SM Journal of Food and Nutritional Disorders

Archive Articles

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Does a High Protein Diet Induce Oxidative Damage?

T he purpose of the present letter is to determine the marginal level of high protein diet which modulates oxidative damage. The author hopes that the determination of the marginal level of high protein diet which modulates oxidative damage could contribute to the research for oxidative damage, apoptosis, obesity, cell proliferation, differentiation or cancer. Consumption of a high protein diet is of interest in terms of one of dietary interventions for weight loss. Camiletti-Moirón et al. [1] reported that a high protein diet induces oxidative damage to the brain in rats by means of lipid peroxidation or protein oxidation. In the paper, however, the diet contained 45% dietary protein for the high protein group compared to the basal protein group. If the diet contains more than the content (e.g., 60-80% dietary protein) in the experimental or clinical study, it is my opinion that an “excessive dietary protein” may be the suitable terminology for the level of dietary protein rather than a “high protein diet”.

Sung Jae Shin*


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Effects of HIV/AIDS on Micronutrients

Both HIV/AIDS and malnutrition are common problems in Sub-Saharan Africa particularly in Ethiopia. HIV/AIDS and malnutrition effects are interconnected and worsen one another in a vicious cycle. However, there is limited studies regarding on effects of HIV/AIDS on malnutrition particularly micronutrients.

Dereje Gedle*


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Potential Influence of Adiponectin on Systemic Lupus Erythematosus and Rheumatoid Arthritis Therapy

T here is growing efforts in developing pharmacological and non-pharmacological therapies directed to decrease both the inflammatory status and the metabolic complications associated to Systemic Lupus Erythematosus (SLE) and Rheumatoid Arthritis (RA). Nevertheless, these aims provoke a continuum challenge due to the pathophysiological complexity of these rheumatic diseases. SLE consists in the development of auto antibodies, which can affect several systems, such as mucocutaneous, musculoskeletal, renal and central nervous system [1], whereas the main AR features are pain, swelling and morning stiffness in distal joints [2]. Whereas the impact of infections and active disease on mortality has diminished dramatically over the years due to intensive treatment, Cardiovascular Disease (CVD) has emerged as the leading cause of death in these patients [3]. The incidence of myocardial infarction is 5 times as high in patients with lupus as in the general population, and in young women the age-specific incidence is increased by a factor of as much as 50 [4]. Similarly, patients with RA present higher cardiovascular risk, as shown by one to one and a half fold coronary diseases; two fold congestive heart disease and two to three fold thromboembolism [5].

Renan Grecco Costa1, Ligia Grecco Costa Dall’Aqua1, Andrea Name Colado Simao2 and Isaias Dichi3*


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To Feed and Move the Muscles are Crucial for Healthy Ageing

Ageing is associated with reduced margins and impairments in several physiological systems including increase in body fat and a decline in lean mass called sarcopenia and limiting physical abilities. Disease Related Malnutrition (DRM) becomes prevalent due to increased risk to develop chronic disease by age. To prevent and reduce the loss of muscle mass and function physical activity and nutrition are of importance. The evidence for a combination effect is convincing. Except adequate energy intake protein and vitamin D are of specific importance to maintain muscle mass. Some amino acids seem of key importance. A major cause of sarcopenia is inactivity and anabolic resistance. Physical exercise, mainly resistance training has been shown to be of significant importance for muscle protein synthesis. Adequate muscular function is a prerequisite for independence and quality of life. It is urgent to learn more about how to prevent and treat loss of muscle mass and function in ageing.

Elisabet Rothenberg*


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Effects of Sulfasalazine, Lactobacillus Plantarum (Lp-115) and Fish Oil in Experimental Colitis

Ulcerative Colitis (UC) is a chronic inflammatory disease that affects the gastrointestinal tract, and studies have shown the association of inflammation and oxidative stress on its occurrence. The use of immunomodulatory nutrients and probiotics has resulted in remission phase prolongation and are considered a promising strategy for prevention and treatment of UC. The long chain n-3 fatty acids from fish oil have also shown favorable results in UC decreasing symptoms. This study aimed to evaluate n-3 fatty acids from fish oil and/or the probiotic Lactobacillus plantarum (Lp-115), combined with sulfasalazine, at inflammatory markers in Trinitro-Benzene Sulfonic Acid (TNBS)-induced colitis in male Wistar rats. The study lasted 21 days. Nutritional intervention was performed during all experiment and colitis induction was performed in the 14th day. The rats were divided into f ive groups: (A), control group; (B), sulfasalazine; (C), sulfasalazine with Lactobacillus plantarum fermented milk; (D), sulfasalazine with n-3 fatty acids and (E) sulfasalazine, n-3 fatty acids and Lactobacillus plantarum. All groups received water and food ad libitum and environmental conditions were controlled. Tissue samples were collected for Myeloperoxidase (MPO) determination. A Kruskal-Wallis test with Dunn’s post-test was applied to determine differences at level of 5 % significance (p<0.05) between groups. The results were demonstrated by reduction of tissue levels of myeloperoxidase. Beneficial effects were seen with the use of sulfasalazine with probiotic, but sulfasalazine association with n-3 fatty acids obtained results that were more favorable.

Paroschi TP1, Breganó JW2, Simão ANC2, Dichi I3* and Miglioranza LHS1


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A Program to Improve Quality of Life for those Dealing with Cancer

I was diagnosed with breast cancer in January 1993 while suffering from extreme Multiple Chemical Sensitivity (MCS). After reviewing my treatment options I decided against chemotherapy. My treatment plan involved making dietary changes and eating only organic. But even then I felt that it would be important to incorporate daily physical activity, and continue my usual course of enjoying the small things in life. I founded a cancer advocacy nonprofit Annie Appleseed Project which went online in June 1999. I was also running an educational program called Whole Health in which (mostly) women with cancer discussed options. We discovered early on that the things I did to keep myself well, worked to help those using conventional therapies, well too. We discovered Integrative Oncology. T he main focus was the use of nutrition as a base for better health.

Ann E Fonfa*


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Diet and Clinical Outcomes in Chronic Kidney Disease Stages 3-5: Need for Evidence-Based Interventions

Background: Excessive dietary habits may contribute to kidney function deterioration in Chronic Kidney Disease (CKD). Diet modifications have been used to slow kidney function deterioration. We reviewed the results of dietetic interventions in the outcomes of CKD.

Methods: Revision of clinical trials and meta-analysis reporting the results of dietetic interventions, published until March 2015 in journals indexed in Pubmed/Medline.

Results: moderate protein restriction (0.8 g/Kg/day) may slow the progression of CKD in stages 4-5. There is no evidence supporting protein restriction in CKD stage 3, or there is no advantage more protein restriction in advanced CKD stages. Severe protein restriction can contribute to Protein Energy Wasting (PEW). Restricting sodium intake to 80-100 m Mol/day helps to control hypertension, albuminuria and oedema. However, there is no evidence that sodium restriction prolongs kidney survival. Restricting phosphate intake is not necessary in CKD stage 3-4 and may also contribute to PEW. When necessary, in CKD stage 5 before kidney replacement therapy, hyperphosphatemia can be controlled with phosphate chelating agents. There is limited evidence that fruits and vegetables can control metabolic acidosis and slow CKD progression.

Conclusion: The evidences that dietetic interventions can slow the progression of CKD are weak. Randomized controlled trials searching for hard clinical outcomes and longer follow-up time are necessary before recommending restrictive dietetic interventions.

Fernando Domingos1,2*