Kategoriarkiv: Forskning og artikler

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Sleep in Elite Athletes and Nutritional Interventions to Enhance Sleep

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Beskriver forskjellige måter søvn påvirker atleter, og hvordan søv påvirkes av mat. Nevner at høykarbo mat må inntaes minimum 1t før leggetid.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4008810/

The same research group also increased the sleep time of swimmers from their usual sleep amount to 10 h per night for 6–7 weeks. Following this period, 15 m sprint, reaction time, turn time, and mood all improved [30].

Waterhouse et al. [31] investigated the effects of a lunchtime nap on sprint performance following partial sleep deprivation (4 h of sleep). Following a 30-min nap, 20 m sprint performance was increased, alertness was increased, and sleepiness was decreased when compared with the no-nap trial. In terms of cognitive performance, sleep supplementation in the form of napping has been shown to have a positive influence on cognitive tasks following a night of sleep deprivation (2 h) [32]. Naps can markedly reduce sleepiness and can be beneficial when learning skills, strategy or tactics [32]. Napping may also be beneficial for athletes who have to wake early routinely for training or competition and those who are experiencing sleep deprivation [32].

Pain Perception

It is well accepted that individuals with chronic pain frequently report disturbed sleep (changes in continuity of sleep as well as sleep architecture). However, there is also recent evidence suggesting that sleep deprivation may cause or modulate acute and chronic pain [36]. Sleep deprivation may thus enhance or cause pain, and pain may disturb sleep by inducing arousals during sleep. A cycle may then eventuate, starting with either pain or sleep deprivation, with these two issues maintaining or augmenting each other [36].

Athletes may experience pain as a result of training, competition and/or injury. Evidence, although minimal at this stage, suggests that athletes may also have lower sleep quality and quantity than the general population [16]. Therefore, appropriate pain management as well as adequate sleep is likely to be very important for athletes from both a pain and sleep perspective.

A small number of studies have investigated the effects of carbohydrate ingestion on indices of sleep quality and quantity. Porter and Horne [52] provided six male subjects with a high-carbohydrate meal (130 g), a low-carbohydrate meal (47 g), or a meal containing no carbohydrate, 45 min before bedtime. The high-carbohydrate meal resulted in increased REM sleep, decreased light sleep, and wakefulness [52].

Practical Applications

In the first instance, athletes should focus on utilizing good sleep hygiene to maximize sleep quality and quantity. While research is minimal and somewhat inconclusive, several practical recommendations may be suggested:

  • High GI foods such as white rice, pasta, bread, and potatoes may promote sleep; however, they should be consumed more than 1 h before bedtime.
  • Diets high in carbohydrate may result in shorter sleep latencies.
  • Diets high in protein may result in improved sleep quality.
  • Diets high in fat may negatively influence total sleep time.
  • When total caloric intake is decreased, sleep quality may be disturbed.
  • Small doses of tryptophan (1 g) may improve both sleep latency and sleep quality. This can be achieved by consuming approximately 300 g of turkey or approximately 200 g of pumpkin seeds.
  • The hormone melatonin and foods that have a high melatonin concentration may decrease sleep onset time.
  • Subjective sleep quality may be improved with the ingestion of the herb valerian; however, as with all supplements, athletes should be aware of potential contaminants as well as the inadvertent risk of a positive drug test.
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Mitochondriogenesis and apoptosis: possible cause of vitamin A-mediated adipose loss in WNIN/Ob-obese rats

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Denne nevner at kronisk tilskudd av Vitamin A på 53mg/kg øker produksjon av mitokondrier og derigjennom bidrar til vektnedgang. Denne dosen blir 5300mg for en på 100kg. Studien nevner også at A vitamin aktiverer «uncouling protein» (UCP1) i mitokondriene som bidrar til termogenese (produksjon av varme i cellen). Det betyr at metabolismen øker men uten at man produserer mer frie radikaler.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4190477/

Background

Previously, we reported that vitamin A-enriched diet (129 mg/kg diet) intake reduces the adiposity development in obese rats of WNIN/Ob strain. Here, we hypothesize that dose lesser than 129 mg of vitamin A/kg diet would also be effective in ameliorating the development of obesity in these rats.

Methods

Five-month-old male lean and obese rats designated as A & B were divided into four subgroups (I, II, III and IV) consisting of 8 rats from each phenotype and received diets containing 2.6 mg (control group), 26 mg, 52 mg and 129 mg vitamin A/kg diet as retinyl palmitate for 20 weeks. Body composition and morphological analysis of brown adipose tissue (BAT) was analyzed. Expression of uncoupling protein 1 (UCP1), retinoic acid receptor α (RARα) and retinoid X receptor α (RXRα) in BAT and levels of Bcl2 and Bax in epididymal white adipose tissue (eWAT) were determined by immunoblotting.

Results

Vitamin A supplementation to obese rats at doses of 52 and 129 mg/kg diet showed reduced body weight gain and adiposity compared to control diet-fed obese rats receiving 2.6 mg of vitamin A/kg diet. In BAT of obese rats, vitamin A supplementation at doses of 26 and 52 mg of vitamin A/kg diet resulted in increased UCP1 expression with concomitant decrease in RARα and RXRα levels compared to control diet-fed obese rats. Further, transmission electron microscopy study revealed an increase in number of BAT mitochondria of obese rats supplemented with 26 and 52 mg of vitamin A/kg diet. Also, obese rats fed on 52 mg/kg diet resulted in increased apoptosis by altering the ratio of Bcl2 to Bax protein levels in eWAT. Notably, most of these changes were not observed in lean rats fed vitamin A-enriched diets.

Conclusion

In conclusion, chronic consumption of 52 mg of vitamin A/kg diet seems to be an effective dose in ameliorating obesity possibly through mitochondriogenesis, UCP1-mediated thermogenesis in BAT and apoptosis in eWAT of obese rats. Therefore, the role of dietary vitamin A in correcting human obesity would be of unquestionable relevance and can only be addressed by future studies.

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The effect of vitamin A supplementation on thyroid function in premenopausal women.

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Tyroid problemer er svært vanlig. Det gir trøtthet, depresjon, lav energi, og et hav av medfølgende plager. En viktig del av øke tyroidea ar å få nok A-vitamin. Her er en studie som nevner at 25000 IU A-vitamin (7500mg) gir en signifikant reduksjon i TSH (som hemmer tyroidea).

http://www.ncbi.nlm.nih.gov/pubmed/23378454

OBJECTIVE:

Vitamin A and its retinoid derivates play an important role in regulation of normal growth and development. Vitamin A has been shown to regulate thyroid hormone metabolism and inhibit thyroid-stimulating hormone (TSH) secretion via down regulation of TSH-β gene expression; however, the effect of vitamin A on thyroid function in obese individuals who are at higher risk of subclinical hypothyroidism is still unclear. In the present study we investigate the impact of vitamin A supplementation on thyroid function in obese women.

METHOD:

A 4-month randomized, double blind controlled trial was conducted among 84 healthy women aged 17-50 years old: 56 were obese (body mass index [BMI] 30-35 kg/m(2)) and 28 were nonobese (BMI 18.5-24.9 kg/m(2)). Obese women were randomly allocated to receive either vitamin A (25,000 IU/d retinyl palmitate) or placebo. Nonobese women received vitamin A. At baseline and 4 months after intervention, serum concentrations of TSH, total thyroxine (T4), total triiodothyronine (T3), retinol-binding protein (RBP), and transthyretin (TTR) were measured.

RESULTS:

Baseline concentrations of thyroid hormones, RBP and TTR were not significantly different between groups. Vitamin A caused a significant reduction in serum TSH concentrations in obese (p = 0.004) and nonobese (p = 0.001) groups. Serum T3 concentrations also increased in both obese and nonobese vitamin A-treated groups (p < 0.001). Serum T4 decreased in all 3 groups after treatment. The results showed a significant reduction in serum RBP in the obese group after vitamin A supplementation (p = 0.007), but no significant change was seen in serum TTR.

CONCLUSIONS:

Serum TSH concentrations in vitamin A-treated subjects were significantly reduced; therefore, vitamin A supplementation might reduce the risk of subclinical hypothyroidism in premenopausal women.

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Elevated Inflammatory Markers in Response to Prolonged Sleep Restriction Are Associated With Increased Pain Experience in Healthy Volunteers

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Denne nevner at 10 dager med redusert søvn (4 timer) øker betennelsesfaktorer i kroppen. 4 timers søvn er svært lite og de fleste sover nok mer enn dette, men studien nevner at 25% reduksjon (6 timer) også gir en økning i betennelsesfaktorer, dog ikke like kraftig.

Den nederste grafen viser hvordan ubehag i kroppen henger sammen med økning i betennelsesfaktorer.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1978405/

Conclusion:

Insufficient sleep quantity may facilitate and/or exacerbate pain through elevations of IL-6. In disorders where sleep disturbances are common, insufficient sleep quantity itself may establish and maintain its co-occurrence with pain and increased inflammation.

Acute sleep loss of up to 3 nights15,17,18 as well as more commonly experienced forms of sleep loss, i.e., sleep reduced by 25%-50% across consecutive days,18,19 have been shown to induce an increase of interleukin-6 (IL-6) and C-reactive Protein (CRP) levels. In addition, increased levels of IL-6 have been found in patients suffering from primary insomnia.20,21

Pain is a hallmark of inflammatory processes. Prostaglandins, in particular PGE2, are classical pain mediators, but in the last decade a variety of novel pain modulators have been identified. For example, proinflammatory cytokines such as interleukin-6 (IL-6) and tumor necrosis factor α (TNF-α) have been found to be potent pain-inducing and pain-facilitating agents, able to sensitize primary sensory neurons.26

Ten days of sleep restriction to 50% of the habitual time led to an IL-6 increase of 1.16 pg/mL in the current study. Sleep restriction to approximately 25% of usual sleep time over one week has been found to lead to a slightly smaller IL-6 increase of 0.75 pg/mL compared to the present result.19 This may suggest a dose-response relationship between chronicity/severity of sleep restriction and elevation of IL-6 levels, and warrants further investigation.

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Pain Sensitivity and Recovery From Mild Chronic Sleep Loss

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Denne viser at økt søvnmengde reduserer smerte. Ved å øke antall timer søvn fra (under) 8 timer til 10 timer ble deltakerene mindre sensitive for smertestimuli. Den nevner også at vi sover mindre nå enn vi gjorde på 60-tallet. Nå er vi nede i 6 timer eller mindre, mens på 60-tallet sov vi 8 timer eller mindre. Den nevner også vi vi får 24%-31% mindre smertetåleranse om vi får 50% dårligere søvn 1 enkelt natt.

Studien beskriver at 4 dager med 10 timers søvn reduserer smertesensitivitet med 25%.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3490359/

Abstract

Study Objectives:

To determine whether an extended bedtime in sleepy and otherwise healthy volunteers would increase alertness and thereby also reduce pain sensitivity.

Setting:

Outpatient with sleep laboratory assessments.

Participants and Interventions:

Healthy volunteers (n = 18), defined as having an average daily sleep latency on the Multiple Sleep Latency Test (MSLT) < 8 min, were randomized to 4 nights of extended bedtime (10 hr) (EXT) or 4 nights of their diary-reported habitual bedtimes (HAB). On day 1 and day 4 they received a standard MSLT (10:00, 12:00, 14:00, and 16:00 hr) and finger withdrawal latency pain testing to a radiant heat stimulus (10:30 and 14:30 hr).

Results:

During the four experimental nights the EXT group slept 1.8 hr per night more than the HAB group and average daily sleep latency on the MSLT increased in the EXT group, but not the HAB group. Similarly, finger withdrawal latency was increased (pain sensitivity was reduced) in the EXT group but not the HAB group. The nightly increase in sleep time during the four experimental nights was correlated with the improvement in MSLT, which in turn was correlated with reduced pain sensitivity.

Conclusions:

These are the first data to show that an extended bedtime in mildly sleepy healthy adults, which resulted in increased sleep time and reduced sleepiness, reduces pain sensitivity.

In the 1960s sleep duration was estimated to be approximately 8 hr per 24-hr period, whereas by 2005 it was reported that sleep duration was 7 hr or less.3 A national survey reported that 21% of the population obtains 6 hr or less of sleep per 24-hr period.4

Partial deprivation, the reduction of bedtime by 50% for one night, reduced finger withdrawal latency (increased pain sensitivity) to a radiant heat stimulus by 24%.7

In the EXT group of the current study finger withdrawal latency was increased by 25%, which reflects a reduction in pain sensitivity.

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Exploring the associations between sleep problems and chronic musculoskeletal pain in adolescents: A prospective cohort study

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Denne nevner at søvnproblemer i ungdommen gir utgangspunkt for smerteproblemer senere i livet. Det er vanlig å tro at smerteproblemer gir søvnproblemer, men denne viser at søvnproblemer ofte kommer før smerteproblemer.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4197758/

Abstract

BACKGROUND:

The prevalence of musculoskeletal chronic pain in adolescents is estimated to be approximately 4% to 40%. The development of musculoskeletal pain during teenage years could have a marked impact on physical, psychological and social well-being.

OBJECTIVE:

To examine whether sleep problems during adolescence are associated with musculoskeletal pain, particularly chronic regional pain and chronic widespread pain.

METHODS:

Using data from the Avon Longitudinal Study of Children, the relationship between sleep problems at 15 years of age and the presence of chronic regional and widespread pain at 17 years of age was explored. Pain data were not available at 15 years of age. A total of 2493 participants with complete data were identified. Relationships among sleep problems and musculoskeletal pain were examined using logistic regression. ORs were calculated after adjusting for sex, ethnicity, socioeconomic position and depression (15 years of age).

RESULTS:

Sleep disturbance (usually wakes up more than two or three times), difficulties with hypersomnolence and poor subjective sleep perception were associated with the presence of both musculoskeletal regional and widespread pain. Finally, using ordered logistic regression, poor subjective sleep perception was also found to be associated with greater pain severity in participants with chronic musculoskeletal regional and widespread pain.

DISCUSSION:

The results of the present study suggest an association between sleep problems during adolescence and the presence of musculoskeletal pain at a later stage. These findings are consistent with adult literature suggesting a link between sleep problems and musculoskeletal pain. Given these associations, sleep problems in adolescence may be an important risk factor for musculoskeletal pain.

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Motor Imagery in People With a History of Back Pain, Current Back Pain, Both, or Neither

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Nevner at for mennesker med ryggsmerte er hjernens opplevelse av kroppen og dens bevegelser dårligere. Hjernens kart over kroppen blir utydelig. Dette kartet er noe av det første vi vil gjenopprette. Det er en viktig del av behandling, og en av de viktigste årsakene til at vi anbefaler daglige øvelser, som f.eks. Foundation trening.

http://www.ncbi.nlm.nih.gov/pubmed/24535054

Introduction:

There is mounting evidence that cortical maps are disrupted in chronic limb pain and that these disruptions may contribute to the problem and be a viable target for treatment. Little is known as to whether this is also the case for the most common and costly chronic pain—back pain.

Objectives:

To investigate the effects of back pain characteristics on the performance of left/right trunk judgment tasks, a method of testing the integrity of cortical maps.

Methods:

A total of 1008 volunteers completed an online left/right trunk judgment task in which they judged whether a model was rotated or laterally flexed to the left or right in a series of images.

Results:

Participants who had back pain at the time of testing were less accurate than pain-free controls (P=0.027), as were participants who were pain free but had a history of back pain (P<0.01). However, these results were driven by an interaction such that those with current back pain and a history of back pain were less accurate (mean [95% CI]=76% [74%-78%]) than all other groups (>84% [83%-85%]).

Discussion:

Trunk motor imagery performance is reduced in people with a history of back pain when they are in a current episode. This is consistent with disruption of cortical proprioceptive representation of the trunk in this group. On the basis of this result, we propose a conceptual model speculating a role of this measure in understanding the development of chronic back pain, a model that can be tested in future studies.

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Neuropathic pain: diagnosis, pathophysiological mechanisms, and treatment

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Denne nevner det aller meste om diagnostisering og behandling av nevropatiske smerter. Her fokuseres på medisiner, men de nevner at en interdisiplinær behandling er viktig.

http://www.thelancet.com/journals/laneur/article/PIIS1474-4422(10)70143-5/fulltext

Neuropathic pain develops as a result of lesions or disease affecting the somatosensory nervous system either in the periphery or centrally. Examples of neuropathic pain include painful polyneuropathy, postherpetic neuralgia, trigeminal neuralgia, and post-stroke pain. Clinically, neuropathic pain is characterised by spontaneous ongoing or shooting pain and evoked amplified pain responses after noxious or non-noxious stimuli. Methods such as questionnaires for screening and assessment focus on the presence and quality of neuropathic pain. Basic research is enabling the identification of different pathophysiological mechanisms, and clinical assessment of symptoms and signs can help to determine which mechanisms are involved in specific neuropathic pain disorders. Management of neuropathic pain requires an interdisciplinary approach, centred around pharmacological treatment. A better understanding of neuropathic pain and, in particular, of the translation of pathophysiological mechanisms into sensory signs will lead to a more effective and specific mechanism-based treatment approach.

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Lions Mane sopp

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Lions Mane er en matsopp som har vist seg å kunne stimulere NGF (Nerve Growth Factor) og bidra til å reparere skader på nerver, samt dempe betennelse og beskytte mot skader på nerver. En sært interessant medisinsk sopp som har noe forskning bak seg.

Examine.com sin komplette gjennomgang: http://examine.com/supplements/Yamabushitake/

Nevner at man kan ta 3000mg daglig.

Medicinal properties of Hericium erinaceus and its potential to formulate novel mushroom-based pharmaceuticals.

Hericium erinaceus (Bull.: Fr.) Pers., a medicinal mushroom, activates peripheral nerve regeneration.

H. erinaceus is capable of promoting peripheral nerve regeneration after injury.

Anti-inflammatory activity of mycelial extracts from medicinal mushrooms.

These results indicate that extracts from medicinal mushrooms exhibited anti-inflammatory activity that might be attributable to the inhibition of NO generation and can therefore be considered a useful therapeutic and preventive approach to various inflammation-related diseases.

Hericium erinaceus (Bull.: Fr) Pers. cultivated under tropical conditions: isolation of hericenones and demonstration of NGF-mediated neurite outgrowth in PC12 cells via MEK/ERK and PI3K-Akt signaling pathways.

Taken together, this study suggests that hericenone E potentiated NGF-induced neuritogenesis in PC12 cells via the MEK/ERK and PI3K/Akt pathways.

Protective effects of Hericium erinaceus mycelium and its isolated erinacine A against ischemia-injury-induced neuronal cell death via the inhibition of iNOS/p38 MAPK and nitrotyrosine. Hele studien her: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4200813/

These findings confirm the nerve-growth properties of Hericium erinaceus mycelium, which include the prevention of ischemic injury to neurons; this protective effect seems to be involved in the in vivo activity of iNOS, p38 MAPK and CHOP.

Hericium erinaceus (Yamabushitake): a unique resource for developing functional foods and medicines.

 In this article, we provide an overview of the biochemical and pharmacological studies on HE, especially of its antitumor and neuroprotective functions, together with a survey of recent developments in the chemical analysis of its polysaccharides, which comprise its major active components.

Neurotrophic properties of the Lion’s mane medicinal mushroom, Hericium erinaceus (HigherBasidiomycetes) from Malaysia.

In conclusion, the aqueous extract of H. erinaceus contained neuroactive compounds which induced NGF-synthesis and promoted neurite outgrowth in NG108-15 cells.

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Informasjon om Palmitoyletanolamide

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Palmitoylethanolamide (PEA) er et svært interessant produkt som har mye forskning bak seg, men er svært lite kjent og lite tilgjengelig. I Italia, Spania og Tyskland selges det som «mat til medisinsk formål», mens i Nederland selges det som kosttilskudd, men da uten noen påstander knyttet til produktet.

Det kan bestilles fra Nederland her: http://www.rs4supplements.com/en/peapure-capsules-info

PEA er et naturlig fettstoff som kroppen produserer selv. Det finnes i mange matvarer, særlig i kjøtt, egg, soyabønner og andre peanøtter.

Kroppen produserer PEA spesielt ved betennelsestilstander, og man ser det øker i konsentrasjon lokalt der betennelsen er. PEA har en beskyttende rolle i en betennelsestilstand. Men om betennelsestilstandende vedvarer kan kroppens naturlige PEA brukes opp. Da får man mindre beskyttelse og det blir lettere å få andre plager eller vedvarende plager. Siden det er kosttilskudd må man regne med å bruke minst 2-3 måneder for å se om det hjelper.

PEA gjør at kroniske betennelsesreaksjoner lettere kan brytes slik at regenerering kan inntre igjen. PEA er spesielt interessant fordi det virker på nervetråder. Nevropati (ødelagte nervetråder) er en svært vanskelig tilstand å behandle, men PEA har potensiale til å være både et effektivt og bivirkningsfri tilskudd for å starte regenereringen av nervetråder. PEA er et endokannabinoid-lignende stoff. Man får alle de medisinske og smertedempende effektene lik kannabinoider, men uten noen form for rus.

Her er en lang rekke med studier som har blitt gjort på nevropati og PEA:

Micronized palmitoylethanolamide reduces the symptoms of neuropathic pain in diabetic patients. (Free in PMC)

These results suggest that PEA-m could be considered as a promising and well-tolerated new treatment for symptomatology experienced by diabetic patients suffering from peripheral neuropathy.

Chronic idiopathic axonal neuropathy and pain, treated with the endogenous lipid mediator palmitoylethanolamide: a case collection. (Free in PMC)

In all these patients, PEA reduced pain significantly, without side effects. PEA can be administered in addition to other analgesics, without negative drug-drug interactions, or can be used as a stand-alone analgesic. Due to a favorable ratio between efficacy and safety, PEA should be considered more often as a treatment for neuropathic pain.

Palmitoylethanolamide is a disease-modifying agent in peripheral neuropathy: pain relief and neuroprotection share a PPAR-alpha-mediated mechanism. (Free in PMC)

These results strongly suggest that PEA, via a PPAR- α -mediated mechanism, can directly intervene in the nervous tissue alterations responsible for pain, starting to prevent macrophage infiltration.

Therapeutic utility of palmitoylethanolamide in the treatment of neuropathic pain associated with various pathological conditions: a case series. (Free in PMC)

Probably due to the fact that PEA is an endogenous modulator as well as a compound in food, such as eggs and milk, no serious side effects have been reported, nor have drug-drug interactions.

Palmitoylethanolamide restores myelinated-fibre function in patients with chemotherapy-induced painful neuropathy.

In a severe condition such as painful neuropathy associated with multiple myeloma and chemotherapy, a safe substance such as PEA provides significant restoration of nerve function.

Use of palmitoylethanolamide in the entrapment neuropathy of the median in the wrist.

The data support the hypothesis of protection against inflammatory and neuropathic pain by PEA.

Palmitoylethanolamide in CNS health and disease.

Overall, the integration of these different modes of action allows PEA to exert an immediate and prolonged efficacious control in neuron signaling either on inflammatory process or neuronal excitability, maintaining cellular homeostasis.

Palmitoylethanolamide, a naturally occurring disease-modifying agent in neuropathic pain.

Collectively, the findings presented here propose that palmitoylethanolamide merits further consideration as a disease-modifying agent for controlling inflammatory responses and related chronic and neuropathic pain.

Mast cells, glia and neuroinflammation: partners in crime?

N-Palmitoylethanolamine has proven efficacious in mast-cell-mediated experimental models of acute and neurogenic inflammation.

Her er en rekke studier som har blitt gjort på betennelser og PEA:

Gastric bypass in morbid obese patients is associated with reduction in adipose tissue inflammationvia N-oleoylethanolamide (OEA)-mediated pathways.

Palmitoylethanolamide regulates development of intestinal radiation injury in a mast cell-dependent manner.

Palmitoylethanolamide normalizes intestinal motility in a model of post-inflammatory accelerated transit: involvement of CB₁ receptors and TRPV1 channels.

Palmitoylethanolamide inhibits rMCP-5 expression by regulating MITF activation in rat chronic granulomatous inflammation.

Palmitoylethanolamide and luteolin ameliorate development of arthritis caused by injection of collagen type II in mice.

An apPEAling new therapeutic for ulcerative colitis?

Palmitoylethanolamide improves colon inflammation through an enteric glia/toll like receptor 4-dependent PPAR-α activation.

A new co-ultramicronized composite including palmitoylethanolamide and luteolin to prevent neuroinflammation in spinal cord injury.

Glia and mast cells as targets for palmitoylethanolamide, an anti-inflammatory and neuroprotective lipid mediator.

New insights in mast cell modulation by palmitoylethanolamide.