Mindfulness-based cognitive therapy added to usual care improves eating behaviors in patients with bulimia nervosa and binge eating disorder by decreasing the cognitive load of words related to body shape, weight, and food.

BACKGROUND: This study aimed to investigate the effectiveness of mindfulness-based cognitive therapy (MBCT) as a complementary approach in patients with bulimia nervosa (BN) or binge eating disorder (BED), and to assess how the reduction of the cognitive load of words related to eating disorders (ED) could constitute an intermediate factor explaining its global efficacy. METHODS: Eighty-eight women and men participated in clinical assessments upon inscription, prior to and following 8-week group MBCT. Mindfulness skills were assessed using the five facet mindfulness questionnaire; eating behaviors were assessed using the Three Factor Eating Questionnaire (TFEQ); comorbid pathologies were assessed using the beck depression index and the state-trait anxiety inventory. The cognitive load of words associated with ED was assessed through a modified version of the Stroop color naming task. RESULTS: Mindfulness skills improved significantly (p < .05) after group MBCT. The improvement of TFEQ scores was accompanied by reduced levels of depressive mood and trait anxiety. The positive impact of MBCT on TFEQ score was directly related to an improvement of the performance in the Stroop task. CONCLUSIONS: MBCT represents an interesting complementary therapy for patients with either BN or BED, at least when cognitive and behavioral domains are concerned. Such efficacy seems to be mediated by the reduction of the cognitive load associated with ED stimuli, which offers a possible explanation of how MBCT could reduce binge-eating behaviors. Other studies are needed, in independent centers, to focus more directly on core symptoms and long-term outcome.

[GABAergic approach of postpartum depression: A translational review of literature]. / Approche GABAergique de la dépression du post-partum : une revue critique translationnelle.

INTRODUCTION: Prevalence of postpartum depression (PPD) ranges from 10 to 15 % of parturients. The impact of the PPD is major on the maternal bond and the health of both mother and child. Its physiopathological mechanisms appear to differ from other types of depression. Today, pharmacotherapy is based on nonspecific treatment, and recent therapeutic advances in this field require a comprehensive approach of the implication of the GABAergic system in the development of PPD. Neurosteroid levels during pregnancy and after parturition and the GABA-A-r modulation are thought to be involved in PPD. OBJECTIVE: To evaluate if the GABAergic approach is relevant in postpartum depression management. METHODS: We conducted a systematic review of literature based on the MEDLINE database with the following Medical Subject Headings (MeSH): "postpartum depression", "GABA", "ganaxolone", "brexanolone", "allopregnanolone", prior to September 2019. We selected articles in English: preclinical and clinical studies, literature review, observational and therapeutic studies. RESULTS: Preclinical models (mouse and rat) show changes in GABAergic inhibition in the peripartum period and correlation between allopregnanolone and GABA-A-r plasticity. This plasticity in the peripartum period maintains levels of inhibition adapted despite increased neurosteroid levels. KO models for the GABA-A-r δ subunit develop depression and anxiety symptoms in the postpartum period, and a change in the expression of the gene coding for the GABA-R alpha-4 subunit was found. Artificial inhibition of progesterone metabolism during post-partum increased depression symptoms. GABAergic fluctuation seems to be interrelated with other systems such as those of oxytocins. A synthetic neurosteroid (SGE-516) was tested on mouse models of PPD, KO for δ-GABA-A-r or KCC2, and showed decreased depressive symptoms and better mothering. Clinical studies confirm neurosteroid fluctuation and changes in the GABAergic system during the peripartum period. Allopregnanolone is the neurosteroid the most studied in PPD, and it is elevated in the brain during the pregnancy. Studies disagree on the presence of significant differences in allopregnanolone plasma levels during pregnancy or postpartum between women with PPD or not. Women with a history of PPD have greater susceptibility to neurosteroid withdrawal. Imagery and genetical data also show a link between allopregnanolone and PPD. The GABA-A-r may not recover in time following a reduced number during pregnancy, and this mismatch between neurosteroid levels and their receptor may trigger PPD. Several randomized controlled trials investigated brexanolone administrated IV, a synthetic formulation of allopregnanolone, and demonstrated a rapid and well tolerated reduction in depressive symptoms. In March 2019 brexanolone obtained FDA approval in PPD indication under the name Zulresso. However, there are differences in the time of beginning of PPD, which could constitute different subgroups of this disease, and which physiopathology could respond to different mechanisms. Prenatal depression does not respond to a GABAergic approach, but women without any risk factor or previous mood disorder developing PPD in the weeks following childbirth could be particularly responsive to this kind of treatment. CONCLUSION: Disability to modulate GABA-A-r expression during pregnancy and restore its previous state after parturition appears to trigger PPD. The GABAergic system is a promising pharmacotherapy target. From preclinical to clinical studies for about twenty years the GABAergic system has been incriminated and targeted in this challenging mental disease.

Hawthorn extracts inhibit LDL oxidation.

Polyphenol-rich diet decreases cardiovascular risk. LDL oxidation is the primary event in atherosclerosis plaque formation and antioxidants such as polyphenols were shown to inhibit LDL oxidation and atherosclerosis development. Hawthorn (Crataegus) and derived pharmaceuticals are rich in polyphenols and already prescribed to treat moderate heart failure, nervousness and sleep disorders. Extracts either from fresh plant parts (flower buds, flowers, young leaves or green fruits) or from dried pharmaceutical parts (flowers and flowering tops) were previously shown to be effective inhibitors of lipoperoxidation and scavengers of oxygen species. In this study, the capacity of total and ethyl-acetate extracts from dried pharmaceutical flowers, tops and fruits to inhibit Cu(2+)-induced LDL oxidation was tested. This capacity was positively linked to their content in total polyphenols, proanthocyanidins (global and oligomeric forms), as well as to their content in two individual phenolics: a flavanol, the dimeric procyanidin B2 and a flavonol glycoside, hyperoside. Flavanol-type phenolics showed to be higher active than the majority of the flavonoids tested in inhibiting Cu(2+)-induced LDL peroxidation. This study suggests that hawthorn could be a source of polyphenols able to inhibit LDL oxidation.

Fatty acid abnormalities in chronic pancreatitis: effect of concomitant diabetes mellitus.

OBJECTIVE: Patients with chronic pancreatitis suffer from malabsorption and nutritional deficiencies. However there is little data available concerning the fatty acid profile in chronic pancreatitis. Diabetes mellitus, a common complication of this disease, could interfere with the metabolism of fatty acids. SUBJECTS: We therefore compared the fatty acid composition of LDL from four groups of male patients with (a) chronic pancreatitis without diabetes (ND-CP; n=12), (b) diabetes secondary to chronic pancreatitis and insulin-treated (CP-D; n=35); (c) type 1 diabetes (n=25); and (d) controls (n=20). RESULTS: The patients in both groups of chronic pancreatitis (ND-CP and CP-D) had lower mean values for linoleic acid than that seen in the type 1 DM and control groups, whereas monounsaturated fatty acids (MUFA; 18 : 1(n-9) and (16 : 1(n-7)) were significantly increased in these two groups (ND-CP and CP-D). Docosa-hexaenoic-acid (22 : 6(n-3)) was significantly decreased in the CP-D group (P>0.05), a response that could be explained by the effects of diabetes mellitus and by selenium deficiency. In this way, diabetes was associated with a decrease in the docosa-hexaenoic-acid (22 : 6(n-3); r=0.30, P=0.005), and selenium was correlated with DHA (r=0.28, P=0.029) and with the 22 : 6(n-3)/20 : 5(n-3) ratio (evaluating the delta 4 desaturation); r=0.31, P=0.022), independently of the diabetes effect. Selenium was negatively correlated with 20 : 4(n-6)/20 : 3(n-6) ratio (evaluating the delta 5 desaturase; r=-0.30; P=0.025). These results suggest that these two factors may have a role in the regulation of the desaturation process. If we consider that a ratio of 16 : 1(n-7)/18 : 2(n-6) greater than 0.086 in plasma indicates an EFAn-6 deficiency, 40% of our CP patients, 57.6% of CP-D patients and 13.6% of type 1 DM patients were involved. CONCLUSIONS: The consequences of these deficiencies are not evaluated in this disease. However, correction of the fundamental deficiencies in essential fatty acids and in selenium seems desirable in chronic pancreatitis.

Phenylpropanoids from Ballota nigra L. inhibit in vitro LDL peroxidation.

From the European plant Ballota nigra L. various polyphenols including phenylpropanoid derivatives were isolated. There is increasing evidence that oxidized low-density lipoproteins (Ox-LDL) might be involved in the pathogenesis of atherosclerosis and it has been reported that polyphenols inhibit LDL peroxidation and atherogenesis. The goal of this study was to test whether the major polyphenolic compounds extracted from Ballota nigra, four phenylpropanoid glycosides, verbascoside, forsythoside B, arenarioside, and ballotetroside and one non-glycosidic phenylpropanoid, caffeoyl-L-malic acid, inhibit Cu(2+)-induced LDL peroxidation. The effectiveness of these compounds was compared to the activity of quercetin, a well-known polyphenol inhibitor of Cu(2+)-induced LDL oxidation. Antioxidant efficacious doses (ED 50) of arenarioside and ballotetroside were 1.8 microM and 7.5 microM respectively, while in the same conditions, the ED 50 of forsythoside B and verbascoside were similar (1 microM) and those of quercetin and of caffeoyl-L-malic acid were 2.3 microM and 9.5 microM respectively. Spectrophotometric studies show that quercetin is a Cu(2+) chelator while phenylpropanoid glycosides and caffeoyl-L-malic acid are not Cu(2+) chelators. Therefore, phenylpropanoid glycosides are strong inhibitors of Cu(2+)-induced LDL oxidation, independent of any capacity to act as Cu(2+) chelators.

Recent developments in the treatment of hypertriglyceridemia.

Hypertriglyceridemia is now recognized as an independent risk factor of coronary artery disease (CAD). A recent secondary prevention study of CAD with a statin suggested that it may be prudent to target fasting triglycerides to less than 150 mg/dL. Secondary prevention trials of CAD with drugs acting primarily on triglycerides (fibrates) have shown that reducing triglycerides and increasing high-density lipoprotein (HDL) cholesterol, without significantly affecting low-density lipoprotein cholesterol slows down coronary artery luminal narrowing (Lopid Coronary Angiography Trial [LOCAT], Bezafibrate Coronary Atherosclerosis Intervention Trial [BECAIT], Bezafibrate Infarction Prevention [BIP]). Furthermore, Veterans Administration-HDL Intervention Trial (VA-HIT) and Gruppo Italiano per lo Studio della Sopravvivenza nell'Infarto-1 (GISSI) studies recently showed that gemfibrozil and fish oils, respectively, decreased CAD mortality in secondary prevention trials. Statins are also capable of significantly reducing high triglyceride levels. Further clinical studies are necessary to confirm in terms of mortality the beneficial effect of reducing triglycerides and increasing high-density lipoprotein cholesterol in secondary CAD prevention; whereas, in primary prevention the beneficial effect of drastically reducing triglycerides by the way of pharmacology needs to be proved.

Rapid quantification of alpha-tocopherol in plasma and low- and high-density lipoproteins.

We have developed two methods for measuring the alpha-tocopherol content in plasma and lipoproteins (LDL and HDL). In procedure 1, plasma or lipoproteins are deproteinized with ethanol containing delta-tocopherol as internal standard and then extracted with hexane or ethyl acetate. The organic layer is removed and evaporated, and the residue is redissolved in methanol and injected into a reversed-phase HPLC. In procedure 2, plasma or lipoproteins are diluted in a methanol and ethanol mixture containing the same internal standard. The solution is vortex-mixed, centrifuged, and directly injected into the column. The tocopherols are eluted with an isocratic methanol mobile phase at a flow rate of 1 mL/min and detected by fluorescence (lambda(exc)= 295 nm, lambda(em)= 330nm). Recoveries are approximately 100% in both cases. Between-run CVs were 8.39% for procedure 1 and 6.55% for procedure 2. Small sample requirement, simplicity of sample preparation, short assay time, and good reproducibility make procedure 2 ideal for clinical or research use. This method was applied to determination of alpha-tocopherol in plasma of patients whose diet was supplemented with alpha-tocopherol and in LDL and HDL.