PharmaNutrition最新文献

Background

Pregnancy interventions, potentially including consumption of nutraceuticals like probiotics, represent possible avenues for preventing non-communicable diseases. However, evidence syntheses indicate that probiotic interventions, while effective in managing some pregnancy complications (e.g., gestational diabetes), do not confer health benefits to uncomplicated pregnancies. Messaging around probiotics in pregnancy is mixed, such that people with low-risk pregnancies may nevertheless feel pressure to spend limited resources on (costly) probiotics. To tailor knowledge exchange and support safe, equitable access to pregnancy probiotics when their prescription may be warranted, we need to understand who takes probiotics during pregnancy and under what conditions.

Methods

We used chi-square and logistic regression analyses of anonymous, cross-sectional survey data from 341 pregnant Canadians of diverse socio-demographic backgrounds to assess which respondents, by socio-demographic characteristics and pre-pregnancy/pregnancy health indicators, were relatively likely to: perceive probiotics as beneficial to pregnancy health and/or report taking probiotics during pregnancy.

Results

Forty-seven percent of respondents perceived probiotics as beneficial to pregnancy health; 51 % reported consuming them. Probiotic attitudes and consumption were socio-demographically-patterned: higher-income, post-secondary-educated respondents disproportionately perceived probiotics as healthy and consumed them. There was no evidence of variation in probiotics attitudes or use by pregnancy health indicators.

Conclusion

Socio-economic factors may be more important determinants of pregnancy probiotic use in this sample than indications for pregnancy complications. Clear guidelines on pregnancy probiotics that reflect current evidence are needed. Equitable access to probiotics should be facilitated for pregnant people likely to benefit from interventions (i.e., those with certain complications), supporting long-term health equity.

Background

Soy isoflavone daidzein protects cells from oxidative stress. Oxidative stress causes several neurodegenerative diseases via damaging mitochondria and inducing cell death.

Methods

In this study, we analyzed protective mechanisms of daidzein on nitric oxide (NO) induced neuronal Neuro2a cell death, and quantitated mitochondrial amount, that was analyzed by cytometric analysis and western blots of mitochondrial molecules.

Results

Daidzein reduced cell death against NO stress and increased mitochondrial amount even in the presence of NO. Regarding the mechanism of mitochondrial increase, daidzein increased the expression of mitochondrial biogenesis regulator Peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC1α) and induced nuclear translocation of PGC1α. Following this, we analyzed if the reduction of PGC1α reduces the protective function of daidzein against oxidative stress. Knockdown of PGC1α abolished the cell-protective function. It strongly suggests that PGC1α activation followed by the mitochondrial increase is critical for the cell protection. Next, we focused on 5′-adenosine monophosphate-activated protein kinase (AMPK) for clarifying how daidzein activates PGC1α. Daidzein increased the expression and phosphorylation of AMPK, indicating that daidzein stimulates AMPK activation. AMPK inhibitor dorsomorphin abolished the cell protection and suppressed the nuclear translocation of PGC1α. Additionally, dorsomorphin prevented the increase of mitochondria by daidzein.

Conclusion

Our study strongly suggests that daidzein protects Neuro2a cells via AMPK activation followed by PGC1α activation and mitochondrial biogenesis.

Background

Milk contains polar lipids may confer health benefits upon consumption. Therefore, polar lipids have received considerable attention for development in the nutraceutical and pharmaceutical space. We review the prophylactic and therapeutic potential of milk polar lipids and their current market trends.

Methods

The following databases were used to retrieve articles for this narrative review: SCOPUS, ScienceDirect, PubMed, and Google Scholar. The search criteria included the following keywords and synonyms combined: (“milk polar lipids” or “milk phospholipids” or “milk glycerophospholipids” or “milk sphingolipids”) AND (“anti-inflammatory” or “cardiovascular” or “cancer” or “cognitive health” or “nutraceutical” or “pharmaceutical” or “supplement”).

Results

Milk polar lipid supplementation appears to improve cognitive health in both child development and age-associated cognitive decline. Milk polar lipids modulate cardiovascular risk factors including lipid levels, inflammation, and platelet function in preclinical studies, but evidence is limited in humans. Milk polar lipids may also affect colon cancer pathogenesis through anti-inflammatory mechanisms. Polar lipids are gaining attention in the nutraceutical and pharmaceutical space for their use in the development of novel therapeutics and pharmaceutical delivery systems.

Conclusions

Milk polar lipids exhibit a multitude of health benefits that may be of value in the nutraceutical and pharmaceutical industries as reflected in current market and research trends for the use of polar lipids and the development of products targeting infant cognitive development, cognitive decline in the aged, cardiovascular diseases, and cancer. Further clinical studies are required to assess efficacy and safety of milk polar lipid supplementation in human diseases.

Background

Despite recent advances that have been made in cancer treatment, we still lack complementary approaches to significantly improve the effectiveness of current anti-cancer therapies. The high-fat, low-carbohydrate ketogenic diet can cause metabolic changes in the tumor microenvironment, thus targeting cancer metabolism, making it an attractive candidate for adjuvant cancer therapy. This review is an attempt to explore the origin and trace the historical use of the ketogenic diet as a metabolic therapy in medical oncology.

Methods

A detailed literature review was conducted through specialized databases. Only those articles pertinent to the specific needs of the review were included. Relevant references in those articles were also followed.

Results

There is a sound biological rationale for the anti-tumor force of the ketogenic diet primarily manifested through its anti-Warburg effect. It is no less true that Otto Warburg’s experiments have based the ketogenic diet in cancer research on solid footing. However, precisely tracing the initial, original anti-tumor use of the ketogenic diet in medical oncology literature has indeed proved to be a hard needle to thread. The currently available data are considered promising in the pre-clinical rodent models. Yet, the number of rigorous human trials is small and suffers from methodological limitations.

Conclusions

Further research, both pre-clinical and clinical, is needed to accurately define the anti-tumor effect of the ketogenic diet and to overcome the current methodological limitations that hinder us from deriving a sound judgment about the use of the ketogenic diet in clinical practice.

To explore the impact of CoQ10 supplementation on periodontitis, a systematic review of controlled trials (PROSPERO: CRD42021274876) was performed from 1970 to November 2022 through Web of Science (ISI), Google Scholar, Embase, CENTRAL, PubMed/MEDLINE, Scopus, and ProQuest. A random-effect model was used considering clinical attachment loss (CAL), plaque index (PI), gingival index (GI), bleeding index (BI), and probing depth (PD). Of 97 records, eight trials were included. CoQ10 supplementation significantly reduce CAL (WMD, –0.66 (–0.81 to –0.50), P < 0.0001; I² = 93.4 %) and GI (WMD, –0.20 (–0.40–0.00), P = 0.05; I² = 98.5 %), but it could not affect PI (WMD, –0.07 (–0.16–0.02), P = 0.11, I² = 91.2 %), PD (WMD, –0.28 (–0.67–0.12), P = 0.17; I² = 98.4 %), and BI (WMD, –0.58 (–1.40–0.24), P = 0.17; I² = 99.5 %) significantly. CoQ10 had a stronger reduction effect on PI and GI in individuals ≥ 40 years old and in doses of ≤ 60 mg CoQ10. Longer duration of CoQ10 supplementation was also more effective in reducing PD. CAL reduced greater when CoQ10 was administered for longer than 12 weeks, in a dose of > 60 mg, and in younger individuals. CoQ10 supplementation in periodontitis may have beneficial effect on GI and CAL. Further investigations in this regard are needed to draw conclusive results.

Background

Nephropathy is a type of complication of type 2 diabetes, and medium chain triglycerides (MCTs) potentially improve metabolic abnormalities. This study examined whether MCT intake inhibits nephropathy development in a type 2 diabetic mouse model.

Methods

Six-week-old control non-diabetic ICR mice and type 2 diabetic Nagoya Shibata Yasuda (NSY) mice were fed a diet enriched with long-chain saturated/mono-unsaturated triglycerides, including palmitic-, stearic-, and oleic acids (C16/C18-rich group). NSY mice were fed a diet containing medium-chain triglycerides with either caprylic acid (C8-rich group) or capric acid (C10-rich group). Feeding was performed for 20 weeks. Plasma biomarker levels were measured using ELISA or enzymatic methods. Kidney pathology was evaluated using periodic acid–Schiff staining, and the expression of redox genes and proteins were determined using qRT-PCR and western blotting.

Results

The C16/C18-rich group of NSY mice exhibited expansion of the mesangial region in the kidney. Plasma cystatin C and creatinine concentrations were not different between ICR mice and C16/C18-rich group of NSY mice and between C16/C18-rich and C8- or C10-rich groups of NSY mice. The C8- and C10-rich groups had suppressed mesangial region than the C16/C18-rich groups. The mRNA expression of Sod1, Prdx1, and Gpx2, and SOD1 protein levels were higher in the C8- and/or C10-rich groups than in the C16/C18-rich group of NSY mice.

Conclusions

MCT intake in NSY mice at the stage without increased markers indicating glomerular filtration decrease, reduces glomerulosclerosis, with induction of redox gene expression, in the kidney.

Background

Visceral obesity and the metabolic syndrome that often accompanies it are robust and well-established risk factors for postmenopausal breast cancer. This increased risk is thought to be mediated, in large part, by increased aromatase expression in the breast. stromal adipocytes and in mammary epithelium; this results in a high local concentration of estrogen capable of supporting the cancerous transformation of estrogen receptor-positive (ER+) epithelial cells. Aromatase, a member of the cytochrome 450 family, is expressed in the endoplasmic reticulum. After menopause, it converts androgens produced within the adrenal cortex (androstenedione and testosterone) into estrogens (estrone and estradiol, respectively. Therefore, the main objective of this narrative article is to review dietary and nutraceutical remedies for the prevention of menopause. Breast cancer: leading strategies to suppress breast aromatase

Methods

The research articles to carry out this work were focused based on many searches and reviews in the following databases: Google Scholar, MDPI, PubMed, ScienceDirect and using the following keywords and combined synonyms: ("nutraceuticals" or "supplements" or "aromatase inhibitors" or "aromatase" or "antioxidants”) AND (“breast cancer” or “vascular function” or “inflammation”). The keywords were also searched in the references of the original articles included in this study

Conclusion

A number of nutraceutical, dietary, and lifestyle measures hold promise for breast cancer prevention and may be considered practical options by women seeking to minimize their risk. for this cancer, particularly as these measures appear to have few downsides and are likely to work in other ways to promote health.

Background

Yogurt, as one of the mass consumption dairy products worldwide, has been made a carrier of bioactive compounds, such as polyunsaturated fatty acids (PUFAs). Since cardiovascular disease (CVD) remains the leading cause of mortality worldwide dietary trends, including PUFAs-enriched yogurts, can be used to address this public health issue and contribute to a better healthcare.

Objective

This work describes the effects of the consumption of yogurt enriched with PUFAs on cardiovascular biomarkers.

Methods

A systematic review following the PRISMA methodology was done by gathering relevant published randomized controlled trials in adult population from 2000 to 2021 through Cochrane, PubMed, and Scopus. To control bias, we examined Cochrane Handbook recommendations.

Results

In the works reviewed, PUFAs-functionalized yogurt led to a reduction of triglycerides (TG) in plasma and an increase in the expression of the peroxisome proliferator- activated receptor gamma (PPARγ). PUFA supplementation in yogurt did not alter body weight or low-density lipoprotein (LDL) plasma levels. A dose of 200 g/d of PUFAs-enriched yogurt (PUFAs content range between 0.64% and 16.02% w/w) was identified. Among the tested PUFA sources (plant, seaweed, and animal), with which yogurt was supplemented, fish oil resulted in the best cardiovascular health benefits across interventions.

Conclusions

Although, all of the reviewed interventions with PUFAs- functionalized yogurt revealed variable effects on cardiovascular health, these still represent a limited number, and more studies are necessary to draw stronger conclusions and actionable information.

Background

In Europe, allergic diseases are the most common chronic childhood illnesses and the result of a complex interplay between genetics and environmental factors. A new approach for analyzing this complex data is to employ machine learning (ML) algorithms. Therefore, the aim of this pilot study was to find predictors for the presence of parental-reported allergy at 4–6 years of age by using feature selection in ML.

Methods

A recursive ensemble feature selection (REFS) was used, with a 20% step reduction and with eight different classifiers in the ensemble, and resampling given the class unbalance. Thereafter, the Receiver Operating Characteristic Curves for five different classifiers, not included in the original ensemble feature selection technique, were calculated.

Results

In total, 130 children (14 with and 116 without parental-reported allergy) and 248 features were included in the ML analyses. The REFS algorithm showed a result of 20 features and particularly, the Multi-layer Perceptron Classifier had an area under the curve (AUC) of 0.86 (SD 0.08). The features predictive for allergy were: tobacco exposure during pregnancy, atopic parents, gestational age, days of: diarrhea, cough, rash, and fever during first year of life, ever being exposed to antibiotics, Resistin, IL-27, MMP9, CXCL8, CCL13, Vimentin, IL-4, CCL22, GAL1, IL-6, LIGHT, and GMCSF.

Conclusions

This ML model shows that a combination of environmental exposures and cytokines can predict later allergy with an AUC of 0.86 despite the small sample size. In the future, our ML model still needs to be externally validated.

Background

Despite the beneficial pharmacological effects, poor oral bioavailability limits the nutritional efficacy of fisetin, a dietary flavonoid. To this end, herein we report the bioavailability and efficacy of an innovative formulation of fisetin using a fenugreek-galactomannan hydrogel scaffold (FF-20).

Methods

In the first phase of the study, female Wistar rats (n = 42) were randomly divided into two groups (n = 21/group) and orally administered with either unformulated (UF) or FF-20 (50 mg/kg b. wt.) and plasma concentration of fisetin was estimated by UPLC-ESI-MS/MS. In the second phase, the relative influence of FF-20 on alcohol-induced neurotoxicity was followed on animals (n = 24) randomized into four groups, Group I – vehicle control, Group II – ethanol treated, Group III – ethanol+ UF, and Group IV – ethanol + FF-20 and treated at 50 mg/kg b. wt. per day for 14 days.

Results

Area under plasma concentration verses time curve showed 9.83-fold enhancement in bioavailability for FF-20, with significantly enhanced pharmacokinetic parameters (*** P < 0.001). Behavior studies revealed significant improvement in reference memory errors, working memory errors, and anxiety among fisetin-treated animals and the improvement was significant in FF-20, compared to UF (* P < 0.05). Neurotransmitters and gene expressions of NMDAR, MAO A&B, and KLF-11 were altered by alcohol treatment; but were restored/improved in FF-20 group. Histopathology of brain tissues also indicated the reversal of alcohol-induced necrosis and tissue damage by FF-20.

Conclusion

FF-20 enhanced the oral bioavailability and significantly alleviated alcohol-induced neurotoxicity in experimental rats.