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    So you have a case, now what? First, gather your information in a clear, concise manner. A worksheet is provided here for reference. Once the information is gathered, it needs to be put together. The components of a case report can vary, again depending on whom or where you are writing for and how much time and energy you have. At the very least, a case report should contain 1) an introduction, 2) a presentation of the case, and 3) a discussion. If you are writing for the purpose of sharing academic knowledge, then it should include 1) an abstract, 2) an introduction with literature support, 3) an in-depth analysis of the case, 4) the discussion with literature documentation, and 5) a conclusion with recommendations or hypothesis generating ideas. A final and important point is that the key to writing a good case report is to be clear about the “single message” that you want to deliver. What is the priority message that you want the reader to take away? Clear description of this and development of why this is so will provide a meaningful addition to the literature and offer real benefit to your colleagues.

    Components of a case report in detail

    1. The abstract provides a concise synopsis of your case report to allow potential readers a quick glimpse into the content of your article. Depending on the journal, the length of an abstract may be 100 to 250 words.

    2. The introduction provides the background to why the case may be of interest to the reader. Literature support on theoretical or research basis of the case may be presented here.

    3. The case presentation gives the detailed description of the case (i.e. presenting symptoms, treatments and outcomes) and analysis of the findings. However, this does not mean you should go on ad nauseam on the details of the case. The goal is to provide essential information and noteworthy features that may be of interest to your reader.

    4. The discussion is the most important part of the case report. This is where the significance of the case is discussed; what the outcomes are, what features are unique and interesting to the reader, and why this case is important. Supporting literature that is relevant to the case should be included here as well as ideas for generating hypotheses for future research.

    5. The conclusion gives a brief summary to what you have learned from the case, any implications to clinical care and recommendations that other clinicians could learn from.

    Other Considerations

    A case report is the medical history of a person and the clinical/therapeutic approach used to treat the person and achieve the outcome. The bottom line is that it is about a person. Thus, as an author, it is proper etiquette for you to get consent from your patient. In fact, obtaining consent from the patient is not only good medical practice, but also mandatory for some journals. In the consent form, you can inform your patient about your intentions, the types of information being shared, and any known or potential risks/ benefits. It is your responsibility to ensure your patient’s confidentiality and anonymity. For example, if photographs are used, anonymity may not be guaranteed. In such a situation, the patient needs to be informed.

    A case report is derived from the detailed reporting of events that take place within the context of treating and observing a single patient (i.e. case). The report is an in-depth longitudinal examination that is essentially qualitative in nature although it may well contain quantitative data. A case report is anecdotal in that it provides informal observations that are uncontrolled, not subject to the scientific method, and cannot be independently confirmed. Although such anecdotal evidence is not regarded as strictly scientific, it is often regarded as an invitation to more rigorous scientific study. For example, in an analysis of 47 case reports detailing side effects of drug therapy, 35 were found to be “clearly correct”. Primarily a case report is a way of communicating information to the medical world through the elucidation of unique and characteristic feature(s) of a condition, complications, and adverse effects and benefits of specific interventions. Case reports may also serve as a valuable research and educational tool. Robert Iles notes that most medical case reports consider one of five topics:

    1. An unexpected association between diseases or symptoms

    2. An unexpected event in the course of observing or treating a patient

    3. Findings that shed new light on the possible pathogenesis of a disease or an adverse effect

    4. Unique or rare features of a disease

    5. Unique therapeutic approaches

    Why write a case report?

    The objectives for writing a case report are mainly to 1) inform/educate; 2) share new knowledge/insight; and 3) document processes and procedures. Furthermore, within the naturopathic context, case reports can serve as a method for building evidence for naturopathic healthcare practice and expanding our Materia Medica. Having well-written case reports published in a reputable medical journal adds to the credibility of the naturopathic profession. The goal of a case report is to provide information of value to the audience (i.e. interesting and relevant). Information provided in a report should contain unique features about the condition, the treatment, the outcome, and anything else pertinent to the case. A case report differs from a clinical case intake in that a case report is systematic, and includes a greater depth of detail, in-depth analysis, literature support guidelines and conclusions about the findings. Case reports can also provide findings that are hypothesis generating.

    As naturopathic doctors, there will likely be a strong desire to maintain a humanistic and holistic approach to care. While called a ‘case’ report, do not lose sight that we are talking about people. After all, we do not treat cases; we treat patients with presenting symptoms. Case reports provide us with a great tool for learning. Thus, case reports should be written about cases with both positive and negative outcomes, with the emphasis being on learning. In fact, as practitioners, we know that we often learn more from the negative cases. Furthermore, by writing a case report, practitioners will likely add to their own knowledge base.

    H was given a protocol to follow with goals of alleviating side effects; the modalities included nutrition, hydrotherapy, supplements, and exercise. A whole foods diet was implemented for weight optimization. The diarrhea was treated with eating organic yogurt and kefir as a source of probiotics. L-glutamine powder 7 g/d was recommended for rebuilding the gut as well as treating diarrhea. Zinc gluconate 20 mg/d was added for the restoration of taste. The CIPN was treated with Neurosol at one softgel twice daily.(4) The hydrotherapy consisted of home treatments including warming socks and gloves nightly to increase peripheral circulation and Epsom salt soaking baths twice weekly. The exercise protocol was a daily walk for 20 minutes. When H presented for the 11th cycle of FOLFOX, the peripheral neuropathy had completely resolved as determined by patient interview before administration of the chemotherapy. At this point H had received a cumulative dose of oxaliplatin of approximately 850 mg/m2. The dose-limiting neurotoxicity occurs with a cumulative dose between 780 and 850 mg/m2 in oxaliplatin treatment.(3) At no point during the remaining nine cycles (cycles 12-20) did H present with complaints of CIPN. The CIPN treatment of Neurosol and home hydrotherapy was continued throughout the FOLFOX treatment and discontinued after the last cycle of FOLFOX, October 2004. (Figure 1) H had excellent partial remission and was switched to irinotecan and bevacizumab, and later cetuximab. The partial remission continued through June 2005. Unfortunately, by October 2005 the cancer was found to be progressive as evidenced by CT scan and CEA (carcinoembryonic antigen) levels rising. At this point, a second round of FOLFOX (13 cycles) was started April 2006. The oxaliplatin dose was 85 mg/m2 with a cumulative dose of approximately 1000 mg/ m2. On two of the cycles the oxaliplatin dose was reduced to 75 mg/m2 due to neutropenia, but not reduced due to neurotoxicity or CIPN. H resumed a similar protocol as for the first FOLFOX treatment, including the same diet therapy of whole foods and yogurt, and a meal of organic liver and onions 1-2 times weekly to guard against chemotherapyinduced anemia. Other therapies included Epsom salt baths, Neurosol (one softgel bid), omega-3 fish oil capsules, and one tablet of silymarin 80% bid (equal to 56mg silymarin/tab). The use of silymarin is currently in question with regards to potential interactions from hepatic metabolism of other medications the patient may be on. The specific concern is that silymarin modulates the activity of cytochrome P450 enzymes and may increase the levels of toxic medications in a patient. 5 The silymarin was prescribed for liver health due to the progressive metastatic cancer in the liver. The FOLFOX combination contains three medications, none of which are hepatically cleared,6 so the use of silymarin was not contraindicated in this patient.

    Since H began naturopathic integrative care his weight stabilized and was considered healthy for his height (+/- 5 pounds) for 15 months while undergoing chemotherapy. In addition, the patient experienced a complete elimination of the CIPN. The Neurosol was discontinued after recovery from the neuropathy and this symptom had not returned as of December 2006. H has had regular bowel movements without significant constipation or diarrhea with the exception of chemotherapy days when he experienced one day of diarrhea that affected daily activities. This is a reduction from seven days of diarrhea post chemotherapy before initiating integrative medical care.

    In August and September 2006, while undergoing FOLFOX treatments, H enjoyed fishing trips to British Columbia and a vacation to Puerto Vallarta. H has had enough energy to be able to exercise and take pleasure in life. After the 13th cycle of FOLFOX in October 2006, H met with the oncologist and in a review of symptoms had no fevers, unusual anorexia, weight loss, peripheral neuropathy, unusual aches or pains, anxiety, depression, or rashes. There are limitations to this case report. No validated tools were used to objectively evaluate the quality of life, ADLs, and CIPN. The data was retrieved through interview and chart notes from the physicians caring for H. In summary, during the naturopathic care that the patient received, H experienced a reduction in all major side effects from the chemotherapy, increased quality of life as evidenced by the ability to not only leave the house, but also to take vacations and engage in hobbies that were previously difficult.

    In general, many large epidemiological and case-control studies have resulted in data describing conflicting outcomes examining the relationship between colorectal cancer and fiber intake. A combined analysis of 13 case-control studies found relative risks of colon cancer to be 0.53 with high versus low fiber intakes. Similarly, a case-control study of 2000 cases found intakes high in fiber correlated with a low relative risk. In contrast, large epidemiological studies such as the Nurses’ Health Study(48) and the Health Professionals Study did not find any such relationships. Lupton (2000) suggests that a higher intake in fermentable fiber is more protective because it results in lower colonic pH and production of the short-chain fatty acid butyrate, a primary energy source for colon cells. The recent review from Obrador examined the evidence supporting the role of dietary fiber in the prevention of colorectal cancer. While most epidemiological and intervention studies analyzed in this review show little strength in terms of cancer prevention, meta-analyses on case control studies report reductions of up to 50% in the risk of colorectal cancer associated with higher intakes of dietary fiber. However, the evidence remains weak since case-control designs are often associated with various biases, namely recall bias and the influence of the subject’s health status on the validity of self-reporting.

    Among factors contributing to the inconsistency in the data available are the source and form of fiber. While some studies have shown both soluble and insoluble sources to be protective, others state that insoluble fiber is the only form that could play a role in cancer prevention. The diet accompanying fiber intake could play an important role as well, as it is hypothesized that the type of fat consumed affects gut susceptibility to cancer. Namely, oils that induce apoptosis, such as fish oil, may be more protective. Confounding the effect of dietary fiber on colorectal cancer is the natural presence of phytochemicals in such food groups as fruits, vegetables and whole grains. In fact, polyphenols and others have shown great antioxidant, antiproliferative and apoptotic activities and could be responsible for the anti-carcinogenic effect of high-fiber foods.

    Although there seems to be a significant body of evidence in favor of dietary fiber as a prevention of colorectal cancer, data from well-designed studies characterized by large sample sizes show no effect of dietary fiber on cancer development or progression. Confounding factors such as composition of meals accompanying fiber intake and antioxidant properties of fiber-rich foods have made the relationship between dietary fiber and colorectal cancer inconclusive, creating the need for further research to isolate the effect of fiber on cancer development. Moreover, it should be noted that cancer itself is a complex disease that can arise secondary to other health conditions, diet and lifestyle. Health claims pertaining to colorectal cancer prevention cannot be justified based on the current literature, however given the natural benefits of fiber containing foods, a potential health claim which states that regular consumption of fiber may decrease the risk of colon cancer could be appropriate in orienting the consumer towards healthier food choices. In conclusion, evidence shows that soluble fiber reduces the risk of cardiovascular disease, and that insoluble fiber protects against disturbances of the digestive tract. Although more extensive research is needed to confirm the beneficial role of dietary fiber in the prevention of colorectal cancer and diverticulosis, the fact remains that fiber is an important and safe component of a healthy diet and has been positively linked to lower incidences of these diseases.

    Human studies have concluded that total dietary fiber given at doses ranging from 20-26 g helps to normalize and improve bowel function by decreasing the incidence of constipation in elderly populations. In these studies, ingestion of fiber-rich foods or supplements resulted in significant improvements of clinical symptoms of constipation and discontinuation of laxatives. Fiber supplementation in children with chronic constipation demonstrated that the recommended ‘age in years plus 5 g/day’ dosage of total fiber resulted in a reduction in the frequency of clinical symptoms. Similar results were observed in a crossover trial using 100 mg/kg body weight of the soluble fiber glucomannan. Constipation is also commonly faced by patients administered enteral feeding. To this end, Silk et al (2001) studied the effect of fiber supplementation of enteral formulas on bowel function. Results show a reduction in gut transit time and an increased stool wet weight as compared to fiber-free formula. Although two metaanalyses examining randomized controlled trials have shown no benefits to dietary fiber in alleviating the symptoms of constipation, the choice of a study population composed of irritable bowel syndrome patients decreases the applicability of the authors’ findings to the general population. In fact, an earlier systematic review, looking at a more heterogeneous population, argued that fiber supplementation did lead to a modest improvement in bowel movement frequency and a decrease in abdominal pain. The review outlines data from 1815 patients with chronic constipation having participated in 36 controlled trials. Although special populations, namely patients with irritable bowel syndrome and diverticulosis, were included in three studies, these populations only accounted for 45 patients of the total sample size. The beneficial effect of dietary fiber on constipation is supported by the evidence in the literature linking the intake of fiber to reduced intensity and frequency of symptoms in the general population. Therefore, health claims on the benefits of dietary fiber for constipation are well founded, especially in populations at risk where more fiber is associated with the need for less laxative medication and accompanying side effects.
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    Fiber Effect on Diverticulosis Prevention
    In the 1960s and 1970s, Painter and colleagues first proposed a low fiber diet as a cause of diverticular disease called “a disease of Western civilization” for its high prevalence in developed countries. A suggested mechanism for the development of diverticulosis is that low fiber intake results in greater water absorption due to slower gut transit. Thus, smaller, firmer stools are produced, leading to high intraluminal pressure which, in turn, results in excessive segmentation. However, to date no human studies exist which confirm this mechanism. Nonetheless, low fiber diets have repeatedly been correlated with the incidence of diverticulosis. In fact, epidemiological studies predicted that 60% of individuals over 60 years of age, from Westernized countries, will be diagnosed with diverticular disease, partly due to a low intake of dietary fiber.

    Fiber supplementation has been examined in animal models in order to explain a possible mechanism through which fiber may act to prevent the disease. It was suggested that fiber may influence the nature of collagen cross-linking in the bowel through decreased production of short chain fatty acids by gut microflora. Although animal models have shown a positive response to high-fiber diets, to date very little evidence exists on fiber supplementation and its link to diverticulosis. Results from a prospective study involving a cohort of healthy males show a more significant inverse relationship between diverticulosis and insoluble fiber than it does for soluble fiber. While no recent randomized placebo-controlled trials have been conducted to evaluate the effect of fiber on diverticular disease, earlier human trials do not hold enough evidence qualifying dietary fiber as a treatment for diverticulosis symptoms. Although patients diagnosed with the disease are commonly prescribed a high fiber diet, there is a need for further investigation into the role of fiber in the development and/or progression of diverticulosis through placebo-controlled clinical trials. At present, consumption of a diet low in fiber is considered a main cause of diverticulosis, therefore there should be a preventative health claim on the risks of diverticulosis linked to a low-fiber intake.

    A dose response effect of soluble fiber appears to exist, where an increase in the amount consumed is associated with a greater reduction in blood lipids, mainly total cholesterol and LDL cholesterol, however, no optimal dose is evident in the literature. One study examined the lipid-lowering effects of 0.4 g, 3 g, or 6 g of beta-glucan in conjunction with a Step 1 diet which consists of 50% of energy from carbohydrates, 20% from protein and 30% fat, with less than 10% contributed by saturated fat and less than 300 mg/day of cholesterol in the diet. Results of the trial showed that LDL cholesterol levels were reduced by around 4%, 10%, and 14%, respectively,20 compared to a Step 1 diet alone. Considering that 3 g of soluble fiber can be found in approximately one cup of oat cereals, it is clear that such improvements in cholesterol levels can be attained with fairly low intakes of soluble dietary fiber.

    Average daily intakes of total dietary fiber in Europe and the USA lie between 15 and 20 g, while the dietary review papers recommended intakes for fiber are reported to be 38 g/day and 25 g/day for men and women, respectively, with no upper tolerable intake set to this date. Adequate intakes can be attained by consuming the recommended servings of whole grains, fruits and vegetables, making fiber supplementation unnecessary. However, it is clear that an adequate consumption of soluble fiber plays a role in reducing the risk of coronary heart disease by decreasing total and LDL cholesterol levels.

    The American Heart Association’s year 2000 dietary guidelines state that there is a moderate cholesterol-lowering effect of soluble fiber over and above the effect of a diet low in saturated fat and cholesterol. As well, the US Food and Drug Administration has authorized a health claim stating that soluble fiber in certain foods such as whole oats reduces risk of coronary heart disease.
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    Fiber Prevents Constipation

    Insoluble dietary fiber plays an important role in promoting normal bowel movement by acting like a sponge in the distal colon, therefore increasing stool bulk. Through such action stool movement through the colon is promoted, thus reducing transit time.(27) In addition to the type of fiber, the effect of fiber on stool output is dependent on the amount of fiber present. Regular consumption of dietary fiber will help increase water content and plasticity of stools, thus promoting regularity. Since the stool holds more water as a result of fiber intake, it is important to increase fluid consumption to a recommended 2 L per day in order to further the action of fiber on stool movement.

    Abstract

    The bulk of the research on dietary fiber started in the 1970s when what had been considered as a fad, lacking scientific evidence, gained the interest of the scientific community as improved designs and analytical methods were used to examine the health benefits of dietary fiber. Since then, epidemiological studies and clinical trials have highlighted the potential role for dietary fiber in the prevention of cardiovascular and gastrointestinal disease. Today, nutrition societies consider dietary fiber to be an essential part of a balanced diet for disease prevention. Health authorities have now approved health claims on the benefits of moderate to high fiber intakes, based on the increasingly available scientific evidence. The purpose of this review is to identify those claims, analyze the supporting evidence behind the role of soluble and insoluble fiber as health promoters, and examine the potential for further health claims, based on recent studies in fiber research.

    Methods

    The literature was searched using mainly PubMed (accessed in 2006 and 2007). References cited in this review comprise peer-reviewed original research articles, reviews, metaanalyses as well as government regulation reports. The bulk of the evidence includes work published after the year 2000; although, findings published between 1960 and 1990 were also used to illustrate the early work in the field of fiber research.

    Fiber Efficacy for Lowering Total and LDL Cholesterol, and Decreasing Risk of Coronary Heart Disease

    Recent animal studies show a significant effect of fiber on blood lipids and suggest potential lipid-lowering mechanisms including satiety effects and moderate to low bile acid-binding capacities. In humans, there is little evidence showing a link between insoluble fiber and coronary heart disease risk factors as well as mortality. A common limitation to human studies examining the lipid-lowering effects of insoluble fiber is a lack of control on the diet and lifestyles of subjects or populations assessed. Thus, there is a contributing confounder by way of the effect of a healthy lifestyle on blood lipid levels. A review by Truswell (2002) showed that 27 of 34 human studies testing efficacy of insoluble fiber saw no reductions in plasma total cholesterol. In addition, experiments that did show significant reductions had inherent weaknesses such as short durations and one-way designs (control-test) where subjects ate ad libitum. Thus, the controversy behind the efficacy of insoluble fiber in decreasing risk factors of cardiovascular disease remains unresolved.

    In contrast, there is an abundance of evidence supporting beneficial effects of soluble fiber on plasma lipid levels. At least forty human trials have indicated high efficacy of oatmeal or oat bran in reducing plasma lipids. Doses of soluble fiber ranging from 3 g to 8 g have induced significant reductions ranging from 2.0% to up to 24% in total and low-density-lipoprotein (LDL) cholesterol in both hypercholesterolemic and non-hypercholesterolemic individuals. Unlike human studies involving insoluble fiber, the clinical trials mentioned here are characterized by their strong designs, including large sample sizes and controlled study diets, reinforcing the validity of their findings. A pooled analysis of cohort studies conducted in the United States and Europe showed that incremental intakes of 10 g/day of cereal and fruit fiber intakes were associated with 25% and 30% reduction in coronary death, respectively. In addition, studies have demonstrated that higher intakes of soluble fiber may reduce the incidence of metabolic syndrome characterized by elevated LDL cholesterol levels, decreasing the risk of cardiovascular disease. Cholesterol lowering action of soluble dietary fiber was explained by Yoshida et al (2005) as a result of an increased fecal sterol excretion and/ or production of short-chain fatty acids previously shown to play a role in the suppression of cholesterol biosynthesis.

    Medium-chain triglycerides (MCT) have unique characteristics relating to energy density and metabolism giving them advantages over more common long-chain triglycerides (LCT). Human consumption of MCT oils is low since naturally occurring sources of MCTs are rare; however, those sources include milk fat, palm kernel oil and coconut oil.

    MCTs are less energy dense and highly ketogenic compared to LCTs. First, the energy density of MCTs is less than that of LCTs due to their shorter chain length. MCTs provide about ten percent fewer calories than LCTs; 8.3 Cal per gram for MCTs versus 9 Cal per gram for LCTs. MCTs also differ from LCTs in their metabolic pathway because they are easily oxidized and utilized as energy, with little tendency to deposit as body fat. Consequently, the intake of MCTs can decrease caloric intake and potentially decrease body weight and body fat in the long term.
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    The literature supports that MCT oil increases energy expenditure and decreases body fat in the majority of studies in both animals and humans. In addition, MCTs may have a greater effect in overweight subjects as opposed to normal weight or obese subjects. Overall, short-term intakes of MCT oil have been shown to promote weight loss; however, chronic intakes of MCTs have shown various effects on energy expenditure, body weight, and fat mass. Yet, appetite control may play a bigger role in weight loss in long-term feedings of MCTs. The exact mechanism for the satiating effects of MCT is unknown, but may perhaps be explained by the distinctive energy density of MCT or the increase in fat oxidation. These studies suggest that replacing LCT with MCT oil could generate body fat loss over long periods of time, with or without reduced energy intake.

    Studies provide varying results concerning the influence of MCT on lipid metabolism such as increased TG concentrations. In addition, several studies have reported that MCTs do not affect blood cholesterol levels; however, others have reported hypercholesterolemic effects of MCTs due to their high saturated fat content. Therefore, the incorporation of other functional foods, such as conventional oils, essential fatty acids or plant sterol may minimize the risk of negative effects of MCT on blood lipids while optimizing decreases in body weight and body fat accumulation. In addition, the ingestion of MCT incorporated into the diet does not appear to cause any adverse symptoms.

    MCTs are easily included in food products without negatively affecting their taste or producing undesirable effects. MCT production is cost-effective compared to other oil-based functional foods. The short-term efficacy of MCT is proven; however, long-term effects of MCT still need to be examined more carefully. Overall, MCT shows a good AECES model and demonstrates the greatest potential for use as a functional fat for weight control.

    All cooking oils naturally contain small quantities of diacylglycerols (DAG), ranging from 0.8% in rapeseed oil to 9.5% in cottonseed oil.39 In addition, DAG is produced in the digestive tract as a metabolic intermediate, as 1,2-diacyl-sn-glycerol (1,2-DAG) or 2,3-diacyl-sn-glycerol (2,3-DAG), after the ingestion of TG.40 In recent years manufacturers have developed an enzymatic process to produce 1,3-diacyl-sn-glycerol (1,3-DAG) by migration of the acyl group with the reverse reaction of the 1,3-specific lipase. DAG oil can be easily incorporated into food products since it is similar in taste, appearance, and fatty acid composition to other oils.

    It is the specific structural differences of DAG isomers and not the fatty acid composition of DAG or TG that appear to explain the different action on lipid metabolism and body weight. The main end products of lipase action on 1,3-DAG are glycerol and free fatty acids, which may be less readily re-synthesized to chylomicron TG. Moreover, larger amounts of fatty acids from digested DAG may be released into the portal circulation rather than being incorporated into chylomicrons, compared with TG oils. In addition to producing lower TG content of chylomicrons, lower serum TG levels in a fasted state and in the postprandial state occur after DAG ingestion. This hepatic exposure to fatty acids by increasing DAG intake may lead to greater fat oxidation by the liver than following TG intake. Enhanced fat oxidation may lead to increased satiety. Thus, decreasing caloric intake may induce a decrease in weight and fat loss in long-term DAG feedings.

    While certain studies indicate that 1,3-DAG has a positive outcome in animal and human trials, other studies show no effect on body weight63-67 or TG levels. This lack of effect may be due to insufficient doses used (10% in the diet) or the heterogeneity across subjects used including overweight or obese versus normal weight individuals. Overweight and obese subjects could have defective fat oxidation; thus, higher fat oxidation may produce greater weight loss. Although the use of DAG oils for weight control is promising, much remains to be clarified regarding the mechanism of dietary DAG.

    DAG oil studies do not indicate any severe adverse health effects related to its consumption. However, it still remains to be seen how DAG oil intake will affect humans on a long-term basis as well as synergistically with other nutrients.

    Overall, DAG oils are easily incorporated into foods without affecting palatability, but have slightly higher costs than conventional oils. The AECES model for DAG shows it being a generally appropriate functional food for weight control; however, DAG oil has not yet been a huge success with consumer acceptance due to conflicting studies on the efficacy of the product. Overall, DAG oil demonstrates potential as a weight loss agent, but future research is needed to elucidate mechanisms responsible for its action on weight loss.

    Conjugated linoleic acid (CLA) is a collective term for a group of positional and geometrical conjugated dienoic isomers of linoleic acid that are found in dairy products and meat. The cis-9, trans-11 CLA is the principal dietary CLA form, but lower levels of the other isomers (trans-10, cis-12 CLA, trans-9, trans-11 CLA, and trans-10, trans-12-CLA) are present in food CLA sources. Naturally, CLA is produced in the rumen of ruminant animals by the fermentative bacteria that isomerize linoleic acid into CLA.

    Mechanisms of action of CLA include: enhanced thermogenesis, increased satiety, augmented fat oxidation, reduced fat cell size as well as fat deposition, increased apoptosis of adipocytes and altered preadipocyte differentiation. Potentially, the combination or additive effects of all these mechanisms of action of CLA may lead to changes in weight and body fat, as no single mechanism fully explains CLA action.

    Studies have shown that CLA, specifically the trans-10, cis-12 isomer, can reduce body weight and fat mass. Most animal studies associated with feeding CLA have shown that CLA lowers body fat and energy retention as well as increases energy expenditure, thereby decreasing weight; yet, others have shown no effects on weight. This may be due to the dose or the CLA isomers used in animal studies. Results demonstrate that body weight and/or fat mass of animals were not affected when they were supplemented with low amounts of CLA mixture (0.5% in the diet), which contained about equal amounts of the trans-10, cis-12 isomer and cis-9, trans-11 isomer. Yet, weight gain was similar to control when high amounts of CLA mixture with mostly the cis-9, trans-11 isomer were given. However, most human studies have not been able to replicate the magnitude of weight lost. Only a few human studies suggest that CLA supplementation has reduced body fat and other studies did not show any effect. The variety of species used in studies may also explain the discrepancy of results obtained.

    In animals, CLA supplements appear to have some undesirable side effects such as induced insulin resistance as well as fatty liver and spleen. These animal studies also demonstrate that CLA may have detrimental effects on plasma lipids. Human studies also show evidence that CLA may adversely influence health, in particular insulin sensitivity and blood lipids, but the results are conflicting. CLA is widely available in capsule form that improves its oxidative stability, therefore having an appropriate matrix, cost, and sensory quality for consumers. However, the efficacy of CLA is questionable because the animal evidence is more convincing than the human data. The lack of clarity on the mechanism of action can explain the inconsistencies in the research results. In addition, human studies should be carried out to determine the long-term effects of CLA and whether any adverse outcomes occur. In summary, the data available from literature demonstrates a poor AECES model. More research is needed to investigate the efficacy and the safety aspects before CLA will have optimal consumer acceptance.