occlusion) , -tube- feeding related diarrhea, chronic secretory diarrhea, carcinoid syndrome-associated diarrhea, gastrointestinal peptide tumors, endocrine tumors, chronic diarrhea associated with thyroid disorders, chronic diarrhea associated with bacterial overgrowth, chronic diarrhea associated with gastrinoma, choleraic diarrhea, chronic diarrhea associated with giardiasis, antibiotic-associated chronic diarrhea, diarrhea-predominant irritable bowel syndrome, chronic diarrhea associated with maldigestion and malabsorption, chronic diarrhea associated with idiopathic primary gastrointestinal motility disorders, chronic diarrhea associated with collagenous colitis, surgery- associated acute diarrhea, antibiotic-associated acute diarrhea, acute and chronic infectious diarrhea, cirrhosis, chronic alcohol dependence, pancreatic insufficiency, total pancreatic resection, cholestatic liver diseases, celiac sprue, long-term parenteral nutrition, gastrointestinal bypass surgeries, Whipple's disease, anorexia nervosa, bulimia (and other eating disorders) , enteropathy of AIDs, endocrinopathies such as thyrotoxicosis and hypoparathyroidism, protein-losing gastroenteropathies, and the like. Short bowel syndrome generally refers to a condition in which there is less than 150 cm of remaining small bowel, and a coinciding massive loss of absorptive capacity. Short bowel syndrome is characterized by severe diarrhea and malabsorption. Affected patients often experience malabsorption of water, electrolytes, vitamins, protein, carbohydrate, and fat, resulting in chronic thirst, electrolyte depletion, vitamin deficiencies, diarrhea, fecal incontinence, calorie depletion, steatorrhea, and weight loss. Functional pancreatic insufficiency may also cause steatorrhea after gastric resection. Steatorrhea is the presence of excess fat in the feces. It is usually caused by a defect in gastrointestinal digestion and/or absorption. Steatorrhea rarely exists without malabsorption of other substances. For example, conditions such as osteo alacia related to calcium and vitamin D deficiency, or anemia due to selective iron or B12 deficiencies, are often associated with the malabsorption that occurs in steatorrhea. Weight loss occurs due to the loss of nutrients and calories. Diarrhea and chronic thirst are other major symptoms associated with steatorrhea. It is present in 80-97% of patients with malabsorption. Dumping syndrome is one of the most common causes of morbidity after gastric surgery. This syndrome is characterized by both gastrointestinal and vasomotor symptoms. Gastrointestinal symptoms include postprandial fullness, crampy abdominal pain, nausea, vomiting, and explosive diarrhea. Vasomotor symptoms include diaphoresis, weakness, dizziness, flushing, palpitations, and an intense desire to lie down. These symptoms occur as a direct result of rapid transit and abnormal presentation of nutrients to the small intestine. With poorly controlled presentation of food, an abnormally large load of nutrients or abnormally large chunks of food (poorly fragmented) spill into the small intestine. Such spilling of food results in an exaggerated length of spread of nutrients through the gut. Patients with severe dumping symptoms may limit their food intake to minimize symptoms, and as a result lose weight and become malnourished. As a last resort in severe cases, surgical treatment of dumping syndrome has been utilized. Current pharmaceutical treatments for dumping syndrome include octreotide acetate (Sandoz) , a long acting somatostatin analogue, which has been used with some success. Octreotide is administered subcutaneously and acts to slow gastric emptying, inhibit insulin release, and decrease enteric peptide secretion in a nonselective way. Unfortunately, since some degree of gut peptide release (seen with normal presentation of nutrients) is needed for normal digestive physiology, octreotide use is accompanied by several complications, including injection site pain, tachyphylaxis, iatrogenic diabetes, malabsorption, and cholelithiasis. Diarrhea is a common problem associated with many gastrointestinal diseases and abdominal operations. Current treatment includes simple dietary changes, opiates and/or opioid-type drugs such as the combination of diphenoxylate hydrochloride and atropine sulfate (available from Searle as Lomotil™) , loperamide hydrochloride (available from Janssen as Imodium™) , camphorated tincture of opium (available from Lilly as Paregoric™) , and the combination of camphorated tincture of opium, opium, pectin, and kaolin (available from Rhone-Poulenc Rorer as Parepectolin™) , antidiarrheal agents such as attapulgite (available from Key as Diasorb™ or from UpJohn as Kaopectate™) , the combination of kaolin, hyoscyamine sulfate, atropine sulfate, and scopolamine hydrobromide (available from Robins as Donnagel™) , opium in Donnagel™ (available from Robins as Donnagel-PG™) , the combination of difenoxin hydrochloride and atropine sulfate (available from Carnick as Motofen™) , and bismuth subsalicylate (available from Proctor & ■ Gamble as Pepto-Bismol™) , for inhibitory effect on intestinal transit. Each modality of treatment, however, has had limited success, and with the exception of dietary changes, all have negative side effects associated with use. Since many patients with diarrhea complain of abdominal cramping pains (due to abnormal transit and resultant exaggerated distension of the gut) , a variety of antispasmodics are also prescribed including the combination of phenobarbital, hyoscyamine sulfate, atropine sulfate and hyoscyamine hydrobromide (available from Robins as Donnatal™) , dicyclomine hydrochloride (available from Marion Merrell Dow as Bentyl™) , hyoscyamine sulfate (available from Schwarz Pharma as Levsin™) , and propantheline bromide (available from Searle as Pro-banthine™) . Unfortunately, these agents are associated with even greater adverse side effects. Diarrhea is also a common complication associated with enteral feeding. Multiple etiologies for diarrhea are postulated, and its genesis may be a multifactorial process (Edes et al., Am. J. Med. 88:91-93 (1990)). Causes include concurrent use of antibiotics or other diarrhea-inducing medications, altered bacterial flora, formula composition, rate of infusion, a dominant accelerating effect of flow over nutrient-triggered inhibitory feedback on the speed of intestinal transit, hypoalbuminemia, and enteral formula contamination. The composition of formula may also affect the incidence of diarrhea. The efficacy of using fiber- containing formulas to control diarrhea related to tube feeding is unsettled (Frankenfield et al. , Am. J. Clin . Nutr. , 50:553-558 (1989)). Malnutrition is a common problem in patients with inflammatory bowel diseases such as, for example, Crohn's disease or ulcerative colitis. Weight loss is found in 70- 80% of patients with Crohn's disease and 18-62% of patients with ulcerative colitis. The role of nutritional support as a primary therapy for inflammatory bowel diseases is not well established. Given the natural history of inflammatory bowel diseases, with frequent relapses and spontaneous remissions, and the difficulty and variability in quantifying disease activity, it has been difficult to design clinical trials that definitively establish the role of nutrition as a primary therapy for inflammatory bowel diseases. The use of elemental diets as primary therapy for inflammatory bowel diseases has also been examined. Parenteral nutrition and elemental diets appear to have limited utility in the long-term treatment of patients with inflammatory bowel diseases. Many drugs and dosage formulations have been and continue to be developed because of the need to suppress the gut inflammation associated with inflammatory bowel disease and to overcome the physiological and physicochemical limitations associated with drug delivery (e.g., poor stability, short biological half-life, inefficient absorption and poor bioavailability) . Many patients have abnormally accelerated intestinal transit (residence in small intestine of less than 1 hour) . In this setting, current applications of controlled release technology have attempted to move toward control of drug absorption via slowing the release of active drug from formulations containing such medication. This has simply worsened the dissociation between the time required for the release of active drug, and the time available for drug absorption (short intestinal transit time) . As a result, much of the medication enters the colon or toilet unabsorbed. Patients fail to respond to oral medication, not because the drug is not effective, but rather the presentation of the drug to the absorptive site failed due to the altered gut motility and the speed of intestinal transit. Recent pharmaceutical attempts to alter gastric emptying and small intestinal transit times, including the use of bioadhesives, have not been very successful. (Khosla and Davis, J. Pharm. Pharmacol . 39:47-49 (1987); Davis et al., Pharm. Res . 3:208-213 (1986); Davis, p. 58, in "Drug Delivery to the Gastrointestinal Tract" (1989)). Thus, a need exists for controlling gastrointestinal transit, i.e., the amount of time available for digestion and absorption of nutrients, and/or dissolution and absorption of oral drugs. To optimize absorption of ingested nutrients and/or pharmacologically active agents in the small intestine it is necessary to have an effective means of controlling gut transit, thereby preventing and/or reducing ineffectiveness of these substances due to malabsorption. Most drugs have short biological half lives. Therefore, to achieve sustained therapeutic levels of such drugs in the circulation, frequent dosing is required. Frequent dosing presents problems of poor patient compliance (it is difficult to consistently take a drug four times a day chronically) . With the rapid rise and fall of the plasma drug level that is typical of a drug with a short half life (sharply oscillating drug peak and valley effect) , it is necessary to administer a relatively large dose so that the plasma drug level remains within the therapeutic range long enough that the next dose is not required immediately. For a drug with a narrow range of therapeutic plasma concentrations, such a high dose may then be associated with the risk of toxicity. Such wide oscillatory swings may also be dangerous and undesirable in the treatment of many diseases, e.g., widely swinging bronchodilator levels in an asthmatic could lead to clinical relapse. Organ rejection may be the consequence of the level of an immunosuppressive agent falling even temporarily below the therapeutic range. Providing drugs at frequent intervals also causes undesirable and unpredictable accumulations of drugs in the body. For example, later doses may add to remnants of earlier doses to elevate the plasma level ever higher. There is already strong evidence that controlled delivery of drugs is useful. For example, in the case of sustained-release formulations of nitroglycerin, benefits have included the need for smaller doses (with the beneficial occurrence f lesser side effects) and reduced incidence of chest pain (Winsor et al. , Chest, 62:407 (1972) ) . In the case of procainamide, an anti-arrhythmic agent, the sustained-release formulation has lengthened the dosing interval from 3 to 6 hours (Graffner et al. , Clin . Pharmacol . Ther. , 17:414 (1975)). It has been proposed that any drug with a half life of 4 hours or less would benefit from a controlled, sustained-release strategy (Heimlick et al. , J. Pharm. Sci . , 50:232 (1961)). Since drugs with long biological half lives are few (e.g., bishydroxycoumarin, chlordiazepoxide, chlorphenteramine, chlorpropamide, diazepam, etchlorvynol, digitoxin, digoxin, meprobamate, phenytoin and warfarin) (Lee and Robinson "Drug Properties Influencing the Design of Sustained or Controlled Release Drug Delivery System" in "Sustained and Controlled Drug Delivery Systems", J.R. Robinson (Ed.) Marcel Dekker (1978) ) , the number of drugs that can benefit from controlled presentation to the gastrointestinal tract is immense. For drugs with a narrow therapeutic window, such as cyclosporin (an immunosuppressive drug used to prevent rejection of transplanted organs) , a strategy would be highly desirable that could blunt the sharp peak plasma profile so that the drug level can rise into and then remain in the therapeutic range for a prolonged period without a high peak (that may be associated with toxicity) or a low valley (that may be associated with rejection complication) . To date, the efforts of the pharmaceutical industry towards achieving this goal of sustained, controlled release have not been very successful. The efforts have been mostly directed at changing the-physico- chemical properties of the drug formulation. In other words, all of the efforts have been focused on the drug delivery system rather than the organs where the drugs are absorbed and to which the drugs are targeted. These efforts can be divided into physical alterations, chemical alterations and biologic alterations (Lee and Robinson (1978)) . Physical alterations employed in the art include: 1. prolonging the dissolution time and the release of the active drug via enteric coatings, microencapsulation, polymer coatings, multiparticulate systems, and other delayed release products (Healey, J.N.C., "Enteric Coating and Delayed Release" in "Drug Delivery to the Gastrointestinal Tract", Davis and Wilson (Eds.) , pp. 97- 110, Ellis Horwood Ltd. (1989)); 2. slowing the diffusion of drug; 3. using an osmotic pump that releases the active ingredient by taking advantage of the driving force of osmotic equilibration across a semi-permeable membrane (e.g., Osmet™, Oros™, and Alzet™ (Alza Corp.) (Davis and Fara, "Osmotic Pumps" in "Drug Delivery to the Gastrointestinal Tract", Davis and Wilson (Eds.), pp.97- 110, Ellis Horwood Ltd. (1989)) ; 4. using a mechanical pump; 5. using ion exchange; 6. using a hydrodynamically balanced capsule (Sheth and Taussounian, U.S. Patent 4,167,558 (1979)); 7. using hollow capsule/solid foam (Watanabe et al., U.S. Patent 3,976,764 (1976)); 8. using an expandable balloon (Michaels et al. , U.S. Patent 3,901,232 (1975)); 9. using a swellable polymer matrix (Mamajek and Moyer, U.S. Patent 4,207,890 (1980)) ; and 10. using a bioadhesive polymer (Ch'ng et al. , Proc. Amer. Pharm . Assoc . Acad. Pharm . Sci . , 13:137 (1983)) . Chemical alterations employed in the art include: _ . ' the use of analogs; and 2. the use of prodrugs. Biological alterations employed in the art include the use of enzyme inhibition to delay the metabolism of the active drug. With the exception of the use of enzyme inhibitors to slow the rate of metabolism of a drug, all of above-mentioned efforts have been directed at the oral drug formulation and have not been very successful. No efforts have been directed at modulating the movement of the drug formulation through the gastrointestinal tract. According to Dressman, "To date, no reproducible method for prolonging the small intestinal residence time has been demonstrated in humans". ("Kinetics of Drug Absorption from the Gut" in "Drug Delivery to the Gastrointestinal Tract", Davis and Wilson (Eds.), pp. 195-219, Ellis Horwood Ltd. (1989)). In spite of all the efforts by those of skill in the art, it is not surprising that the goal of controlled, sustained drug delivery has not been achieved. It is not surprising that there is wide variability in drug bioavailability. For example, it is known that food increases the bioavailablity of some drugs while decreasing the bioavailability of other drugs (this effect is also nutrient and load dependent; see Wilson, "Relationship between Pharmacokinetics and Gastrointestinal Transit" in "Drug Delivery to the Gastrointestinal Tract", Davis and Wilson (Eds.), pp. 161-178, Ellis Horwood Ltd. (1989) ) . The proximal and mid-small intestine (duodenum and proximal jejunum) are the main sites of drug absorption. Yet those of skill in the art are directing their efforts largely at creating delayed-release drug formulations. This strategy is not likely to be successful in patients with diarrhea on the basis of rapid transit (e.g., patients with resected terminal ileum), as the retention time of the drug in the small intestine may be as little as 15-30 minutes. Even in patients with a normal rate of transit (about 2 to 4 hours) , the drug may pass through this absorptive window too quickly for full absorption to occur. Therefore, the only result of delayed-release strategies may be the slow release of active drug into the colon or the toilet rather than achieving truly controlled presentation of pharmacologically active agents to the absorptive sites of the small intestine. A need therefore exists for means to enhance the bioavailability and effectiveness of pharmacologically active agents by controlling the rate of transit through the small intestine. The present invention satisfies these needs and provides related advantages as well. SUMMARY OF THE INVENTION The present invention provides methods and compositions for slowing gastrointestinal transit and prolonging residence time in the small intestine, optimizing digestion of nutrients or dissolution of pharmacologically active agents, as well as their absorption in the small intestine. Invention methods prevent and/or reduce ineffectiveness of nutrients and/or pharmacologically active agents due to malabsorption. In general, invention methods comprise administering to a subject a composition comprising an active lipid in an amount sufficient to slow gastrointestinal transit and/or to prolong the residence time of a substance in the small intestine. The present invention further provides methods and compositions for enhancing the bioavailability and therapeutic effectiveness of pharmacologically active agents. In addition, the present invention provides methods and compositions for treating diarrhea, for reducing atherogenic serum lipids, and for reducing the inhibitory effect of nicotine on gastrointestinal motility mechanisms. BRIEF DESCRIPTION OF THE FIGURES Figure 1 comprises two parts, each presenting a graph (labeled Fig. 1A and Fig. IB) demonstrating the slowing of intestinal transit in separate stable inflammatory bowel disease patients having diarrhea as a result of rapid transit, when treated according to invention methods. Figure 2 is a graph demonstrating the improvement in bioavailability of a marker drug, acetaminophen, when the marker drug was ingested by a dog after administration of a composition according to the invention. DETAILED DESCRIPTION OF THE INVENTION In accordance with the present invention, there are provided methods of slowing gastrointestinal transit, thereby prolonging the residence time of a substance in the small intestine of a subject, for an amount of time sufficient for digestion and absorption of the substance to occur. Invention methods comprise administering to a subject a composition comprising an active lipid in an amount effective to slow the transit of said substance through the small intestine for an amount of time sufficient for absorption of said substance to occur. In a preferred embodiment, the active lipid is administered in the form of a premeal, or pretreatment, about 0 to 24 hours before ingestion of a substance, so that the substance is presented to the gastrointestinal tract for the optimal amount of time. Invention compositions comprise an active lipid and a pharmaceutically acceptable carrier. In a preferred embodiment, invention compositions comprise an active lipid which is administered as a premeal or a pretreatment. One function of invention compositions is to slow gastrointestinal transit and control gastrointestinal residence time of a substance so as to enable substantial completion of luminal and mucosal events required for absorption of the substance in the small intestine. Another function of invention compositions is to control the presentation of a substance to a desired region of the small intestine for absorption. In a preferred embodiment, invention compositions especially prolong the residence time of a substance in the proximal region of the small intestine (duodenum and proximal jejunum) . The present invention further provides methods and compositions for treating diarrhea in a subject, said methods comprising administering to said subject a composition comprising an active lipid in an amount sufficient to prolong the residence . time in the small intestine of the luminal contents thereof. This will allow for greater absorption of liquid and thereby decrease stool volume (less diarrhea) . The present invention also provides pharmaceutical oral articles and enteral formulas that slow gastrointestinal transit and prolong residence time of a substance. Invention compositions enhance dissolution, absorption, and hence bioavailability of pharmacologically active agents ingested concurrently therewith or subsequent thereto. Without wishing to be bound by any theory, it is presently believed that the most important physiological functions affected by invention compositions are the ileal brake in the distal intestine (Read et al. , Gastro . , 86(2):274-80 (1984); Spiller et al. , Gut, 29 (8) :1042-51 (1988); Spiller et al. , Gut, 25(4):365-74 (1984)) and the jejunal brake in the proximal intestine (Lin et al. , Dig. Dis . Sci . , 41(2): 326-329 (1996)). These nutrient- triggered mechanisms function when sufficient numbers of nutrient sensors in the intestine are triggered by the presence of appropriate signals (e.g., end-products of digestion) . The magnitude of inhibition of intestinal transit depends on the number of nutrient sensors recruited to generate inhibitory feedback signals. These mechanisms for slowing transit may be significantly impaired in gastrointestinal diseases such as inflammatory bowel disease. The ileal brake (Spiller et al. (1988)) may be impaired due to active disease of the ileum, or may be missing entirely in IBD patients with ileal resections. While a nutrient-triggered brake in the proximal gut is available (Lin et al. , (1996)), it is less potent than the ileal brake (Zhao et al., Gastro. , 108(4):A714 (1995)). In active disease states, it is likely that the jejunal brake is not engaged because transit through the proximal gut is so rapid, there are probably insufficient amounts of end products of digestion present, and insufficient time of contact available with the small intestine, to fully activate this braking mechanism. The invention contemplates a range of optimal residence times which are dependent upon the character of the substance being delivered. As used herein, "substance" encompasses anything that has been ingested or placed in the lumen of the gastrointestinal tract. This includes, for example, digested and partially digested foods and nutrients, pharmacologically active agents, electrolyte- containing fluids, and the like. As used herein, "digestion" encompasses the process of breaking down large molecules into their smaller component molecules, by enzymatic and other processes of the gastrointestinal tract, so that nutrients go into solution, as well as disintegration (breaking down large particles into their smaller component particles) and dissolution (e.g., release of active drug into solution) of insoluble materials (e.g., pharmacologically active agents) . As used herein, "absorption" encompasses the transport of a substance from the intestinal lumen through the barrier of the mucosal epithelial cells into the blood and/or lymphatic systems. As used herein, "active lipid" encompasses molecules having a structure substantially similar to an end-product of fat digestion, that are capable of activating the system of inhibitory and stimulatory motility mechanisms of the gastrointestinal tract. Examples of end products of fat digestion are molecules such as glycerol and fatty acids. In a preferred embodiment, the active lipid comprises a saturated or unsaturated fatty acid, mono- or di-glyceride, or glycerol, as well as mixtures of any two or more thereof. Fatty acids contemplated by the invention typically have between 4 and 24 carbon atoms. Examples of fatty acids contemplated for use in the practice of the present invention include caprolic acid, caprulic acid, capric acid, lauric acid, myristic acid, oleic acid, palmitic acid, stearic acid, palmitoleic acid, linoleic acid, linolenic acid, tran -hexadecanoic acid, elaidic acid, columbinic acid, arachidic acid, behenic acid, eicosenoic acid, erucic acid, bressidic acid, cetoleic acid, nervonic acid, Mead acid, arachidonic acid, timnodonic acid, clupanodonic acid, docosahexaenoic acid, structured lipids, and the like, as well as mixtures of any two or more thereof. In a preferred embodiment, the active lipid comprises oleic acid. Invention active lipids are preferably formulated in well dispersed form in a pharmaceutically acceptable carrier. As used herein, "pharmaceutically acceptable carrier" encompasses any standard pharmaceutical carrier, as are well known to those of skill in the art. Dispersion can be accomplished in various ways, e.g., as a solution. Lipids can be held in solution in a variety of ways, e.g., if the solution has the properties of bile (i.e., solution of mixed micelles with bile salt added) , a detergent (e.g., solution of Tween) , or a solvent. Alternatively, a dispersion may be in the form of an emulsion, which is a 2-phase system in which one liquid is dispersed in the form of small globules throughout another liquid that is immiscible with the first liquid (Swinyard and Lowenthal, Pharmaceutical Necessi ties, p. 1296, REMINGTON'S PHARMACEUTICAL SCIENCES, 17th ed. , AR Gennaro (Ed.), Philadelphia College of Pharmacy and Science (1985)) . As yet another alternative, a dispersion may be in the form of a suspension with dispersed solids (e.g., a microcrystalline suspension) . Additionally, any emulsifying and suspending agents that are acceptable for human consumption can be used as a vehicle for dispersion of the composition. For example, beeswaxes, glycowaxes, castor waxes, carnauba waxes, 1,6-hexanediamines, starches, polyvinylchlorides, polyvinylpyrrolidones, gelatin coacervates, styrene-maleic acid copolymers, shellacs, nylons, acrylic resins, silicons, 2-hydroxymethacrylate,- 1,3-butylene glycol dimethacrylate, ethylene glycol dimethacrylate, Tweens, acetylated monoglycerides, hydroxypropylmethyl celluloses, gum acacias, agars, sodium alginates, bentonites, carbomers, carboxymethylcelluloses, sodium carboxymethylcelluloses, carrageenans, powdered celluloses, cholesterol, gelatins, glycerol palmitostearate, glycerol monostearate, ethylcelluloses, cellulose acetates, cellulose acetate phthalates, cellulose acetate butyrates, methacrylate hydrogels, polyethylene glycols, poly(dl-lactic acids) , hydroxyethyl celluloses, hydroxypropyl celluloses, hydroxypropyl methylcelluloses, methylcellulose, octoxynol 9, oleyl alcohol, polyvinyl alcohols, povidones, propylene glycol monostearate, sodium lauryl sulfate, sorbitan esters, stearyl alcohol, tragacanths, xantham gums, chondrus, glycerin, trolamine, coconut oils, propylene glycol, ethyl alcohol, malts, malt extracts, and the like, can be employed. Any of these solutions, emulsions or suspensions can be incorporated into capsules, or microspheres or particles (coated or not) contained in a capsule, or as the coating of particles, capsules, tablets or caplets. Pharmaceutical compositions of the present invention can be used in any of a wide variety of formf e.g., in the form of a solid, a solution, an emulsion, a dispersion, a micelle, a liposome, and the like, wherein the resulting composition contains one or more active lipids according to the present invention, as an active ingredient, in admixture with an organic or inorganic carrier or excipient suitable for enteral or parenteral applications. The active ingredient may be compounded, for example, with the usual non-toxic, pharmaceutically acceptable carriers for tablets, caplets, troches, lozenges, pellets, capsules, dispersible powders or granules, solutions, emulsions, suspensions, syrups, elixirs, enteral formulas, sustained or delayed release systems, and the like. Those of skill in the art understand that a variety of carriers can be used, including glucose, lactose, calcium carbonate, calcium phosphate, sodium phosphate, alginic acid, gum tragacanth, gum acacia, gelatin, mannitol, starch paste, magnesium trisilicate, magnesium stearate, stearic acid, talc, corn starch, keratin, colloidal silica, potato starch, urea, medium chain length triglycerides, dextrans, vegetable oils, liquid paraffin, and the like. Pharmaceutical compositions of the invention can be in solid, semisolid, or liquid form. Compositions intended for oral use may be prepared according to any of a variety of methods as are known in the art. Such compositions may contain one or more agents selected from the group consisting of a sweetening agent (such as sucrose, lactose, aspartame, or saccharin) , flavoring agents (such as peppermint, oil of wintergreen or cherry) , stabilizing agents, thickening agents, coloring agents, perfumes, preserving agents, and the like, in order to provide pharmaceutically elegant and palatable preparations. Any fluid that allows for dispersion of the active lipid is suitable for use with the invention, e.g., shake-like drinks such as Carnation Instant Breakfast™, protein supplement formulas such as high nitrogen Vivonex Plus (Ross) , nondairy coffee creamers such as Coffeemate™, gravies such as Heinz™ ready made gravy, and other edible solutions, emulsions, or suspensions. In a particular preferred embodiment, an active lipid is blended with a nutrient-rich drink, such as Ensure™ brand drink (Ross) , and ingested about 0 to about 24 hours prior to a meal. Pharmaceutical oral articles may be uncoated or they may be coated by known techniques to delay disintegration and absorption in the gastrointestinal tract, thereby providing sustained action over a longer period. For example, a time delay material such as glyceryl monostearate or glyceryl distearate may be employed. Pharmaceutical oral articles may also be coated to form osmotic therapeutic tablets for controlled release employing the techniques described in U.S. Pat. Nos. 4,256,108, 4,167,558, 4,160,452, and 4,265,874, each of which is hereby incorporated by reference. Other techniques for preparation of controlled release compositions, which may be used in the formulation of invention pharmaceutical compositions include those described in the U.S. Pat. Nos. 4,193,985, 4,690,822, 3,976,764, 3,901,232, 4,207,890, and 4,572,833, each of which is hereby incorporated by reference. Without wishing to be bound by any theory, it is presently believed that early in gastric emptying, before inhibitory feedback is activated, the load of fat entering the small intestine may be variable and dependent on the load of fat in the meal. Thus, while exposure to fat may be limited to the proximal small bowel after a small meal, a larger meal, by overwhelming proximal absorptive sites, may spill further along the small bowel to expose the distal small bowel to fat. Thus, the response of the small intestine to fat limits the spread of fat by reducing the rate of transit, so that more absorption can be completed in the proximal small intestine and less in the distal small intestine. If this is so, then intestinal transit is inhibited in a load-dependent fashion by fat. Thus, precise regulation of intestinal transit theoretically occurs whether the region of exposure to fat is confined to the proximal gut or extended to the distal gut. In accordance with the present invention it has been observed that inhibition of intestinal transit by fat depends on the load of fat entering the small intestine. More specifically, intestinal transit is inhibited by fat in a load-dependent fashion, whether the nutrient is confined to the proximal segment of the small bowel or allowed access to the whole gut. In modern society, the gastrointestinal tract not only serves as the site of nutrient absorption, but also of drug absorption. Oral pharmaceutical preparations account for more than 80% of all drugs prescribed. It is essential, therefore, to control the multiple factors that influence their intestinal absorption of pharmaceuticals and thus the ultimate therapeutic effectiveness thereof. Before a drug can be absorbed in the gastrointestinal tract, it must be solubilized. Drugs ingested in solid form must first dissolve in the gastrointestinal fluid before they can be absorbed, and tablets must disintegrate before they can dissolve. The dissolution of a drug in the gastrointestinal tract is often the rate-limiting step governing its bioavailability. In any given drug, there can be a 2- to 5-fold difference in the rate or extent of gastrointestinal absorption, depending on the dosage or its formulation. Therefore, invention methods are especially useful for improving the bioavailability of solid drug formulations, as these require longer intestinal residence time when compared with liquid drug formulations. The rate of gastric emptying bears directly on the absorption of ingested drugs and on the bioavailability thereof. Some drugs are metabolized or degraded in the stomach, and delayed gastric emptying reduces the amount of active drug available for absorption. Since invention methods and compositions can also delay gastric emptying (Davis, pp. 55 and 57, in "Drug Delivery to the Gastrointestinal Tract" (1989) ) , protective coatings may be necessary to prevent gastric inactivation of some drugs, due to the increase in time spent in the stomach. The pharmaceutical industry has extensively developed slow and/or sustained-release technology. These efforts have been directed at delaying gastric emptying and slowing the release of active drug using controlled, sustained, or delayed release systems. Sustained-release formulations employ several methods. The most common is a tablet containing an insoluble core; a drug applied to the outside layer is released soon after the medication is ingested, but drug trapped inside the core is released more slowly. Capsules containing multiparticulate units of a drug with coatings that dissolve at different rates are designed to give a sustained-release effect. However, the basic problem with sustained-release medications is the considerable variability in their absorption due to an inability to control gastrointestinal transit. During fasting, a sustained-release formulation moves rapidly out of the stomach and through the gastrointestinal tract. When fasting, motility cycles to phase III of the major migratory complex (MMC) , a period of intense, lumen obliterating contractions that propagate from the stomach to the distal small intestine. Phase III of the MMC is responsible for transit of solid drug formulations. Since the duration of MMC is highly variable (90-120 minutes) , the transit (and thereby absorption) of a solid formulation depends on the time from ingestion to the next phase III of MMC. Since it is unknown at the time of drug ingestion whether one's fasting motility is in phase III, II or I, the transit and bioavailability of the drug may be unpredictable (i.e., require as little as a minute to move through the gut if phase III of MMC starts as soon as the drug is ingested, or hours to move to the absorptive sites if the next phase III of MMC does not come for hundreds of minutes) . After eating a meal, the motility pattern converts to a noncyclical pattern known as fed motility. During the fed state, mouth-to-colon transit averages 2-4 hours. Accordingly, slow release of a drug (i.e., over many hours) in the absence of slow transit in the gut is useless for optimizing drug bioavailability and prolonging the duration that the drug is within the therapeutic range in the plasma. A more dangerous problem may arise when a doctor must overprescribe an oral medication in order to achieve the desired medical result. If the patient, such as an IBD patient, is suffering from rapid transit, then simultaneous multiple doses of a drug may need to be administered so that one effective dose of the drug is absorbed by the intestinal mucosa. Obviously, this is wasteful of the drug. This problem becomes dangerous when, for whatever reason, the rapid transit of substances through the patient's system ceases. When this happens, the patient may suddenly be able to absorb all of the multiple doses of the drug, resulting in toxicity problems. This is especially dangerous for drugs that have a narrow therapeutic window (i.e., toxicity occurs at a concentration that is close to the effective range) . For such drugs, the practice of overprescribing may be too dangerous, and the patient must instead do without the full benefit of the drug. The present invention solves the above-described bioavailability problem. Invention methods and compositions enable one to manipulate the balance of disintegration, dissolution, and gastrointestinal transit by increasing gastrointestinal residence time. To facilitate drug absorption in the proximal small intestine, the present invention provides a method for prolonging the gastrointestinal residence time, which will allow drugs in any dosage form to more completely dissolve, go into solution, and be absorbed. Since invention compositions slow gastrointestinal transit (i.e., delay both gastric emptying and small intestinal transit) , dosage forms that dissolve relatively slowly are handled well, although more rapidly dissolving dosage forms will have drug bioavailability that is primarily controlled by the invention methods and compositions. Invention methods and compositions are beneficial for pharmacologically active agents that have slow dissolution characteristics. Since the active agent is released slowly, such as in formulations that are enterically coated or packaged in sustained-release form, there is great potential for the drug to be passed into the colon still incompletely absorbed. One object of the invention is to increase the gastrointestinal residence time to allow poorly dissolving drugs to be more fully absorbed. The benefit of the invention methods and compositions are also beneficial for pharmacologically active agents that have rapid dissolution characteristics, as these agents are held in contact with the absorptive sites for a prolonged period, thus providing them with controlled transit sustained absorption. Invention methods and compositions can also affect the formation of serum lipids. Postprandial serum lipids result from the absorptive transfer of cholesterol, triglycerides, and other lipids from the intestinal lumen into the mesenteric, lymphatic, and finally the circulatory system. Since cholesterol and triglycerides are so insoluble in lymph and plasma, the transport of these lipids occurs through the use of lipoprotein-containing carriers called chylomicrons. While fat absorption from the lumen is rate-limiting for the proximal half of the small intestine, chylomicron synthesis or release is rate- limiting for the distal half of the small intestine. As a result, chylomicrons formed by the distal small intestine are larger than those from the proximal small intestine (Wu et al., J. Lipid Res . , 16:251-57 (1975)). In the capillary bed of the peripheral circulatory system, the enzyme lipoprotein lipase hydrolyzes and removes most of the triglycerides from the chylomicron. The lipoprotein that remains, now rich in cholesterol esters and potentially atherogenic, is called a chylomicron remnant. This postprandial lipoprotein is then removed from the circulation by the liver (Zilversmit, Circulation, 60(3) :473 (1979)). Elevated levels of atherogenic serum lipids have been directly correlated with atherosclerosis (Keinke et al. , Q. J. Exp. Physiol . , 69:781-795 (1984)) . The present invention provides a novel method to minimize atherogenic postprandial lipemia by optimizing fat absorption in the proximal gut. In other words, the present invention provides a novel method by which atherogenic postprandial serum lipids can be controlled preabsorptively by the fed motility response of the small intestine to luminal fat. Preabsorptive control depends on the triggering of a specific pattern of proximal intestinal motility systems that slow transit, thereby minimizing the spread of fat into the distal gut. After a small meal of cholesterol-containing, fatty foods, the small intestine limits the site of fat absorption to the proximal small intestine by generating braking, nonpropagated motility to slow intestinal transit. Since chylomicrons produced by the proximal small intestine are small in size, the size distribution of postprandial lipoproteins is shifted to minimize postprandial lipemia. However, during gorging of a high cholesterol, high fat meal, the ability of the small intestine to optimize proximal fat absorption is reduced by the time-dependent fading of the effect of fat on nonpropagated motility. As a result, after the first 1-2 hours, faster intestinal transit works to displace luminal fat into the distal small intestine where large, cholesterol-enriched, atherogenic chylomicrons are formed and released into the circulation. Limiting the spread of fat to the proximal small intestine also slows the entry of fat into the circulation in the postprandial period. Since chylomicron formation depends on the availability of lipoprotein (apo-A IV) and the synthesis of apo-A IV by the proximal small intestine is stimulated by the exposure of the distal small intestine to fat (Kalogeris et al. , Gastro . , 108:A732 (1995)), the present invention reduces serum lipids by reducing distal gut stimulation of proximal gut apo-A IV synthesis. By slowing intestinal transit, the invention methods and compositions increase fat absorption by the proximal small intestine, and thereby decrease the amount of fat entering the distal small intestine. With less fat coming into contact with the distal gut, there is less stimulation of apo-A IV production by the proximal small intestine, and slower entry of chylomicrons into the circulation (lower peak postprandial concentration of lipids reduces atherogenic risk of a fatty meal) . The present invention also provides novel methods and compositions for decreasing the rate of intestinal transit in smokers. Studies suggest that nicotine inhibits intestinal motility (Carlson et al. , J. Pharm. Exp . Ther. , 172:367-76 and 377-383 (1970); Weissbrodt et al. , Eur. J. Pharmacol . , 12:310-319 (1970)). In the postprandial situation, this nicotine-related inhibitory effect diminishes the potentially protective, braking or nonpropagated pattern of motility normally triggered by fat. As a result, nicotine may facilitate the spreading of ingested lipids into the distal small intestine and impair the preabsorptive control exerted by lipids. The methods of the present invention provide means to minimize the nicotine-induced inhibition of this postprandial nutrient- triggered motility response. In addition, methods of the invention provide means to maximize proximal gut fat absorption by reducing the rate of gastrointestinal transit and reducing the spread of ingested lipids into the distal small intestine. The methods and compositions of the invention require an effective amount of active lipid. An effective amount of active lipid is any amount that is effective to slow gastrointestinal transit and control presentation of a substance to a desired region of the small intestine. For example, an effective amount of active lipid, as contemplated by the invention, is any amount of active lipid that can trigger any or all of the following reflexes: intestino-lower esophageal sphincter (relaxation of lower esophageal sphincter) ; intestino-gastric feedback (inhibition of gastric emptying) ; intestino-intestinal feedback (ileo-jejunal feedback/ileal brake, jejuno-jejunal feedback/jejunal brake (for control of motility and transit as well as intestino-intestinal reflexes for enhancing intestinal obsorption) , intestino-CNS feedback (for example, intensifying intestinal signaling of satiety)); intestino-pancreatic feedback (control of exocrine enzyme output) ; intestino-biliary feedback (control of bile flow) ; intestino-mesenteric blood flow feedback (for the control of mucosal hyperemia) ; intestino-colonic feedback (so- called gastro-colonic reflex whereby the colon contracts in response to nutrients in the proximal small intestine) . In a preferred embodiment, invention compositions are administered in a manner which ensures that the dispersion of active lipid is presented to a predetermined length of the small intestine. An example is presentation to the entire length of intestine. Such spread of active lipid will trigger the maximal response of the reflexes referred to above. Since a smaller dose will trigger a weaker response (i.e., less slowing of transit), administration of active lipid is preferably in a dosage such that the desired effect is produced. In a preferred embodiment, the amount of active lipid administered to an adult human patient is from about 0.25 grams to about 20.0 grams per dose. In a more preferred embodiment, the amount of active lipid administered to an adult human patient is from about 0.5 grams to about 6.0 grams per dose. As used herein, "premeal" encompasses any solid or liquid formulation that comprises an amount of an active lipid effective to substantially increase the residence time of a substance in the small intestine, and which is administered to a patient about 0 to 24 hours prior to ingesting the substance. In another embodiment, the premeal is administered about 0 to 2 hours prior to ingesting the substance. In a preferred embodiment, the premeal is administered about 15 to 45 minutes prior to ingesting the substance. Thus, an important aspect of the premeal is the timing of its administration such that the active lipid component will activate the system of inhibitory and stimulatory motility mechanisms of the gastrointestinal tract, thereby optimizing the residence time of the substance in the small intestine. The use of invention compositions in enteral feeding contemplates adding the composition directly to the feeding formula, in addition to the premeal strategy. Invention compositions can be compounded into the enteral formula as needed by the user when the rate of formula delivery is known (i.e., add just enough composition to deliver the desired amount of active lipids) . Alternatively, invention compositions can be compounded at the factory so that the enteral formulas are produced having different concentrations of the active lipid composition and can be used according to the rate of formula delivery (i.e., higher concentration of active lipids for lower rate of delivery) . The residence time for optimal absorption of digested foods and nutrients in the small intestine can be calculated using an average orocecal (mouth-to-cecum) transit time as a reference. The normal orocecal transit time is approximately 1 to about 6 hours in the fasted state and 2 to about 4 hours in the fed state. Invention compositions preferably target an intestinal residence time within or above the average time frame of approximately 2-4 hours, when being used to promote absorption of ingested nutrients. The pharmaceutical industry has published a great deal of information on the dissolution time for individual pharmacologically active agents and compounds. Such information is found in numerous pharmacological publications which are readily available. For example, if the in vi tro model for dissolution and release of agent "X" is 4 hours, then the residence time for optimal absorption of agent "X" in the small intestine should be at least 4 hours and would also include additional time allowing for gastric emptying to occur in vivo. Thus, for pharmacologically active agents, the appropriate residence time is dependent on the time for release of the active agent. The invention provides the opportunity of manipulating two variables at the same time, the gastrointestinal transit time and the time for release of the active agent. Many potential variations are then possible for creating drug bioavailability profiles ideal for each drug and each disease. In order to extend biologic activity so that one has a convenient, daily dosage regimen, the present invention contemplates that invention compositions are administered as a premeal, e.g., prior to ingestion of the food, nutrient, and/or pharmacologically active agent to be delivered. In a preferred embodiment, invention compositions (depending on the formulation) are administered up to a period of 24 hours prior to ingestion of the food, nutrient and/or pharmacologically active agent. When delivered as a premeal, the active lipid is ingested about 0 to 24 hours (0 to 2 hours in another embodiment, or 15 to 45 minutes in a currently preferred embodiment) prior to ingestion of the target meal or pharmacologically active agent. The period of time prior to ingestion is determined by the precise formulation of the invention composition and the targeted pharmacologically active drug. For example, if the active lipid formulation itself is incorporated in a controlled release system, the time required for release, and the duration of release, of the active lipid will determine the time for administration of the composition. Sustained- release formulations of the composition are useful to ensure that the intestinal feedback effect is sustained, since exposure of the intestines to invention active lipids will be prolonged. When invention compositions are added to an enteral formula, and the formula was continuously delivered into the small intestine, the composition that is initially presented with the nutrient formula would slow the transit of nutrients that are delivered then and later. Except for the start of feeding (when transit may be too rapid because the inhibitory feedback from the composition has yet to be fully activated) , once equilibrium is established, it is no longer logistically an issue of delivering the composition as a premeal although the physiologic principle is still the same. Methods of administration are well known to those of skill in the art and include, but are not limited to oral administration, tube administration and enteral administration. In one embodiment of the present invention, the active lipid is presented in an enterically coated or sustained-release form such that intestinal transit is slowed for a prolonged period of time. The pharmacologically active agent can also be packaged in an enterically coated or sustained-release form so that it can also be released slowly. This combination would probably have the longest biologic activity and be favored if a high initial drug plasma peak is not desired. In an alternative embodiment, invention pharmaceutical articles may be formulated for controlled release (enterically coated or sustained-release form) of active lipid, in combination with a pharmacologically active agent formulated for rapid release (tablet or capsule with rapid dissolution characteristics or composition in a liquid form) . This simpler strategy would be used to "hold" the active drug in the proximal small intestine for a period long enough for complete absorption of the drug to take place whenever a high initial peak of the drug is desired. Another embodiment of the present invention contemplates a rapid release formulation of the invention composition. This form would be administered along with or following slow release of the pharmacologically active agent, which is enterically coated or in a sustained- release form. Also contemplated by the present invention is the combination of a rapid release form of the invention composition and a rapid release form of the pharmacologically active agent. Accordingly, the methods and compositions of the present invention can be combined with existing pharmaceutical sustained-release technology to provide control over not only the gastrointestinal transit and residence time of a pharmacologically active agent, but also over the time of release of the active agent. More specifically, the combination of invention methods and compositions with existing sustained-release technology provides control over the multiple factors that influence intestinal absorption of a pharmacologically active agent. The ability to control such factors enables optimization of the bioavailability and ultimate therapeutic effectiveness of any pharmacologically active agent. The following examples are intended to illustrate, but not limit, the present invention. EXAMPLE I Oleate Application to the Proximal Intestine Indicates the Existence of the Jejunal Braking System Although fat absorption has long been considered an exclusive function of the proximal small intestine (Borgstrδm et al. , Gastro. , 45(2) :229-38 (1963)), recently, this concept was found to be flawed (Lin et al., Gastro . , 107:1238a (1994); Lin et al. , Am. J. Physiol . , in press (1996b) ) . Instead, during the course of a typical meal (fat load of 60 g) , both the proximal and distal small intestine participate in the absorption of this nutrient. The idea that fat presents normally to the distal small intestine is crucial to understanding not only the normal control of intestinal transit but the rapid transit that develops in IBD patients. Direct infusion of fat into the ileum slows gastric emptying and intestinal transit through action of the ileal brake (Read et al., (1984) ; Spiller et al., (1984)) . This response depends specifically on the availability of fatty acids as the end product of fat digestion. Since these initial reports of the ileal brake, this distal gut response has been considered as the only nutrient-triggered control mechanism governing intestinal transit. However, in short bowel patients with no ileum, fat absorption still managed to increase in a load- dependent manner (Woolf et al. , Gastro . , 84 (4) :823-828 (1993)). Since the triggering of the ileal brake was not possible in these patients and the surface area available for absorption was fixed, this response suggested the existence of an inhibitory mechanism in the proximal gut. Recently such a mechanism has been found, i.e., a jejunal brake that responds to oleic acid, a product of fat digestion (Lin et al. , (1996)). Thus, in 6 dogs equipped with duodenal (10 cm from pylorus) and midgut (160 cm from pylorus) fistulas, intestinal transit was compared across an isolated (occluding Foley catheters were placed in the distal limb of each fistula to achieve a water-tight seal) 150 cm test segment (between fistulas) while 0, 15, 30, or 60 mM oleate was delivered into the proximal half of the gut (between fistulas) as a solution of mixed micelles in pH 7.0 phosphate buffer at 2 ml/min for 90 minutes. 60 minutes after the start of the perfusion, -20 μCi of 99m Tc-DTPA (diethylenetriamine pentaacetic acid) was delivered as a bolus into the test segment. Intestinal transit was then measured by counting the radioactivity of 1 ml samples collected every 5 minutes from the completely diverted output of the midgut fistula. Intestinal transit was calculated by determining the square root of the area under the curve (AUC) of the cumulative percent recovery of the radioactive marker. The square root AUC (Sqrt AUC) values varied between 0 (i.e., no recovery by 30 minutes) and 47.4 (i.e., theoretical, instantaneous complete recovery at time 0) . Results are reported as mean ± standard deviation. TABLE 1. JEJUNAL BRAKE: CUMULATIVE RECOVERY OP "Tc OVER 30 MINUTES Oleate dose (mM) Mean Cumulative Recovery, % sort AUC 0 (Buffer) 95.5 40.9 + 2.6 15 64.3 33.8 ± 2.9 30 54.7 29.8 ± 3.5 60 38.7 21.5 ± 4.6 It was found that intestinal transit was inhibited by oleic acid in a dose-dependent fashion via the jejunal brake when fat was confined to the proximal half of the small intestine (p<0.005, 1-way ANOVA) . Since the observed jejunal brake is triggered by oleic acid, an end product of fat digestion, inadequate fat hydrolysis (resulting in insufficient availability of end products of fat digestion) may explain the failure of previous investigators to observe inhibition of intestinal transit by fat in the proximal gut (Higham and Read, Gut, 31(4):435-38 (1990); Read et al. , (1984)). EXAMPLE II Fat in Distal Gut Inhibits Intestinal Transit More Potently Than Fat in Proximal Gut Bowel resection is, unfortunately, a frequently necessary therapy in IBD. Depending on the extent of resection and whether a pull-through type of procedure is performed, patients are left with altered anatomy. In the dog, 50-70% of the proximal small intestine may be resected without losing weight or capacity to absorb fat and protein. Mild steatorrhea is the only consequence of this procedure as the fecal fat content increases from about 8-10% (unoperated animals) to about 15-24% (Kremen et al., Ann. Surg. 140 (3) :439-48 (1954)). In contrast, the removal of the distal 50% of the small intestine was far more catastrophic for the animal. Significant weight loss followed the appearance of severe steatorrhea as the fecal fat content increased to about 80- 90%. In the rat, similar resection provided an explanation for the weight loss observed with distal gut resection. Intestinal transit was found to be much faster after distal than proximal resection (Reynell and Spray, Gastro. , 31(4):361-68 (1956)). The weight loss and impaired absorption noted in these rats and in the dogs (Kremen et al. , (1954)) may be explained by the diminished contact time between luminal contents and absorptive surfaces due to rapid transit. Since rapid transit was far worse after distal than proximal resection, intestinal transit and therefore optimal processing of nutrients must depend on the ileal brake as a uniquely potent mechanism that controls transit. To test the hypothesis that intestinal transit is inhibited more potently by fat in the distal (ileal brake) than proximal gut, in 6 dogs equipped with duodenal (10 cm from pylorus) and midgut (160 cm from pylorus) fistulas, intestinal transit was compared across an isolated 150 cm test segment (between fistulas) while 0, 15, 30 or 60 mM oleate was delivered into either the proximal or distal segment of the gut as a solution of mixed micelles in pH 7.0 phosphate buffer at 2 ml/min for 90 minutes. Buffer was perfused into the other segment of the gut. The segment of gut not receiving oleate was perfused with buffer at 2 ml/min. 60 minutes after the start of the perfusion, -20 μCi of 99m Tc-DTPA (diethylenetriamine pentaacetic acid) was delivered as a bolus into the test segment. Intestinal transit was then measured by counting the radioactivity of 1 ml samples collected every 5 minutes from the diverted output of the midgut fistula. Intestinal transit was calculated by determining the square root of the area under the curve (AUC) of the cumulative percent recovery of the radioactive marker. The square root values of the AUC were compared under varying conditions of region of fat exposure and oleate dose using 2-way repeated measures ANOVA (where 0 = no recovery by 30 minutes and 47.4 = theoretical, instantaneous complete recovery by time 0. Results are reported as mean ± standard deviation. For the control, buffer was perfused into both proximal and distal half of the gut, and recovery was 41.4 ± 4.6. TABLE 2. EFFECT OF OLEATE ON PROXIMAL AND DISTAL GUT Oleate dose (mM) Reσion of fat exposure 15 30 60 Proximal half of gut 38.8 ± 2.1 37.8 ± 5.9 29.0 ± 4.0 Distal half of gut 22.4 ± 2.9 15.8 ± 2.4 7.2 ± 2.3 These experiments demonstrate that intestinal transit is slower when fat is exposed in the distal half of the gut (region effect; p <0.01). These experiments also demonstrate that oleate is effective in inhibiting intestinal transit in a dose-dependent fashion (dose effect, p <0.05); and that dose dependent inhibition of intestinal transit by oleate depends on the region of exposure (interaction between region and dose, p <0.01). These experiments show that the ileal brake is more potent than the jejunal brake. When fat was perfused into the proximal half of the small intestine as per this Example, transit times were faster than those in Example I. This difference is the result of the simultaneous perfusion of buffer through the distal half of the small intestine in this Example. Data has been collected supporting the existence of a volume, distension-driven accelerating mechanism in the distal gut, that was presumably triggered by the buffer perfusion in this Example. Particularly after a large load, fat normally appears in the proximal as well as the distal gut early in the course of gastric emptying, triggering the jejunal and ileal brakes. The inhibitory feedback response that is triggered allows adequate time for digestion of nutrients in the proximal gut. In the setting of ileal disease (Weser et al. , Gastro . , 77(2) -.512-13 (1979)) or resection of the ileum, the already rapid transit through the proximal gut (Connell, Rend. Gastro. , 2:38-46 (1970)) becomes even faster, leaving little time for digestion of nutrients. Since the jejunal brake is triggered by end products of fat digestion, this still-remaining mechanism for control of transit does not operate, leading to abnormally rapid transit. As a result, fat malabsorption and subsequent weight loss occur in rat, dog, and man having such altered anatomy. EXAMPLE III Oleate Slows Upper Gut Transit and Reduces Diarrhea in Patients with Rapid Upper Gut Transit and Diarrhea Rapid transit through the upper gut may result in diarrhea, maldigestion, malabsorption, and weight loss; pharmacologic treatment with opiates or anticholinergics is often required. It was tested whether active lipids could be used to slow upper gut transit and reduce diarrhea in patients with rapid transit and diarrhea. Five patients with persistent diarrhea for 3 to 22 months (one each due to vagal denervation, ileal resection for Crohn's disease, and vagotomy and antrectomy, and two due to idiopathic causes) were studied. Each patient demonstrated rapid upper gut transit on routine lactulose breath hydrogen testing (Cammack et al. , Gut 23:957-961 (1982)). This test relies on the metabolism of certain carbohydrate materials (e.g., lactulose) by the microbial flora within the distal gut (i.e., the caecum in a patient with intact gastrointestinal tract) . By generating gas which can be detected in the expired air, it is possible to make some estimation about the time to the initial arrival of the administered material within the colon. For the experimental study, each patient received orally, in random order, 0, 1.6 or 3.2 ml of oleate in 25 ml Ensure™ brand drink, followed by 100 ml water. Thirty minutes after each dose of oleate, patients received 10 g lactulose orally, followed by 25 ml water. Breath hydrogen was measured every 10-15 minutes, and upper gut transit time was defined as the time from ingestion of lactulose until a rise of H 2 of >10 ppm. Data were analyzed using 1-way repeated measures analysis of variance (ANOVA) , and are expressed as mean ± standard deviation. TABLE 3. EFFECT OF OLEATE ON TRANSIT TIME Oleate (ml) 0 1.6 3.2 Transit time (min) 46 ± 8.6 116 + 11.1 140 + 11.5 It can be seen that upper gut transit was significantly prolonged by oleate in a dose-dependent fashion (p <0.005, significant trend). After ingestion of oleate 15-30 minutes prior to meals for a period of 1 to 3 days, all patients reported reduced diarrhea. The patient with Crohn's disease reported complete resolution of chronic abdominal pain as well as postprandial bloating and nausea, and over time gained 22 lbs. In addition, the patient with vagotomy and antrectomy reported resolution of postprandial dumping syndrome (flushing, nausea, light- headedness, abdominal cramps, and diarrhea) . These experiments demonstrate that oleate premeal is effective in slowing of upper gut transit and reducing diarrhea among patients with diarrhea secondary to rapid transit. It is likely that this novel, nutrient-based treatment will be effective in other chronic diarrheal conditions associated with rapid transit. EXAMPLE IV A Premeal Containing Oleate Slows Upper Gut Transit and Reduces Diarrhea in Inflammatory Bowel Disease Patients A premeal containing active lipids has been demonstrated as effective in a large number of patients with rapid transit, as seen in Example III. Therefore, it was next desirable to test its effect in IBD patients. Presented below are the extremely promising data from two IBD patients with ileal resection and reanastomosis. Table 4. Improvement in diarrhea in Crohn's patients Patient 1 Frequency Volume (ml) Appearance Intestinal Transit (min) Without oleic 4 2400 liquid 20 acid premeal With oleic 3 1550 liq/semi- 150 acid premeal solid Patient 2 Frequency Volume (ml) Appearance Intestinal Transit (min) Without oleic 8 975 semi-solid 25.5 acid premeal With oleic 2 250 solid 125 acid premeal IBD patient 1 is a 35-year-old male with Crohn's Disease who was status post ileal resection with reanastomosis. He presented with diarrhea (12-15 times/day) , abdominal cramps, bloating, steatorrhea, poor response to oral medications, weight loss of 30+ lb. , and weakness in association with rapid intestinal transit as measured by lactulose hydrogen breath test (time-to-10 ppm rise of H 2 ) . The effect of active lipid was tested by adding 1.6 or 3.2 g of oleate to a 25 g Ensure™ brand drink premeal fed to the subject. It was found that the time-to- 10 ppm rise of breath H 2 was delayed to 46 min. after a premeal containing 1.6 g of oleate, and to 150 min. when 3.2 g oleic acid was provided (Fig. 1A) . This patient's diarrhea and postprandial symptoms improved significantly on an average dose of 2 g of oleate before each meal. In 3 days, with active lipid premeal, his stool volume dropped from 2400 to 1500 ml and the frequency of bowel movements decreased from 4 to 3 per day. After one month ofactive lipid therapy, his bowel pattern improved even more impressively to an average of 2 bowel movements (semi- solid, formed stools) each day, occurring generally upon rising and in the mid-afternoon. This time-dependent improvement suggests that it may take some time (e.g., as long as a month) to achieve maximal benefit from invention methods. After 2 months of treatment, he had gained 22 lbs. and returned to school full time. IBD patient 2 is an 18-year-old male with ulcerative colitis who underwent colectomy with ileostomy 2 years after the initial diagnosis, followed by ilio-anal pull-through 6 months later. At the time of his presentation, he was having up to 8 movements of liquid/semi-solid stool per day, tired easily, suffered from fecal incontinence, and was socially restricted by his diarrhea. After confirming that his intestinal transit responded to active lipid (Fig. IB) , he was placed on a schedule where a premeal containing 3.2 g of oleic acid was eaten 30 minutes before breakfast, lunch, and dinner. On this treatment, Patient 2 nearly normalized his bowel pattern (Table 3) so that he was able to report solid stools for the first time since his disease began. He also reported recovery of a sense of well-being, a full and unlimited resumption of his social life, and is now looking forward to college. EXAMPLE V A Premeal Containing Active Lipid Increases the Bioavailability of an Orally Delivered Drug Optimal assimilation of all luminal contents depends on adequate residence time in the small intestine (Read, Clin . Gastro . , 15(3):657-83 (1986)). When transit through the small intestine is too rapid, there is insufficient time for digestion and absorption of nutrients and other luminal contents (Bochenek et al. , Ann . Int . Med. , 72(2):205-13 (1970); Thompson, Gastro . Clin . N. Am. , 23(2):403-20 (1994); Weser et al. , Gastro. , 11 (3 ) -.512-19 (1979); Winawer et al. , NEJM, 274(2) :72-78 (1966)) . One of the most important substances in the gut lumen for the IBD patient receiving drug treatment is oral medication. In the setting of the IBD patient with rapid transit, it is reasonable to expect that absorption of oral medications will be impaired. The goal of drug therapy is to deliver sufficient amounts of the appropriate drug to the blood stream and hence the tissue site of disease involvement (Gubbins and Bertch, Pharmacotherapy, 9(5):285-95 (1989)). Among the factors important to the bioavailability of oral medications are the physicochemical properties of the drug, pH of the lumen, presence of food or other drugs in the lumen, gastrointestinal motility, amount of absorptive surface area, and residence time in the small intestine (Dressman et al., J. Pharm. Sci . , 82(9):857-72 (1993); Gubbins and Bertch (1989); Hebbard et al. , Clin . Pharmacokinet . , 28(l):41-66 (1995); Parsons, Clin . Pharmacokinet . , 2(l):45-60 (1977); Toothaker and Welling, Ann . Rev. Pharmacol . Toxicol . , 20:173-99 (1980)) . The same kinds of surgery and pathophysiological abnormalities that cause rapid transit in IBD have been shown to alter drug bioavailability (Dressman et al. (1993) ; Gubbins and Bertch (1989) ; Parsons (1977) ) . Since these patients are often dependent on oral immunosuppressive drugs for treatment, these alterations of drug bioavailability may lead to poor therapeutic outcomes. Anti-diarrheal opiates such as codeine and loperamide are frequently prescribed for IBD patients. These agents act by slowing transit (Barrett and Dharmsathaphorn, J. Clin . Gastro . , 10(l):57-63 (1988)). These agents also lead to greater overall bioavailability of other drugs taken concurrently (Greiff and Rowbotham, Clin . Pharmacokinet . , 27(6):447-61 (1994)), suggesting that drug bioavailability may be enhanced by slowing intestinal transit. However, these drugs are not completely effective and have serious side effects (Barrett and Dharmsathaphorn (1988) ) . Responses to oral medications are erratic for individual IBD patients and among the patient population as a whole (Gubbins and Bertch (1989) ) . The causes of this day to day variation are not clear, but may involve the state of disease activity (quiescence versus acute relapse) , and the physical formulation of a drug (liquid versus solid; Gubbins and Bertch (1989) ) . During acute relapse in IBD, more powerful drugs with narrower therapeutic windows are prescribed in an effort to reverse the course of disease. Alternatively, or in addition, physicians often resort to prescribing massive doses of drugs to treat the relapse (e.g., 16 Pentasa per day). This could be a potentially dangerous practice if, for example, a drug is more bioavailable in the active disease state, when large doses of drugs are more likely to be prescribed. Therefore, the day to day variation of drug bioavailability can have catastrophic consequences. Rapid intestinal transit in the IBD patient with ileal disease or resection may result in insufficient time for dissolution (equivalent to digestion) and absorption of drugs. This problem is particularly important for the delivery of drugs such as cyclosporin which are absorbed in the proximal small intestine (Brynskov et al. , Scand. J. Gastro . , 21 (A ) -.961- 61 (1992)). Just as there are no end products of fat digestion to trigger the jejunal brake, rapid transit also reduces the amount of "digested" drugs available for absorption. These problems are particularly acute for solid forms of a drug which must undergo dissolution before absorption, a step not needed for the liquid form of a drug. These issues are equally important for drugs that work topically on the mucosa. Ideally, a topically acting drug should have prolonged contact time with the mucosa. The pharmaceutical industry has attempted to address this need with the advance of enteric coatings (e.g., delayed release formulations such as Pentasa) . Unfortunately, uncontrolled, rapid transit through the intestine will diminish the effective contact time regardless of the speed of release. Supporting this idea is the observation that there are considerable variations in bioavailability between liquid and solid formulations of the same drug (Gubbins and Bertch (1989)). In one fistulated dog where chyme was diverted at midgut as a short bowel model, 1 g liquid acetaminophen was delivered into the stomach 30 minutes after a meal of 50 ml Ensure™ brand drink mixed with (w/) or without (w/o) 1.6 ml oleic acid. Blood was then drawn every 30 minutes for 4 hours. Plasma was separated and assayed for acetaminophen levels using a chemical kit (acetaminophen assay kit , Sigma Diagnostics) . Table 5 . ACTIVE LIPID EFFECT ON ACETAMINOPHEN BIOAVAILABILITY IN THE DOG Bioavailability parameter /o Oleic acid w/Oleic acid sqrt AUC 43.9 54.1 C^ (μg/ml) 22 19 t__ (minutes) 30 120 It was found that the bioavailability of acetaminophen was increased by prior administration of active lipid. Specifically, the square root of the area under the curve (AUC) was greater and the time to maximum plasma level (t ^ was delayed 400% (Fig. 2 and Table 5) . This data suggests that active lipids have a significant beneficial effect in the management of oral drug therapy in IBD patients with rapid transit. Drug bioavailability in a human IBD patient with rapid transit is likely to be similar to that observed without active lipid treatment in the fistulated dog, i.e., only a relatively brief period of therapeutic activity with each dose. With slowing of intestinal transit by an active lipid (e.g., oleic acid) premeal, the same drug dose behaves like the idealized extended release formulation. This effect was supported in a preliminary study of one IBD patient with rapid transit. The time to peak plasma concentration of acetaminophen (after a 2g dose) was delayed from 60 to 240 minutes when the drug was taken with 3.2g of oleic acid. The effect of rapid transit on drug bioavailability may be even more profound when the drug is formulated for sustained release. For example, an IBD patient with rapid transit on a regimen of a pharmacologically formulated delayed release drug such as Pentasa (four 250 mg capsules q.i.d.) will be faced with a significant mismatch between rapid transit through the small intestine and the longer dissolution time of the enteric coating (relative to a noncoated drug) . As a result, much of the expensive medication may end up in the toilet. If an active lipid premeal were to be used in conjunction with a delayed release formulation, the increase in drug bioavailability would result in improved efficiency of drug delivery. In the case of a drug like cyclosporin which is generally only 30% bioavailable when delivered orally, and which has a ^ of 3.5 hours (Sandoz "Sandimmune", Physician's Desk Reference, 49th ed. , pp. 2183-2186 (1995)), rapid transit completely eliminates the possibility of effectively delivering the drug via the oral route. Slowing intestinal transit by administration of an active lipid premeal provides a useful way of increasing drug bioavailability. Although the invention has been described with reference to the disclosed embodiments, those skilled in the art will readily appreciate that the specific embodiments taught hereinabove are only illustrative of the invention. It should be understood that various modifications can be made without departing from the spirit of the invention.

Claims: What is claimed is: 1. A method to prolong the residence time of a substance in the small intestine of a subject, said method comprising administering to said subject a composition comprising an active lipid in an amount effective to slow the transit of said substance through the small intestine for an amount of time sufficient for absorption of said substance to occur. 2. A method according to claim 1 wherein the composition is administered prior to said substance. 3. A method according to claim 2 wherein the composition is administered up to about 24 hours prior to said substance. 4. A method according to claim 2 wherein the composition is a premeal, and said premeal is administered about 0 to about 24 hours prior to said substance. 5. A method according to claim 4 wherein said premeal is administered about 0 to about 2 hours prior to said substance. 6. A method according to claim 5 wherein said premeal is administered about 15 to about 45 minutes prior to said substance. 7. A method according to claim 4 wherein said premeal comprises a nutrient-enriched drink. 8. A method according to claim 1 wherein the composition is administered concurrently with said substance. 9. A method according to claim 1 wherein said composition is a liquid or a solid. 10. A method according to claim 1 wherein said composition is administered orally or tube-delivered. 11. A method according to claim 1 wherein said active lipid comprises a digested or partially digested lipid. 12. A method according to claim 11 wherein said digested or partially digested lipid is a fatty acid. 13. A method according to claim 12 wherein said fatty acid is selected from the group of fatty acids having between 4 and 24 carbon atoms. 14. A method according to claim 13 wherein said fatty acid is selected from the group consisting of caprolic acid, caprulic acid, capric acid, lauric acid, myristic acid, oleic acid, palmitic acid, stearic acid, palmitoleic acid, linoleic acid, linolenic acid, trans-hexadecanoic acid, elaidic acid, columbinic acid, arachidic acid, behenic acid eicosenoic acid, erucic acid, bressidic acid, cetoleic acid, nervonic acid, Mead acid, arachidonic acid, timnodonic acid, clupanodonic acid, docosahexaenoic acid, and structured lipids. 15. A method according to claim 14 wherein said fatty acid is oleic acid. 16. A method of slowing gastrointestinal transit of a substance in a subject having a gastrointestinal disorder, said method comprising administering to said subject a composition comprising an active lipid in an amount sufficient to prolong the residence time of the substance in the small intestine. 17. A method according to claim 16 wherein the residence time in the small intestine is prolonged for an amount of time sufficient for substantial digestion and substantial absorption of said substance to occur therein. 18. A method according to claim 16 wherein the prolonged residence time in the small intestine results in increased absorption of said substance. 19. A method of enhancing the digestion and absorption of nutrients and/or pharmacologically active agents in a subject, said method comprising administering to said subject a composition comprising an active lipid in an amount sufficient to prolong the residence time of said nutrients and/or pharmacologically active agents in the small intestine. 20. A method for treating diarrhea in a subject, said method comprising administering to said subject a composition comprising an active lipid in an amount sufficient to prolong the residence time of the luminal contents of the small intestine. 21. A method of reducing the level of atherogenic serum lipids in a subject wherein said atherogenic serum lipids are derived from an ingested substance, said method comprising administering to said subject a composition comprising an active lipid in an amount sufficient to prolong the residence time of said substance in the small intestine. 22. A method according to claim 21 wherein the amount of said composition is sufficient to limit the spread of and to control the presentation of said substance to the proximal segment of the small intestine. 23. A method of enhancing the bioavailability of an orally ingested pharmacologically active agent in a subject, said method comprising orally administering to said subject a composition comprising an active lipid in an amount sufficient to prolong the residence time of the pharmacologically active agent in the small intestine. 24. A method according to claim 23 wherein said composition is administered prior to said pharmacologically active agent. 25. A method according to claim 24 wherein said composition is administered from about 0 to about 24 hours prior to said pharmacologically active agent. 26. A method according to claim 25 wherein said composition is administered from about 0 to about 2 hours prior to said pharmacologically active agent. 27. A method according to claim 25 wherein said composition is administered from about 15 to about 45 minutes prior to said pharmacologically active agent. 28. A method according to claim 23 wherein said composition is administered concurrently with said pharmacologically active agent. 29. A method according to claim 23 wherein the residence time in the small intestine is prolonged for a time sufficient for dissolution and absorption of said pharmacologically active agent to occur therein. 30. A pharmaceutical oral article comprising a core having an active lipid coating thereon, wherein said core is a pharmacologically active agent and wherein said coating is substantially absorbed in the small intestine prior to release of said pharmacologically active agent. 31. An article according to claim 30, wherein said coating comprises an active lipid in an amount effective to prolong the residence time of said active pharmacologically active agent in the small intestine for a time sufficient for dissolution and absorption of said pharmacologically active agent to occur therein. 32. A pharmaceutical oral article comprising a plurality of particles, wherein said particles comprise an active lipid with a controlled release coating thereon, wherein said particles are substantially absorbed in the small intestine to effect and sustain a slowing of gastrointestinal transit. 33. An enteral formula comprising essential nutrients and an active lipid in an amount effective to prolong the residence time of said essential nutrients in the small intestine for a time sufficient for digestion and absorption of said nutrients to occur therein. 34. A gelatin capsule comprising a diluent and an active lipid in an amount effective to prolong the residence time of essential nutrients in the small intestine, for a time sufficient for digestion and absorption of said nutrients to occur therein. 35. A gelatin capsule according to claim 34, wherein said diluent is selected from the group consisting of calcium carbonate, calcium phosphate, kaolin, liquid paraffin, or an edible oil. 36. A method of counteracting the nicotine-induced inhibition of intestinal motility in a subject, said method comprising administering to said subject a composition comprising an active lipid in an amount sufficient to prolong the residence time of said substance in the small intestine in the presence of nicotine.

Inventors: LIN HENRY C, LIN, HENRY, C.
Applicants: CEDARS SINAI MEDICAL CENTER, LIN HENRY C, CEDARS-SINAI MEDICAL CENTER, LIN, HENRY, C.
Application year: 1996
Main classification: A61K31
IPC codes: A61K31