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Healthy Cooking Techniques
Published in Nicole M. Farmer, Andres Victor Ardisson Korat, Cooking for Health and Disease Prevention, 2022
Joel J. Schaefer, Mary Schaefer
Sodium is present in foods as part of a wide variety of many ingredients and has many names other than salt. MSG is a flavor enhancer. Many other sources of sodium start with the word sodium, so be aware of these products. Sodium benzoate is a preservative. Sodium nitrite is a source of sodium found in hot dogs and lunch meats and is also used as a preservative in many foods. Another example is sodium phosphate, which is a generic term for a variety of salts and sodium and phosphate. (Figure 10.1).
Ornithine transcarbamylase deficiency
Published in William L. Nyhan, Georg F. Hoffmann, Aida I. Al-Aqeel, Bruce A. Barshop, Atlas of Inherited Metabolic Diseases, 2020
William L. Nyhan, Georg F. Hoffmann, Aida I. Al-Aqeel, Bruce A. Barshop
In chronic management of OTCD (Table 26.1), citrulline is substituted for arginine, as it is more palatable. Most patients are also treated with phenylbutyrate [65] as a source of phenylacetate. To many, phenylbutyrate is so unpalatable that a gastrostomy tube is required in order to avoid poor compliance, and even then, patients complain of a taste. For these reasons, sodium benzoate is preferred by some patients and some authorities. Most patients require restriction of the intake of protein, and most receive mixtures of essential amino acids to minimize the intake of nonessential nitrogen. Protein restriction and the use of benzoate/phenylbutyrate and deficiency of essential amino acids may lead to Kwashiorkor. Acrodermatitis-like skin lesions have been reported [66]. Complexities of management of OTCD were discussed in a patient diagnosed prenatally with a deletion who developed neurologic disease and anasarca, despite exemplary management and avoidance of hyperammonemia. Whole genome sequencing led to the diagnosis of a contiguous gene deletion involving chronic granulomatous disease, retinitis pigmentosa, and McLeod syndrome [10]. The authors stressed the need for detailed genetic analysis.
Chemophobia and the Boy Who Cried Wolf
Published in David Lightsey, The Myths about Nutrition Science, 2019
Panera Bread’s advertisement involved sodium benzoate, which is used as a preservative in many foods and is simply the sodium version of the naturally occurring chemical benzoic acid. Panera Bread states in the caption below the video: Sodium Benzoate is an artificial preservative found in sauces, jellies and pickled foods. It’s also an active ingredient in fireworks. So, to celebrate our removal of all artificial preservatives from Panera food, we staged an Independence Day firework show in Johnston City, Illinois. The town hadn’t seen fireworks in 10 years. Of course, Panera Bread wishes those watching the advertisement will assume that Panera Bread is all about “natural” food ingredients with no “nasty” preservatives, which purportedly makes their food better for you. This is not true. In food, sodium benzoate is used to inhibit the growth of mold, yeast, and bacteria. In other words, it delays spoilage and extends the shelf life and safety of products where it is used. Again, this is part of sustainable agriculture by reducing food waste. Natural food sources of benzoic acid include fruits, vegetables, cheeses, and yogurt, as well as other foods. Sodium benzoate is perfectly safe and rapidly excreted from the body.
Update on novel antipsychotics and pharmacological strategies for treatment-resistant schizophrenia
Published in Expert Opinion on Pharmacotherapy, 2022
Andrea de Bartolomeis, Mariateresa Ciccarelli, Licia Vellucci, Michele Fornaro, Felice Iasevoli, Annarita Barone
The NMDAR hypofunction hypothesis has been implicated in the pathophysiology of schizophrenia and may potentially play a prominent role in poor response to D2R-occupying agents [147]. NMDAR function can be enhanced by increasing the levels of D-amino acids. In this regard, sodium benzoate, a DAAOI, inhibits the enzyme that metabolizes D-amino acids (Figure 1) [141]. In two placebo-controlled clinical trials, sodium benzoate demonstrated high efficacy and tolerability [74,148]. Preliminary results showed that add-on therapy with sodium benzoate improved overall and positive symptoms in CRS patients [74] and enhanced neurocognitive functions in patients with chronic schizophrenia [148]. Further studies are needed to provide insight into the optimal dose and duration of treatment, as well as its potential use for CRS [74]. However, several lines of evidence have identified features that limit the use of DAAOIs, such as low bioavailability and poor ability to cross the BBB [149]. An adaptive phase II/III clinical trial is currently running to evaluate their safety and efficacy in TRS [150]. While the efficacy results are encouraging and may enable clinicians with a second-line option in difficult-to-treat patients, the pharmacokinetic issues may strongly affect the development and marketing of these agents.
Toxicological impact of sodium benzoate on inflammatory cytokines, oxidative stress and biochemical markers in male Wistar rats
Published in Drug and Chemical Toxicology, 2022
Ishfaq Shafi Khan, Khalid Bashir Dar, Showkat Ahmad Ganie, Md. Niamat Ali
Use of sodium benzoate in food and pharmaceutical products is widely acknowledged as safe as per food and drug administration (Nair 2001). However some sources have claimed that negative impacts arise by long term or short term uptake of sodium benzoate (Fujitani 1993). At concentration of 647–825 mg/kg b.wt of SB the International Program on Chemical Safety observed no detrimental impact on humans (Wibbertmann et al. 2005). The Turkey's Ministry of Health declared the appropriate dose of SB in 2003 is 500–1000 mg/kg. The Joint FAO/WHO Committee on Food Additives (JECFA) has approved an appropriate dosage of 0–5 mg/kg of sodium benzoate per day (Yadav et al. 2016). Food and drug administration permits 300 mg of sodium benzoate per kg b.wt. Despite the small daily intake dose of SB, its continuous long term intake may be harmful for users. Sodium benzoate was proved to be highly mutagenic when human blood cells were treated with varying doses of SB (6.25–100 µg/mL) (Zengin et al. 2011).
Emerging therapeutic targets for schizophrenia: a framework for novel treatment strategies for psychosis
Published in Expert Opinion on Therapeutic Targets, 2021
Susan F. Sonnenschein, A Grace
Numerous glutamate-targeting compounds have been evaluated in clinical trials. NMDA receptor co-agonists, including D-cycloserine, D-serine, and glycine, were among the earliest studied in an effort to enhance NMDA-mediated interneuron function [90], thereby increasing inhibition of pyramidal neurons. Despite initial promise in clinical trials, none of these compounds passed phase 2 or phase 3 clinical trials as either a monotherapy or adjunct to current treatments [91,92]. Selective glycine transporter 1 (GlyT1) inhibitors, such as sarcosine and biopertin have also been tested as an alternative method to increase the availability of glycine at NMDA receptors [93]. Sarcosine has demonstrated success in clinical trials as an adjunct treatment in early clinical trials in improving positive, negative, and cognitive symptoms [94,95] with some evidence for greater efficacy than NMDA receptor agonists [96]. However, not all trials have shown significant results with GlyT1 inhibitors, such as when added to clozapine or tested as a monotherapy [97–99]. D-amino acid oxidase (DAAO) inhibition with compounds such as sodium benzoate has also recently been explored as a method of enhancing NMDA receptor activation by blocking D-amino acid metabolism. Sodium benzoate has produced promising results as an adjunctive therapy in early clinical trials [100–102]. Larger clinical trials are needed to better assess the potential benefits of NMDA receptor-targeting drugs.