General Nutrition/MS Research

[jimmylegs]

Human Peptidoglycan Recognition Proteins Require Zinc to Kill Both Gram-Positive and Gram-Negative Bacteria, and Are Synergistic with Antibacterial Peptides
http://www.jimmunol.org/content/178/5/3116.short
Mammals have four peptidoglycan recognition proteins (PGRPs or PGLYRPs), which are secreted innate immunity pattern recognition molecules with effector functions. In this study, we demonstrate that human PGLYRP-1, PGLYRP-3, PGLYRP-4, and PGLYRP-3:4 have Zn2+-dependent bactericidal activity against both Gram-positive and Gram-negative bacteria at physiologic Zn2+ concentrations found in serum, sweat, saliva, and other body fluids. The requirement for Zn2+ can only be partially replaced by Ca2+ for killing of Gram-positive bacteria but not for killing of Gram-negative bacteria. The bactericidal activity of PGLYRPs is salt insensitive and requires N-glycosylation of PGLYRPs. The LD99 of PGLYRPs for Gram-positive and Gram-negative bacteria is 0.3–1.7 μM, and killing of bacteria by PGLYRPs, in contrast to killing by antibacterial peptides, does not involve permeabilization of cytoplasmic membrane. PGLYRPs and antibacterial peptides (phospholipase A2, α- and β-defensins, and bactericidal permeability-increasing protein), at subbactericidal concentrations, synergistically kill Gram-positive and Gram-negative bacteria. These results demonstrate that PGLYRPs are a novel class of recognition and effector molecules with broad Zn2+-dependent bactericidal activity against both Gram-positive and Gram-negative bacteria that are synergistic with antibacterial peptides.

related:
Peptidoglycan Recognition Proteins Are a New Class of Human Bactericidal Proteins (2006)
http://www.jbc.org/content/281/9/5895.short

[jimmylegs]

related

Inhibition of various gram-positive and gram- negative bacteria growth on selenium nanoparticle coated paper towels
free full text https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4403699/
There are wide spread bacterial contamination issues on various paper products, such as paper towels hanging in sink splash zones or those used to clean surfaces, filter papers used in water and air purifying systems, and wrappings used in the food industry; such contamination may lead to the potential spread of bacteria and consequent severe health concerns. In this study, selenium nanoparticles were coated on normal paper towel surfaces through a quick precipitation method, introducing antibacterial properties to the paper towels in a healthy way. Their effectiveness at preventing biofilm formation was tested in bacterial assays involving Staphylococcus aureus, Pseudomonas aeruginosa, Escherichia coli, and Staphylococcus epidermidis. The results showed significant and continuous bacteria inhibition with about a 90% reduction from 24 to 72 hours for gram-positive bacteria including S. aureus and S. epidermidis. The selenium coated paper towels also showed significant inhibition of gram-negative bacteria like P. aeruginosa and E. coli growth at about 57% and 84%, respectively, after 72 hours of treatment. Therefore, this study established a promising selenium-based antibacterial strategy to prevent bacterial growth on paper products, which may lead to the avoidance of bacteria spreading and consequent severe health concerns.

other studies re selenium vs bacteria in context of contact lenses, wound bandages etc
https://scholar.google.ca/scholar?as_yl ... m-negative"

[jimmylegs]

Serum Retinol Levels are Associated with Brain Volume Loss in Patients with Multiple Sclerosis
http://journals.sagepub.com/doi/full/10 ... 6686261%20

Background: Brain atrophy has been recognised as an endpoint of irreversible tissue loss that is closely associated with disability in patient with multiple sclerosis (MS). Although predicting future brain volume loss is important, studies have been shown only few biomarkers that can predict brain volume loss (BVL).

Objective: The aim of this study is to elucidate the association between longitudinal BVL and serum biomarker candidates.

Methods: This single-centered retrospective observational study intended to cover MS patients during January, 2008 to March, 2016. Inclusion criteria were: 1) patients who have brain MRI two times with intervals of more than 24 months; 2) patients who have blood test at the time or within 3 months of MRI scan. Evaluation of brain volume was done using SIENAX and SIENA in the FMRIB software library (FSL). Three serum biomarker candidates, uric acid (UA), 25-hydroxybitamin D (25(OH)D) levels and retinol binding protein (RBP) levels were measured.

Results: Twenty-three patients with MS were included in this study. We found that serum RBP levels were significantly correlated with percentage brain volume change (PBVC) (p = 0.0079). Furthermore, best subset selection of multiple linear regression models identified baseline normalised brain volume (NBV) and serum RBP as the best predictors of PBVC (R^2 = 0.23, p = 0.027).

Conclusions: Our study shows that lower serum retinol levels are associated with greater longitudinal brain volume loss and that serum RBP and can be a predictor of brain volume loss.

[jimmylegs]

Multiple Micronutrient Deficiencies Exist in Aged-care Residents, with Serum Zinc, not Iron, Being a Major Predictor of Anemia
http://www.fasebj.org/content/31/1_Supp ... 60.2.short

Abstract

Background Anemia is a significant comorbidity in older adults with a complex etiology that is not fully attributable to iron deficiency. Other micronutrient and non-nutritional health-related associations have also been implicated as possible causal factors.

Objective To examine the relations of serum iron, zinc, selenium and vitamin D status with hemoglobin concentrations and anemia in residents of New Zealand aged-care facilities.

Methods A cross-sectional survey of 309 rest-home level care residents from 16 aged-care facilities across New Zealand. Blood samples were analyzed for biomarkers of micronutrient status and inflammation. Multivariate regression was performed to examine the relations of micronutrient and inflammation biomarkers, and socio-demographic and health factors (BMI, medication use, malnutrition and frailty status), with hemoglobin and anemia. Direct and indirect (through zinc) associations between selenium and hemoglobin were investigated using mediation analysis.

Results Data were available for 284 residents with complete hemoglobin and micronutrient results. Mean participant age was 85.1 (± 7.7) years old and approximately two-thirds were female (67.6%). Anemia was present in 89 participants (31.3%) however, less than 2% of participants had either depleted iron stores or iron deficiency (with or without the presence of anemia).
In contrast, 81.7% and 50.7% of participants had low serum zinc (< 10.7 μmol/L) and low serum selenium concentrations (< 0.82 μmol/L), respectively.
Vitamin D deficiency (25OHD < 50 nmol/L) was low, as 75% of all residents were taking monthly high-dose vitamin D supplements.
Proton pump inhibitor (PPI) or H2 antagonist medications were prescribed for 47.4% of participants.
Being female, taking PPI or H2 antagonist medications and having a BMI ≥ 30kg/m2 were negatively associated with hemoglobin, while there was a positive association with serum zinc (P < 0.05).
Selenium had an indirect effect on hemoglobin which was mediated by zinc, with a significant effect of selenium on zinc and zinc on hemoglobin (P < 0.05). The effect of zinc explained 30.1% of the relationship between serum selenium and hemoglobin.
Low serum zinc, PPI or H2 antagonist medications and risk of malnutrition were associated with greater odds of being anemic (P < 0.05).

Conclusion High prevalence of low serum zinc is associated with a greater risk of anemia in elderly aged care residents, and mediates the effect of selenium on hemoglobin. Medications which alter iron absorption are also associated with lower hemoglobin concentrations. These findings emphasize the importance of monitoring the effect of medication on nutritional status in this vulnerable population and consideration of multiple micronutrient deficiencies when interpreting anemia.

i didn't expect to have a number of 'what now?!' reactions to this abstract. but i did and here they are:

1. serum zinc had to be BELOW < 10.7 μmol/L to be considered 'low'?!?!?! wonder if any single subject had serum zinc in the upper teens. so glad at least one of my local labs successfully flagged my 8.6 as outright deficiency (and if my level had been 10.8 or even 11.4 it would have been considered outright deficient per my local hospital too - not just 'low')
2. we're still using outright 'deficiency' at 50 nmol/L for serum 25(OH)cholecalciferol cutoff? hopefully there are subgroups in the full text analysis, such as subjects with levels above 75 nmol/l and 100 nmol/l.
3. tracking who's on PPIs (plus d3!) but not interactions with serum magnesium??

all that aside i did enjoy the extent to which this study examined interactions between different nutrients. looking forward to more research re these complex interrelationships in the body and their implications for human health care.

[jimmylegs]

i found this article by searching the literature for magnesium and d3 interactions. although it only looks at one older female patient, the data is still interesting.
the play by play:

Hypomagnesaemia due to use of proton pump inhibitors – a review
https://www.njmonline.nl/getpdf.php?id=788
Abstract
"Magnesium homeostasis is essential for many intracellular processes and depends on the balance of intestinal absorption and renal excretion. Hypomagnesaemia may arise from various disorders. We review the literature on hypomagnesaemia due to the use of proton pump inhibitors, as illustrated by a case of a 76-year-old woman with muscle cramps and lethargy caused by hypomagnesaemia and hypocalcaemia with a low parathyroid hormone level while using esomeprazole, a proton pump inhibitor (PPI). After oral magnesium repletion both abnormalities resolved. Fractional magnesium excretion was low, excluding excessive renal loss. A causal relation with PPI use was supported by the recurrence of hypomagnesaemia after rechallenge..."

ok interesting. will be good to see where the d3 enters the picture here.

Intro excerpt
"On admission the laboratory findings showed hypocalcaemia (1.26 mmol/l), hypomagnesaemia (0.18 mmol/l), hypokalaemia (3.2 mmol/l) and a low parathyroid hormone (0.9 pmol/l). Her serum vitamin D3 level was normal."

good old normal. what will the actual number be??!! let's find out...

"We started intravenous calcium and magnesium suppletion. In three days the calcium, potassium, magnesium and parathyroid hormone (PTH) level normalised and her
symptoms slowly resolved..."

sounds good, continue...

"After 11 days she was discharged with oral magnesium supplements (magnesium oxide 500 mg three times daily). Two months later the magnesium was discontinued."

holy *actual* $#!+ that poor poor woman. what a couple of months that must have been.

"Within four weeks a dramatic drop in the serum magnesium and calcium followed."

hmm whaddaya reckon that was at least in part because it wasn't taken in a form that would be readily absorbed?

"We discontinued the magnesium supplements and the esomeprazole. The serum magnesium and calcium level did not change in four weeks."

i notice the serum magnesium was circling the drain in terms of being *just* within our familiar and (not) most excellent 'normal' range.

"Because of increasing symptoms of gastro-oesophageal reflux we let her resume the esomeprazole."

hmm wonder what optimizing that serum mag level might have done for that... if someone had bothered... okay i'm still looking for that d3 connection...

"Table 1. Electrolyte balance and other biochemical data at admittance, during and after magnesium supplements and esomeprazole

................................Normal value..........Day 1........6 months
Serum magnesium.....0.65-1.05 mmol/l.....0.18..........0.67
Serum vitamin D3.........30-130 nmol/l......39.............58"

and that is literally the beginning and then end re mention of d3. no connections made in the text.

so the 'normal' serum d3 was just 39 nmol/l to begin, which is atrocious of course.
perhaps unsurprising that using mag oxide, in the context of intermittent PPI use, only allowed this patient to achieve 0.67 mmol/l magnesium in serum (which is clearly suboptimal and would be considered outright deficient at some labs i've frequented)

however, it is interesting to note that without any apparent d3 supplementation *and* with PPI medication in the picture which actively depletes magnesium levels, that a simple (if less than perfect) magnesium supplementation regimen was still associated here with a ~20nmol/L increase in serum d3 levels. fascinating, and consistent with other studies in which folks with low magnesium status have impaired d3 dose response whether from diet, sun or supplements.

[jimmylegs]

Nutritional Considerations for Healthy Aging and Reduction in Age-Related Chronic Disease
free full text: http://advances.nutrition.org/content/8/1/17.2.full.pdf

Excerpts:
"A projected doubling in the global population of people aged >60 y by the year 2050 has major health and economic implications, especially in developing regions. Burdens of unhealthy aging associated with chronic noncommunicable and other age-related diseases may be largely preventable with lifestyle modification, including diet. However, as adults age they become at risk of “nutritional frailty,” which can compromise their ability to meet nutritional requirements at a time when specific nutrient needs may be high.
This review highlights the role of nutrition science in promoting healthy aging and in improving the prognosis in cases of age-related diseases. ...

Coordinated efforts between health care policy makers, health care providers, insurance companies, and nutrition experts are needed to develop comprehensive preventive strategies based on individualized nutritional needs for older adults. Incorporation of “nutrition physical” or screening into the yearly physical examination of older adults will provide the foundation for developing the preventive measures needed."

[jimmylegs]

OT but still auto-immune stuff so:

Decreased zinc in the development and progression of malignancy: an important common relationship and potential for prevention and treatment of carcinomas
free full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5183570/
Abstract
Introduction
Efficacious chemotherapy does not exist for treatment or prevention of prostate, liver, and pancreatic carcinomas, and some other cancers that exhibit decreased zinc in malignancy. Zinc treatment offers a potential solution; but its support has been deterred by adverse bias.
Areas covered
1. The clinical and experimental evidence for the common ZIP transporter/Zn down regulation in these cancers.
2. The evidence for a zinc approach to prevent and/or treat these carcinomas.
3. The issues that introduce bias against support for the zinc approach.
Expert opinion
1. ZIP/Zn downregulation is a clinically established common event in prostate, hepatocellular and pancreatic cancers.
2. Compelling evidence supports the plausibility that a zinc treatment regimen will prevent development of malignancy and termination of progressing malignancy in these cancers; and likely other carcinomas that exhibit decreased zinc.
3. Scientifically-unfounded issues that oppose this ZIP/Zn relationship have introduced bias against support for research and funding of a zinc treatment approach.
4. The clinically-established and supporting experimental evidence provide the scientific credibility that should dictate the support for research and funding of a zinc approach for the treatment and possible prevention of these cancers.
5. This is in the best interest of the medical community and the public-at-large.

re item 3 above, this article is cited as being behind much of the opposition to zinc therapy for cancer:

Zinc Supplement Use and Risk of Prostate Cancer
https://academic.oup.com/jnci/article/9 ... ate-Cancer
Abstract
The high concentration of zinc in the prostate suggests that zinc may play a role in prostate health. We examined the association between supplemental zinc intake and prostate cancer risk among 46 974 U.S. men participating in the Health Professionals Follow-Up Study. During 14 years of follow-up from 1986 through 2000, 2901 new cases of prostate cancer were ascertained, of which 434 cases were diagnosed as advanced cancer. Supplemental zinc intake at doses of up to 100 mg/day was not associated with prostate cancer risk. However, compared with nonusers, men who consumed more than 100 mg/day of supplemental zinc had a relative risk of advanced prostate cancer of 2.29 (95% confidence interval = 1.06 to 4.95; Ptrend = .003), and men who took supplemental zinc for 10 or more years had a relative risk of 2.37 (95% confidence interval = 1.42 to 3.95; Ptrend<.001). Although we cannot rule out residual confounding by supplemental calcium intake or some unmeasured correlate of zinc supplement use, our findings, that chronic zinc oversupply may play a role in prostate carcinogenesis, warrant further investigation.

yep TONS of something is bad, so deficit must be okay... ?!?!?! also wonder if these gents were making sure their zinc intake didn't throw anything else, like copper say, out of whack over their ten year supplementation period (doubtful right)? i'll have to dig in and check out if they mean >100mg/d AND >10 yrs, or >100mg/d OR >10 yrs and if the latter, what intakes represented chronic oversupply. and if they bothered to check out copper status at all.

potentially related piece of the puzzle?
SERUM COPPER AND ZINC AND THE RISK OF DEATH FROM CANCER AND CARDIOVASCULAR DISEASE (1988)
https://academic.oup.com/aje/article-ab ... /352/61085
Abstract
To investigate the association of serum copper and zinc with mortality from cancer and cardiovascular disease, the authors performed a case-control analysis of data obtained in a Dutch prospective follow-up study. Cancer (n = 64) and cardiovascular disease (n = 62) deaths and their matched controls were taken from a cohort of 10,532 persons examined in 1975–1978. Trace elements were measured in baseline serum samples, which had been stored during the six to nine years of follow-up. The adjusted risk of death from cancer and cardiovascular disease was about four times higher for subjects in the highest serum copper quintile (>1.43 mg/liter) compared with those with normal levels. The excess mortality observed in subjects with low copper status suggests a U-shaped relation. No significant change in the risk of death from cancer and cardiovascular disease was found for subjects with low or high baseline levels of serum zinc. However, a protective effect of a high zinc status on the risk of cancer and cardiovascular disease is compatible with the data. For definitive conclusions, analysis of larger prospective data sets is recommended.

GOOD. too much AND too little copper problematic. got it.

interesting new cancer research:

Influencing the Tumor Microenvironment: A Phase II Study of Copper Depletion Using Tetrathiomolybdate in Patients with Breast Cancer at High Risk for Recurrence and in Preclinical Models of Lung Metastases (2017)
http://clincancerres.aacrjournals.org/content/23/3/666
...This study targets copper-dependent processes within the tumor microenvironment known to be critical for establishment of the premetastatic niche in a cohort of patients with breast cancer at high risk of relapse. The premetastatic niche constitutes a local microenvironment that provides optimal infrastructure for disseminated tumor cells to colonize and grow. Using a copper depletion strategy that targets copper-dependent processes critical for creating this niche, we show a markedly reduced infrastructure critical for tumor progression...

crazy thought - what if there were oh, i dunno, some kind of essential nutrient that would handily deplete copper for us??? i wonder how the serum copper levels in the copper zinc study ^^ line up with the depletion levels achieved in the last study above ^. and what the serum copper zinc ratios look like in both cases.

[jimmylegs]

The Evidence for a Beneficial Role of Vitamin A in Multiple Sclerosis
https://link.springer.com/article/10.10 ... 014-0148-4
Vitamin A is an essential nutrient with important roles in immunological responses and in brain development. Its main metabolite is retinoic acid (RA), which is responsible for the neuroimmunological functions related to vitamin A. In the brain, RA is known to have interactions with other nuclear receptor-mediated signalling pathways. RA is involved in plasticity, regeneration, cognition and behaviour. In the peripheral blood, RA plays a major role both in increasing tolerance and in decreasing inflammation, through balancing T-lymphocyte populations. It is likely that RA synthesis may be manipulated by complex cross-talk among cells during infection and inflammation. The role of vitamin A in multiple sclerosis (MS) could be dual: at the same time as it decreases inflammation and increases tolerance of autoimmunity, it may also help in brain protection. The present review discusses the beneficial effects that vitamin A might have for controlling MS, although it must be clearly stated that, at the present time, there is no clear indication for using vitamin A as a treatment for MS. However, the results from the present review should encourage clinical trials with vitamin supplementation as a potential treatment or as an add-on option. Vitamin A acts in synergy with vitamin D, and the immunological homeostasis ensured by these vitamins should not be unbalanced in favour of only one of them.

[jimmylegs]

Increasing serum levels of vitamin A, D and E are associated with alterations of different inflammation markers in patients with multiple sclerosis
https://journals-scholarsportal-info.pr ... mipwms.xml

"Our main findings are that
(i) rising 25(OH)D (vitamin D) levels are positively associated with IL-1Ra and sFRP3, but only before IFN-β treatment,
(ii) rising retinol (vitamin A) levels are negatively associated with PTX3 both before and during IFN-β treatment and
(iii) rising α-tocopherol (vitamin E) levels are positively associated with CXCL16 levels, but only during IFN-β treatment."

well doesn't this just remind me of the old days immediately post-dx... off to wikipedia ;)

https://en.wikipedia.org/wiki/Interleuk ... antagonist
... a natural inhibitor of the pro-inflammatory effect of IL1β

https://www.ncbi.nlm.nih.gov/pubmed/28240822
Reduced skeletal muscle secreted frizzled-related protein 3 is associated with inflammation and insulin resistance

https://en.wikipedia.org/wiki/PTX3
PTX3 behaves as an acute phase response protein, as the blood levels of PTX3, low in normal conditions (about 25 ng/mL in the mouse, < 2 ng/mL in humans), increase rapidly (peaking at 6–8 h after induction) and dramatically (200–800 ng/mL) during endotoxic shock, sepsis and other inflammatory and infectious conditions, correlating with the severity of the disease. Under these conditions, PTX3 is a rapid marker for primary local activation of innate immunity and inflammation

no time for CXCL16 atm, but suspect for now that increase = good.

[jimmylegs]

encountered this study while looking for research on anxiety and magnesium.

thought here would be the most suitable place on the forum to file this tidbit.

Effects of zinc and magnesium supplements on postpartum depression and anxiety: A randomized controlled clinical trial
http://www.tandfonline.com/doi/abs/10.1 ... 16.1235074
ABSTRACT
"Postpartum anxiety and depression are prevalent disorders. The authors of this study aimed to determine the effects of zinc and magnesium supplements on depressive symptoms and anxiety in postpartum women referred to three governmental, educational hospitals in Tabriz, Iran during 2014–2015. In this triple-blind, randomized, controlled clinical trial, the participants were randomly assigned to the zinc sulfate, magnesium sulfate, and placebo groups (n = 33 per group). The intervention groups received a 27-mg zinc sulfate tablet or 320-mg magnesium sulfate tablet per day for 8 weeks, whereas the control group received a placebo tablet each day during the same period. The Edinburgh Postnatal Depression Scale and the Spielberger State-Trait Anxiety Inventory were completed before and 8 weeks after the intervention. Blood samples were drawn from each participant to determine serum levels of zinc and magnesium before intervention at 48 hours after delivery. Also, a 24-hour dietary questionnaire was used during the first and last 3 days of the intervention. Adjusting for baseline scores as well as zinc and magnesium serum levels, no significant difference was observed between groups 8 weeks after delivery in mean scores of depressive symptoms (p = .553), state anxiety (p = .995), and trait anxiety (p = .234). This study concluded magnesium and zinc did not reduce postpartum anxiety and depressive symptoms."

i found this an annoying read due to the study design.

luckily, the authors do review the many studies which counter their findings in the full text discussion, and did pick up on the main issues as noted in the full text's conclusion:

"Conclusion
Considering the results of the present study, which indicated that zinc and magnesium supplements cannot prevent postpartum depressive symptoms and anxiety in non-depressed women, it is recommended that the effects of these two supplements with different doses and with longer follow-ups should be evaluated in future studies. In addition, administration of these supplements should be accompanied by studying their serum levels before and after the intervention"

we already knew that before and after piece, which has been previously included in best practice recommendations for nutrition studies. tsk tsk, edalati fard et al. let's hope we don't have to deal with this particular kind of limitation in future.

given the above, proposed abstract revision:

original - "This study concluded magnesium and zinc did not reduce postpartum anxiety and depressive symptoms."

revision - "Magnesium and zinc, in the formulations and doses used in this study, did not reduce postpartum anxiety and depressive symptoms."

(now that's not to say mg and zinc won't get thrown out with bathwater anyway - other abstracts that read like the proposed revision above have still been used to vilify certain nutrients when it was clearly the formulation causing the problem).

[jimmylegs]

well that would be one of the highest serum mag levels i've ever seen in a healthy controls group.

this is of course assuming, given that the authors do not seem to have specified (!?!), that the units are mg/dl. (if any other typical units, the results are even higher levels).

Evaluation of 25(OH) Vitamin D3 with Reference to Magnesium Status and Insulin Resistance in T2DM
free full text https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3879824/



!!!

[Zyklon]

I guess something is wrong. 3.36 is way too much and 19.55 D3 is alarming for healthy controls.

[jimmylegs]

something's weird. mind you they do specify "Hypovitaminosis D is defined as that, wherein the levels of 25(OH) Vitamin D3 are below 25ng/ml."
healthy controls is a relative thing - it is another situation in which healthy does not mean optimal. it just means 'without type 2 diabetes' in this case

i wouldn't normally expect ppl with super high mag levels to have d3 levels in the basement. d3 intake is either *super* low across the board, or there's some kind of mistake.

[jimmylegs]

Effect of Zinc Supplementation on Growth Performance, Intestinal Development, and Intestinal Barrier-Related Gene Expression in Pekin Ducks (2018)
https://www.ncbi.nlm.nih.gov/pubmed/28895044

Abstract
The current study was conducted to investigate the effect of zinc supplementation on the growth performance, intestinal morphology, and the transcription of the barrier function related genes in Pekin ducks. Seven-hundred and sixty-eight 1-day-old Pekin ducks were randomly assigned into six dietary treatments. Each treatment had eight replicates with 16 ducks per replicates. The ducks were fed either a corn-soybean meal basal diet or basal diets supplemented with 15, 30, 60, 120, and 240 mg zinc/kg from zinc sulfate. This experiment lasted for 5 weeks, and the jejunum sample were harvested at 14 and 35 days of age. Results have shown that diets supplemented with zinc significantly increased the duck body weight, average daily gain, and average daily feed intake in different period of experiment (P < 0.05); feed to gain ratio was decreased as the zinc level increased (P < 0.05). Zinc supplementation increased the villus height and decreased the crypt depth in jejunum of ducks (P < 0.05) at 14 and 35 days of age. The transcription of tight junction protein CLDN1, OCND, ZO-1, and ZO-3 in jejunum were increased (P < 0.05), and the messenger RNA (mRNA) levels of leak protein CLDN2 were decreased as the dietary zinc level increased (P < 0.05) at 14 and 35 days of age. The mRNA levels of chemical barrier-related genes MUC2 and TFF-2 in jejunum at 14 and 35 days of age were increased (P < 0.05) by zinc supplementation, and so did the transcription of immunological barrier-related genes lgA, pIgR, LYZ, and AvBD2 (P < 0.05). In conclusion, dietary zinc supplementation exhibited growth-promoting effect on Pekin duck, improved intestinal morphology, and enhanced the intestinal barrier integrity.

[jimmylegs]

Recent Updates in Imperative Natural Compounds for Healthy Brain and Nerve Function: A Systematic Review of Implications for Multiple Sclerosis
http://www.ingentaconnect.com/contenton ... 3/art00006

Background: The evolution of the Green movement in western society has changed attitudes in the general population who now perceive natural compounds as being inherently harmless and more desirable than artificial chemical products.

Objective: Considering the growing interest towards introducing naturally emerged medicines, the purpose of this review was to overview the ongoing research into prevention and treatment of multiple sclerosis (MS) lesions.

Method: This review was carried out by searching bibliographic databases such as PubMed and Scopus for studies reported between 1st January 2008 to 30th January 2016 on MS patients or animal models of MS, investigating the beneficial effects of natural compounds in MS treatment. In this updated systematic review, the search terms were “multiple sclerosis” or “neurodegeneration” and (“natural compounds” or “medicinal plants”, “traditional medicine” or “native medicine”).

Results: Studies with vitamins (A, B12, D, H), minerals (selenium and lithium), n-3 PUFAs, lipoic acid, statins, resveratrol, marijuana, EGCG and some probiotics have shown significant helpful effects in MS by preventing or delaying the onset of disease. Other natural compounds such as xanthines, anthocyanins, glucosinolates, isoflavones, organosulfurs, steroid glycosides, and alkaloids have also shown protective effects in the treatment of MS in animal models. Adverse effects were also reported in some of the experiments.

Conclusion: Further studies with a focus on the molecular mechanisms of the protective natural compounds are needed to decrease possible side effects and to develop new medicines for MS. Apigenin, chrysin, baicalein, cyanidin, flavone glycoside, daidzein, coumestrol, sulforaphane, bee venom and huperzine A are the candidates for more prospective investigations.