Synbiotics Reduce Oxidative Stress

Yet another example of how keeping the gut microbiome healthy – in this case with a “synbiotic” combination of probiotic and prebiotic – also keeps the rest of the body healthy (reduced oxidative stress and cellular damage).

Oxid Med Cell Longev. 2017;2017:9315375. doi: 10.1155/2017/9315375. Epub 2017 Feb 13.

Influence of Synbiotics on Selected Oxidative Stress Parameters.


The aim of the present study was to assess synbiotic (Lactobacillus casei + inulin) influence on oxidative stress parameters such as concentrations of malondialdehyde (MDA), hydrogen peroxide (H2O2), glutathione, and free sulfhydryl groups content. Experiments were carried out on healthy volunteers (n = 32). The subjects were divided into women group (n = 16) and men group (n = 16) and randomly assigned to synbiotic and control groups. Blood samples were collected before synbiotic supplementation and after 7 wks, at the end of the study. The administration of synbiotic resulted in a significant decrease in MDA (p < 0.01), H2O2 (p < 0.01), and GSSG concentrations (p < 0.05) as compared with the control groups and significant increase in the concentrations of GSHt (p < 0.001), GSH (p < 0.01), and -SH group content (p < 0.05) versus control. Synbiotics containing L. casei plus inulin may have positive influence on selected oxidative stress markers.












Polyphenols & Microbiome…

I’m giving a short talk and participating in an expert panel discussion at UC Davis next week, where I will talk about, “Gut Feelings – the Role of the Microbiome in Mental Wellness” – and touch on aspects of dietary supplements related to probiotics, prebiotics, and “phytobiotics” like polyphenols that can modulate (and be modulated by) our microbiome.

Here is an interesting recent paper on the topic…

Biochem Pharmacol. 2017 Mar 16. pii: S0006-2952(17)30141-7. doi: 10.1016/j.bcp.2017.03.012.

Role of the small intestine, colon and microbiota in determining the metabolic fate of polyphenols.


(Poly)phenols are a large group of compounds, found in food, beverages, dietary supplements and herbal medicines. Owing to their biological activities, absorption and metabolism of the most abundant compounds in humans are well understood. Both the chemical structure of the phenolic moiety and any attached chemical groups define whether the polyphenol is absorbed in the small intestine, or reaches the colon and is subject to extensive catabolism by colonic microbiota. Untransformed substrates may be absorbed, appearing in plasma primarily as methylated, sulfated and glucuronidated derivatives, with in some cases the unchanged substrate. Many of the catabolites are well absorbed from the colon and appear in the plasma either similarly conjugated, or as glycine conjugates, or in some cases unchanged. Although many (poly)phenol catabolites have been identified in human plasma and / or urine, the pathways from substrate to final catabolite, and the species of bacteria and enzymes involved, are still scarcely reported. While it is clear that the composition of the human gut microbiota can be modulated in vivo by supplementation with some (poly)phenol-rich commodities, such modulation is definitely not an inevitable consequence of supplementation, it depends on the treatment, length of time and on the individual metabotype, and it is not clear whether the modulation is sustained when supplementation ceases. Some catabolites have been recorded in plasma of volunteers at concentrations similar to those shown to be effective in in vitro studies suggesting that some benefit may be achieved in vivo by diets yielding such catabolites.

KEYWORDS: Bioavailability; Conjugation; Microbiota; Phenolic acids; Polyphenols

PMID: 28322745 DOI: 10.1016/j.bcp.2017.03.012

Stress, Overeating, and Obesity?

Neurosci Biobehav Rev. 2017 Mar 11. pii: S0149-7634(16)30394-3. doi: 10.1016/j.neubiorev.2017.01.026.

Stress, overeating, and obesity: Insights from human studies and preclinical models.


Eating disorders and obesity have become predominant in human society. Their association to modern lifestyle, encompassing calorie-rich diets, psychological stress, and comorbidity with major diseases are well documented. Unfortunately the biological basis remains elusive and the pharmacological treatment inadequate, in part due to the limited availability of valid animal models. Human research on binge eating disorder (BED) proves a strong link between stress exposure and bingeing: state-levels of stress and negative affect are linked to binge eating in individuals with BED both in laboratory settings and the natural environment. Similarly, classical animal models of BED reveal an association between acute exposure to stressors and binging but they are often associated with unchanged or decreased body weight, thus reflecting a negative energy balance, which is uncommon in humans where most commonly BED is associated with excessive or unstable body weight gain. Recent mouse models of subordination stress induce spontaneous binging and hyperphagia, altogether more closely mimicking the behavioral and metabolic features of human BED. Therefore the translational relevance of subordination stress models could facilitate the identification of the neurobiological basis of BED and obesity-associated disease and inform on the development of innovative therapies.

KEYWORDS: Animal model; Chronic subordination stress; Ecological momentary assessment; Negative affect; Social stress; Stress

PMID: 28292531
DOI: 10.1016/j.neubiorev.2017.01.026

Dementia Metabolism?

Fantastic article with innovative ideas about using amino acid formulations to circumvent the metabolic derangements typical of dementia.

Abstract pasted below and full article at =

Amino Acid Catabolism in Alzheimer’s Disease Brain: Friend or Foe?


There is a dire need to discover new targets for Alzheimer’s disease (AD) drug development. Decreased neuronal glucose metabolism that occurs in AD brain could play a central role in disease progression. Little is known about the compensatory neuronal changes that occur to attempt to maintain energy homeostasis. In this review using the PubMed literature database, we summarize evidence that amino acid oxidation can temporarily compensate for the decreased glucose metabolism, but eventually altered amino acid and amino acid catabolite levels likely lead to toxicities contributing to AD progression. Because amino acids are involved in so many cellular metabolic and signaling pathways, the effects of altered amino acid metabolism in AD brain are far-reaching. Possible pathological results from changes in the levels of several important amino acids are discussed. Urea cycle function may be induced in endothelial cells of AD patient brains, possibly to remove excess ammonia produced from increased amino acid catabolism. Studying AD from a metabolic perspective provides new insights into AD pathogenesis and may lead to the discovery of dietary metabolite supplements that can partially compensate for alterations of enzymatic function to delay AD or alleviate some of the suffering caused by the disease.