Journal of Breastfeeding Biology

Journal Of Breastfeeding Biology

Journal of Breastfeeding Biology

Current Issue Volume No: 1 Issue No: 1

Review Article Open Access Available online freely Peer Reviewed Citation

Breast Feeding and Melatonin: Implications for Improving Perinatal Health

George Anderson 1,   Cathy Vaillancourt 2,   Michael Maes 3,   Russel J. Reiter 4  

1CRC Scotland & London, Eccleston Square, London, UK.

2INRS-Armand-Frappier Institute and Center for Interdisciplinary Research on Well-Being, Health, Society and Environment (CINBIOSE), Laval, QC, Canada.

3Deakin University, Department of Psychiatry, Geelong , Australia

4UT Health Science Centre, San Antonio, Texas

Abstract

The biological underpinnings that drive the plethora of breastfeeding benefits over formula-feeding is an area of intense research, given the cognitive and emotional benefits as well as the offsetting of many childhood- and adult-onset medical conditions that breast-feeding provides. In this article, we review the research on the role of melatonin in driving some of these breastfeeding benefits. Melatonin is a powerful antioxidant, anti-inflammatory and antinociceptive as well as optimizing mitochondrial function. Melatonin is produced by the placenta and, upon parturition, maternal melatonin is passed to the infant upon breastfeeding with higher levels in night-time breast milk. As such, some of the benefits of breastfeeding may be mediated by the higher levels of maternal circulating night-time melatonin, allowing for circadian and antioxidant effects, as well as promoting the immune and mitochondrial regulatory aspects of melatonin; these actions may positively modulate infant development. Herein, it is proposed that some of the benefits of breastfeeding may be mediated by melatonin's regulation of the infant's gut microbiota and immune responses. As such, melatonin is likely to contribute to the early developmental processes that affect the susceptibility to a range of adult onset conditions. Early research on animal models has shown promising results for the regulatory role of melatonin.

Author Contributions
Received 21 May 2016; Accepted 11 Jul 2016; Published 22 Jul 2016;

Academic Editor: Maryann Bozzette, University of Missouri-St. Louis

Checked for plagiarism: Yes

Review by: Single-blind

Copyright ©  2016 George Anderson, et al.

License
Creative Commons License     This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Competing interests

The authors have declared that no competing interests exist.

Citation:

George Anderson, Cathy Vaillancourt, Michael Maes, Russel J. Reiter (2016) Breast Feeding and Melatonin: Implications for Improving Perinatal Health. Journal Of Breastfeeding Biology - 1(1):8-20. https://doi.org/10.14302/issn.2644-0105.jbfb-16-1121

Download as RIS, BibTeX, Text (Include abstract )

DOI 10.14302/issn.2644-0105.jbfb-16-1121

Introduction

Although highly recommended, breastfeeding rates vary across countries, with 30% of USA mothers exclusively breastfeeding, and a further 30% partially breastfeeding 1. Consequently, the majority of women in the USA and most western countries predominantly use formula-feeding, with a number of negative impacts, as compared to breastfeeding, for the developing infant.

Breastfeeding has many benefits, including: lower rates of hospital admissions for respiratory infections 2; lower hospital admissions for neonatal fever 3; decreased levels of childhood obesity at age 2 years 4; decreased levels of offspring cancer 5, as well as a range of other medical conditions, including type 1 and 2 diabetes, obesity, hypertension, cardiovascular disease and hyperlipidemia 6. Such benefits to infant outcome result in substantial financial benefits to countries, at least in part mediated by the improvements in health, cognition and IQ that breastfeeding confers 7, 8.

Such benefits are likely to impact on the susceptibility to a number of other adult onset conditions, including Alzheimer's disease and depression 9, 10, suggesting that breastfeeding may decrease the susceptibility to Alzheimer's disease in the offspring, as well as in the mother 11. Such offspring benefits are likely to be partly mediated via the positive impacts of breastfeeding on offspring obesity and metabolic dysregulation 12. Breastfeeding may also confer some psychoneuroimmunological benefits to mothers (13.

Biological Benefits of Breastfeeding

The biological components and processes that drive the benefits of breastfeeding are the subject of intense investigation. Some of these benefits are thought to be mediated by the effects of immune-associated factors in the maternal milk, which may be modulated by levels of maternal stress 14. These immune-linked factors include cytokines, chemokines, whole cells, immunoglobulins, various growth factors, lysozyme, lactoferrin, oligosaccharides and microbiota 15, 16. Such breast milk derived growth factors, cytokines and chemokines, are proposed to have important roles in the infant's gastrointestinal and immune development 17, 18, with these factors contributing to the immune influence on the maturation and integrity of the gastrointestinal tract, including in part, via the regulation of the infant's inflammatory responses 19. Classical T helper 1 (Th1) cytokines are pro-inflammatory and include interleukin (IL)-1β, IL-18 and gamma-interferon (IFNγ), whilst classical Th2 cytokines, such as IL-10, are generally anti-inflammatory. The levels and balance of such cytokines in breast milk will modulate many aspects of infant development 19. Chemokines are also important players in the regulation of immune responses, primarily via their capacity to chemo attract an array of different immune cells, including neutrophils, monocytes, and lymphocytes. An array of chemokines are found in breast milk 20.

Cytokines, chemokines, and growth factors, such as brain-derived neurotrophic factor (BDNF), are thought to prime intestinal immune cells, contribute to angiogenesis, help develop the intestinal epithelial barrier function, and generally suppress inflammation 21. Human milk has significant levels of secreted immunoglobulin A (IgA), which plays an important role in the gut's mucosal immune defence, with infant gut microbiota eventually inducing secreted (s)IgA as the infant's immune system develops 22. This may be of some importance as sIgA may have a significant role in the selection of 'good' and 'bad' gut microbiota 23. As such, breastfeeding, via a variety of factors, impacts on the development of the infant's immune system, including in the regulation of the gut and gut microbiota. This is likely to be of crucial relevance to infant brain development, given the growing body of data showing the importance of the gut-brain axis to an array of psychiatric and neurodegenerative conditions 24, 25, 26. The impacts of breastfeeding on such processes may be even more important in premature infants, where only limited in utero development of such physiological processes occurs 22.

The neonate is highly dependent on the innate immune system in the first 6 months, prior to the full maturation of the adaptive immune system, which is also compensated for by increased activity of gamma-delta T cells 27, 28. As such, neonates and early infancy is associated with a distinct pattern of immune responses, including in the regulation of the intestine. Consequently, a fuller protection requires human milk. Complex carbohydrates and glycans are rich in human milk and, being prebiotics, increase the gut colonization by probiotic bacteria. Glycans are therefore part of an array of milk component factors that drive the nature of the infants immune response, particularly via effects in the gut 21. Early developmental influences on gut microbiota are being increasingly recognized as important for the susceptibility to adult onset disorders, at least in part by subtle changes in the nature of the immune response that influence the development of an array of different tissues and organs, at least in part driven by increased gut permeability and the leakage of gut microbiota and/or tiny fragments of partially digested food, which lead to low level systemic inflammation 29. Some of the benefits of breastfeeding may be mediated by elevated infant night-time melatonin 30.

Melatonergic Pathways

Melatonin (N-acetyl-5-methoxytryptamine) is a methoxyindole that is present in most plants and animals, with recent work suggesting that it may be expressed in all mitochondria-containing cells 31, 32. In mammals, melatonin has been primarily studied in the context of its night-time release by the pineal gland, which gives it a powerful role in driving circadian rhythms 33. However, as reflected by its possible expression in all mitochondria-containing cells, melatonin has been shown to be released by a growing number of cells, including placental trophoblasts, astrocytes, immune cells and enterochromaffin gut cells 34, 35. In fact, melatonin production by the gut can be up to 400-fold greater than the amount produced by the pineal gland 36. As well as a role in circadian regulation, melatonin is also a powerful antioxidant, anti-inflammatory and antinociceptive, contributing to its crucial role as an immune regulator and optimizer of mitochondrial functioning 37. As such, melatonin is a key regulator of immune defenses and cellular energy processes 38, 39, which requires investigation as to the relevance of melatonin's impact on breastmilk constituents. Melatonin also induces endogenous antioxidant enzymes 40, with these increases being mediated via melatonins induction of the transcription factor NF-E2-related factor 2 (Nrf2) 32, 41. Many melatonin effects seem to be via its regulation of homeostatic processes, contributing to its clinical utility across a wide range of medical conditions.

N-acetylserotonin (NAS) is the precursor of melatonin and is also a powerful antioxidant, immune regulator and modulator of mitochondria functioning 42. NAS is also a BDNF mimic, via its activation of the BDNF receptor, tyrosine kinase receptor-B (TrKB) 43. The synthesis of NAS and melatonin are highly dependent on serotonin availability, given that serotonin is the immediate precursor of NAS. Serotonin is converted to NAS by the enzyme, arylalkylamine N-acetyltransferase (AANAT), with hydroxyindole O-methyltransferase (HIOMT), (also referred to as acetylserotonin methyltransferase), converting NAS to melatonin 44. The melatonergic pathways are therefore highly dependent on tryptophan availability for serotonin synthesis, with lower levels of serotonin, as in depressive episodes or in the course of immune activation, restricting NAS and melatonin synthesis. Both melatonin and NAS are amphiphilic, readily diffusing through the extracellular space and across cell membranes and organelles. Consequently, neither is entirely dependent on plasma membrane receptors for their cellular effects 45.

Many of the melatonin metabolites also have anti-inflammatory and antioxidative, as well as immune system modulatory effects, as previously summarized 41. As a consequence, melatonergic pathway activation produces an array of antioxidants, including Nrf2-induced endogenous antioxidant enzymes, with implications for a host of medical conditions 46, as well as in pregnancy and infancy 47.

With the early developmental period being increasingly recognized as an important factor in the etiology of a host of medical conditions, it is of note that single nucleotide polymorphisms (SNP) in melatonin receptors (MT1r and MT2r) as well as the melatonergic pathway enzymes increase the susceptibility to a wide array of medical conditions, including depression 48, cancer 49, 50, multiple sclerosis 51, 52 and bipolar disorder 53. The role of early developmental melatonin in the modulation of the epigenetic processes that contribute to the risk of such medical conditions is an area of intense investigation, including as to the role of gut microbiota, gut dysbiosis, gut permeability and bacterial translocation in this early developmental etiology 29.

Many biological factors, including those in breast milk such as tryptophan and omega-3 polyunsaturated fatty acids, act to regulate serotonin and therefore melatonin availability, including via the regulation of monoamine oxidase (MAO), which degrades monoamines such as serotonin 54, 55. Chronic stress-induced hypothalamus-pituitary-adrenal (HPA) axis activation, leading to cortisol production, can also increase MAO, as well as increasing tryptophan 2,3-dioxygenase (TDO), which drives tryptophan to tryptophan catabolite (TRYCAT) synthesis and away from serotonin and melatonin synthesis 29. As breastfeeding can limit infant HPA axis cortisol responses 56, this is another means by which breastfeeding is likely to optimize the infant's serotonin and melatonin availability.

Overall, melatonin has many effects, including being: an optimizer of mitochondria functioning; a powerful antioxidant and inducer of endogenous antioxidants; an anti-inflammatory; a regulator of immune and glial cell reactivity; as well as being a circadian rhythm regulator 33, 36, 37, 40, 41. The melatonergic pathway is present in many cell types and tissues/organs, especially in the gut 36. All of these factors are crucial over the course of infancy, suggesting that variations in the presence of melatonin in breast and formula feeding is likely of some importance.

Melatonin: Perinatal and Infancy

Melatonin is highly produced, in a non-circadian fashion, by the placenta, leading to the maintenance of high melatonin levels in the pregnant mother and foetus 57, 58. Upon birth, such continuous melatonin provision ceases, for both the mother and the newborn. However, a growing body of data has highlighted the utility of melatonin during the first year of life.

Melatonin increases survival in struggling premature infants, with melatonin being shown to have adjunctive efficacy in the management of neonatal sepsis 59, 60. Melatonin also has utility in the management of perinatal asphyxia 61, with melatonin decreasing levels of subsequent seizures and white matter damage, as well as preventing the expression of indicants of developmental delay at 6 month follow up 62. Increased levels of melatonin are evident in labor-associated birth (versus caesarean section), which is suggested to decrease the oxidant challenge in the neonate 63. As such, the increasing placental melatonin production over the course of pregnancy and its efficacy in a number of critical neonatal conditions suggests that melatonin is likely to have utility and a high safety profile in the perinatal period 59. Further investigation of this area is, however, urgently warranted.

Melatonin and Breastfeeding

Given the night-time rise in pineal melatonin synthesis levels, there is an increase in circulating melatonin levels in the mother. Consequently, breastfeeding during the night results in the transfer of melatonin, NAS and melatonin metabolites to the suckling infant 30. As such, night-time breastfeeding results in differences in the contents of the mother' milk, with a small sample study showing increased night-time melatonin in the milk of preterm mothers, which correlated with the circulating levels of the antioxidant enzyme, glutathione peroxidase 64. It is not unlikely that such melatonin-containing night-time breast milk will have an impact on the entrainment of the infant's circadian rhythms, as well as providing powerful antioxidant, anti-inflammatory and immune regulatory effects. It is also likely that melatonin will impact on the maturation of gut microbiota and gut permeability, thereby suggesting possible impacts on how such gut microbiota influence infant development 65, including via modulation of the circadian rhythm and the patterning of circadian genes expressed. Circadian genes are important regulators of immune system responses 66.

In the central nervous system (CNS), NAS, melatonin and its antioxidant metabolites may all increase levels of neurogenesis, as shown in a wide range of preclinical studies 67. As such, it requires investigation as to whether the positive effects of breastfeeding on cognition and IQ 68 are mediated, at least in part, via the melatonin contained in the night-time feed. Melatonin may also have impacts on many other aspects of development 69, including via its regulation of circadian genes 70.

To ensure maximal levels of melatonin in breast milk at night, the mother should sleep in a dark room and, likewise, breast feed under very subdued lighting 71. Avoiding blue wavelengths of light, which are present in polychromatic light sources, is of special importance since these light wavelengths are maximally inhibitory to pineal melatonin synthesis 71.

Melatonin also regulates many of the milk-associated factors thought to drive the biological benefits of breastfeeding 72, 73, and is likely to attenuate the effects of maternal stress on such milk-derived factors 74. Maternal melatonin also has a role in the regulation of the maternal production of such proposed beneficial factors 73, indicating that it may also regulate the levels of the infant's endogenous synthesis of these factors. As to whether the circadian regulation of such milk-derived beneficial factors is driven by melatonin in the night-time breast milk requires investigation.

Overall, the role of melatonin in the night-time breastfeed has been significantly under-investigated. Given the lack of melatonin in formula feeds, it could be argued that this is a significant deviation from the evolutionary driven forces that led to the night-time feed containing melatonin. It also requires investigation as to whether variations in maternal melatonin modulate the circadian, antioxidant and immune-associated beneficial factors in the night-time breast feed over the course of normal development.

Consideration should be given to the possibility of supplementing infant formula for use at night-time feeding with melatonin. Thus, there could be both daytime and night-time formulas, differing in their melatonin levels. Indeed, one author (RJR) of the current report was asked about this possibility by a major producer of infant formula.

The utility of melatonin in early infancy, however, may be especially relevant in premature infants. It is common to add protein, fat and carbohydrate fortifiers to breastmilk for premature infants 75. Given that melatonin is highly produced by the placenta 35, it is highly likely that premature infants may gain from the addition of melatonin to all feeds, and not solely to night-time feeds. There is a growing utilization of banked human donor milk for premature babies, which is usually pasteurized by the Holder method 72. As to whether such milk should be fortified with melatonin, as mentioned above, either as a whole or in a sub-sample solely for night-time feeding has still to be investigated. It should also be noted that very low birthweight infants often have little access to breastfeeding 76 and may also benefit from the addition of melatonin to human donor milk or formula feed, as would be the case in situations where the mother is unable to breast feed.

Preclinical studies indicate that providing the dam with melatonin in pregnancy prevents offspring postnatal corticosteroid-induced hypertension 77. This suggests that the addition of melatonin to human donor milk for premature infants may have utility in decreasing the effects of corticosteroids given to women at increased risk of a preterm birth, including the reduced levels of cognition and increased risk of hypertension that are linked to corticosteroid-associated preterm births 78. Placental melatonin is decreased in preeclampsia, which is significantly associated with intrauterine growth restriction and preterm birth 35. This may be of particular relevance in women with preexisting diabetes and nephropathy or microalbuminuria, where complications such as severe preeclampsia and preterm delivery are still common 79. An SNP in the melatonin receptor, MT2, is a genetic susceptibility factor for gestational diabetes 80, with preclinical studies showing that melatonin decreases the increased risk of neural tube defects in gestational diabetes 81. However, it should be noted that it still requires thorough investigation as to the utility and safety of exogenous melatonin during human pregnancy, although there is increasing evidence that melatonin may be beneficial for ensuring successful pregnancy 82. However, it should be noted that an array of medical conditions with a suspected early developmental etiology, such as hypertension and obesity, were evident prior to the development of formula feed in the nineteenth century, indicating that such disorders are multifactorial and not simply due to decreased melatonin provision in early infancy.

Future Directions

General practitioners (GPs) need to improve their knowledge regarding breastfeeding, as their support of breastfeeding significantly increases its rates 83. Perinatologists, neonatologists and pediatricians, as well as GPs also need to improve their knowledge regarding the effects of melatonin, given that little is known other than in regard to its utility in management of 'jet lag'. In this context, it also of note that the benefits of breastfeeding extend to the mother, with psychoneuroimmunological benefits 13, including alterations in pro-inflammatory cytokines and altered stress hormone responses, which are thought to contribute to a decreased risk of Alzheimer's disease 11.

There a number of gaps in the available data on the utility of melatonin in humans, including its use during the perinatal period and infancy. However, an extensive preclinical and limited human literature indicate that there are many potential benefits of perinatal and postnatal melatonin that are likely to be relevant not only to the optimization of infant development, but also for the susceptibility to adult onset disorders 77, 78. As such, many of the benefits of breastfeeding would seem to be mimicked by the effects of melatonin. Much of the data on melatonin has been derived from preclinical studies and is in need of careful investigation in human studies.

Breastfeeding is consistently associated with increased levels of cognition and IQ in the offspring 68 and it requires investigation as to whether such positive cognitive benefits are mediated, perhaps in part, by the melatonin contained in the night-time feed or its effects on the content of breast milk or indeed from their interaction.

Similarly, it requires investigation as to the relevance of melatonin in breast milk for the many other adult onset conditions that are positively regulated by breastfeeding, including: decreased hospital admissions for respiratory infections 2 and neonatal fever 3; lower levels of childhood obesity 4; and lower rates of offspring cancer 5; as well as a range of other medical conditions, including type 1 and 2 diabetes, obesity, hypertension, cardiovascular disease and hyperlipidemia 6. Melatonin is known to positively modulate all of these medical conditions 70, suggesting possible beneficial effects prenatally and in infancy.

Many of the benefits of melatonin may ultimately be mediated by its positive effects on mitochondrial functioning 84, 85, in turn optimizing cellular functioning, including that of immune cells 86, 87. Many of the benefits of melatonin are mediated via its induction of the alpha-7 acetylcholine receptor (a7nAChR), which has cognitive enhancing effects 88, as well as being a significant immune 89 and mitochondrial 90 regulator. It is unknown as to whether any benefits of breastfeeding are mediated via the increased levels and activation of the a7nAChR. This is in need of investigation, especially given the role of the a7nAChR in the regulation of gut permeability 91.

It should also be noted that the constituents of breast milk are highly variable between individuals, with postnatal age and gestational length (preterm versus term) being important predictors of breast milk content 92. It will be important to investigate how variable this is across day- versus night-time breast milk constituents, and as to whether variations in maternal and/or non-circadian melatonin contribute to such individual variance.

Given that the night-time breast feed is likely to have its content determined by circadian factors and that melatonin is significant circadian regulator, there is a need to study the influence of the administration of melatonin to the mother, on the content and benefits of breast milk. Cesarean section and other pro-inflammatory events in the mother are likely to drastically decrease the levels of maternal pineal gland melatonin production 93. Should melatonin benefits in breast milk and/or its influence on the contents of breast milk be prevented by such maternal pro-inflammatory processes, primarily driven by increased levels of pro-inflammatory cytokines, it is likely that the use of melatonin by the mother at night or its addition to breast milk or formula feed would compensate its transient cessation. However, it should be emphasized that supplementation with melatonin should not occur until the content of breastmilk has been thoroughly examined to identify the amount of melatonin that is being transferred during feeding, and the subsequent melatonin serum levels of infants. A safe level of any melatonin supplement for an infant has also yet to be determined.

SIDS

Sudden infant death syndrome (SIDS) is most common between the ages of 1-6 months, the period of time when infant levels of circulating melatonin are often still to develop a circadian rhythm 94, 95. A recent review and meta-analysis found breastfeeding to decrease the risk of SIDS 96, 97. The biological underpinnings of such protection afforded by breastfeeding are still to be determined. A Canadian study indicates that up to 41.4% of gastrointestinal infections, 26.1% of hospitalizations from lower respiratory tract infections and 24.6% of SIDS cases could be prevented in native Canadian infants if they received any breastfeeding 98. Given the beneficial effects of melatonin against oxidative stress 99, mitochondrial functioning 32, infections 100, gut microbiota/permeability 29 and diaphragm muscle fatigue 101, which are all suspected to contribute to SIDS pathophysiology 102, 103, 104, 105, 106, it requires investigation as to whether the efficacy of breastfeeding is mediated, to some degree, by melatonin. If so, this could suggest that the addition of melatonin to the night-time formula feed would lower SIDS cases, as may its administration to the mother following cesarean section. The decreased levels of melatonin (and its precursor serotonin) in SIDS 107 is partly mediated by microglia activation 108 and is prevented by melatonin 109, suggesting that melatonin may well lower the incidence of SIDS and strengthens the case for melatonin inclusion in night-time formula feeds as well as its optimization in breast milk. The role of melatonin in SIDS, including as to whether melatonin would have any efficacy in preventing SIDS cases, is in urgent need of investigation.

Conclusions

The biological underpinnings of the many benefits of breastfeeding over formula feeding is an important and active area of research. The research reviewed above suggests that variations in melatonin may well be an important aspect of the many breastfeeding benefits. As indicated, there are a number of easily achievable investigations that would clarify the role of melatonin in breast milk, including in the regulation of gut microbiota and in the early developmental processes that bias the susceptibility to a range of adult onset conditions. Given that the four major pathophysiological processes associated with SIDS are inhibited by melatonin, it will be important to determine as to whether melatonin in breast milk, or its addition to a night-time formula feed, decreases the incidence of SIDS.

Acknowledgements

Not Applicable

References

  1. 1.L A Smith, N L Geller, A L Kellams, E R Colson, D V Rybin.. (In press) Infant Sleep Location and Breastfeeding Practices in the United States,2011-2014.Acad.Pediatr .
  1. 2.Dagvadorj A, Ota E, Shahrook S, Olkhanud Baljinnyam, Takehara P et al. (2016) Hospitalization risk factors for children's lower respiratory tract infection: A population-based, cross-sectional study in Mongolia. , Sci, Rep 6, 24615.
  1. 3.Netzer-Tomkins H, Rubin L, Ephros M.(In press) Breastfeeding Is Associated with Decreased Hospitalization for Neonatal Fever.Breastfeed.Med.
  1. 4.Bider-Canfield Z, M P, Wang X, Yu W, M P Bautista.(In press) Maternal obesity, gestational diabetes, breastfeeding and childhood overweight at age 2 years. Pediatr. Obes
  1. 5.Blackadar C B. (2016) Historical review of the causes of cancer. , World. J. Clin. Oncol 7(1), 54-86.
  1. 6.Binns C, Lee M, W Y Low. (2016) The long-term public health benefits of breastfeeding. , Asia Pac J. Public. Health 28(1), 7-14.
  1. 7.Walters D, Horton S, A Y Siregar, Pitriyan P, Hajeebhoy N.(In press) The cost of not breastfeeding in Southeast Asia. Health Policy Plan.
  1. 8.Straub N, Grunert P, Northstone K, Emmett P. (2016) Economic impact of breast-feeding-associated improvements of childhood cognitive development, based on data from the ALSPAC. , Br. J. Nutr 1-6.
  1. 9.Maes M, Anderson G. (2016) Overlapping the tryptophan catabolite (TRYCAT) and melatoninergic pathways in Alzheimer’s disease. , Curr. Pharm. Des 22(8), 1074-1085.
  1. 10.Roomruangwong C, Kanchanatawan B, Sunee Sirivichayakul S, Anderson G, Maes M.(In press) IgA / IgM responses to tryptophan and tryptophan catabolites (TRYCATs) are significantly associated with premenstrual syndrome or physio-somatic symptoms at the end of term, while lowered IgA responses to anthranilic acid are associated with perinatal depression. , Mol. Neurobio
  1. 11.Fox M, Berzuini C, L A Knapp. (2013) Maternal breastfeeding history and Alzheimer’s disease risk. , J. Alzheimers. Dis 37(4), 809-21.
  1. 12.V A Moser, C J Pike.(In press) Obesity and sex interact in the regulation of Alzheimer’s disease. , Neurosci. Biobehav. Rev
  1. 13.M W Groer, M W Davis. (2006) Cytokines, infections, stress, and dysphoric moods in breastfeeders and formula feeders. , J. Obstet. Gynecol. Neonatal. Nurs 35(5), 599-607.
  1. 14.Thibeau S, D’Apolito K, A F Minnick, M S Dietrich, Kane B.. , Relationships of Maternal Stress with Milk Immune Components in African American Mothers of Healthy Term Infants. Breastfeed. Med 11, 6-14.
  1. 15.Velasco I, Santos C, Limón J, Pascual E, Zarza L. (2016) Bioactive Components in Human Milk Along the First Month of Life: Effects of Iodine Supplementation during Pregnancy. , Ann. Nutr. Metab 68(2), 130-6.
  1. 16.He Y, N T Lawlor, D S Newburg. (2016) Human Milk Components Modulate Toll-Like Receptor-Mediated Inflammation. , Adv. Nutr 7(1), 102-11.
  1. 17.Groer M W, Luciano A A, Dishaw L J, Ashmeade T L, Miller E. (2014) Development of the preterm infant gut microbiome: a research priority. , Microbiome 2, 38.
  1. 18.W H Oddy. (2002) The impact of breastmilk on infant and child health. , Breastfeed. Rev 10(3), 5-18.
  1. 19.Garofalo R. (2010) Cytokines in human milk. , J. Pediatr 156, 36-40.
  1. 20.Bosire R, B L Guthrie, Lohman-Payne B, Mabuka J, Majiwa M. (2007) Longitudinal comparison of chemokines in breastmilk early postpartum among HIV-1-infected and uninfected Kenyan women. , Breastfeed. Med 2(3), 129-38.
  1. 21.Newburg D S, Walker W A. (2007) Protection of the neonate by the innate immune system of developing gut and of human milk. , Pediatr. Res 61(1), 2-8.
  1. 22.S L Bridgman, Konya T, M B Azad, M R Sears, A B Becker. (2016) Infant gut immunity: a preliminary study of IgA associations with breastfeeding. , J. Dev. Orig. Health. Dis 7(1), 68-72.
  1. 23.McLoughlin K, Schluter J, Rakoff-Nahoum S, A L Smith, K R Foster. (2016) Host Selection of Microbiota via Differential Adhesion. , Cell. Host. Microbe 19(4), 550-9.
  1. 24.Anderson G, Seo M, Carvalho A, Berk M, Maes M.(In press) Gut Permeability and Parkinson’s Disease.Curr.Pharm.Des.
  1. 25.Martin-Subero M, Anderson G, Kanchanatawan B, Berk M, Maes M. (2015) Comorbidity between depression and inflammatory bowel disease explained by immune-inflammatory, oxidative and nitrosative stress, tryptophan catabolite and gut-brain pathways. , CNS. Spectrums 21(2), 184-98.
  1. 26.Anderson G, Rodriguez M, Maes M.(In press) Multiple Sclerosis: the role of increased gut permeability. , Curr. Pharm. Des
  1. 27.D L Gibbons, S F Haque, Silberzahn T, Hamilton K, Langford C. (2009) Neonates harbour highly active gammadelta T cells with selective impairments in preterm infants. , Eur. J. Immunol 39(7), 1794-806.
  1. 28.A K Simon, G A Hollander, McMichael A. (2015) Evolution of the immune system in humans from infancy to old age. , Proc. Biol. Sci 282(1821), 20143085.
  1. 29.Anderson G, Maes M. (2015) The gut-brain axis: the role of melatonin in linking psychiatric, inflammatory and neurodegenerative conditions. , Adv. Integr. Med 2(1), 31-37.
  1. 30.Illnerová H, Buresová M, Presl J. (1993) Melatonin rhythm in human milk. , J. Clin. Endocrinol. Metab 77(3), 838-41.
  1. 31.D X Tan, L C Manchester, Liu X, S A Rosales-Corral, Acuna-Castroviejo D. (2013) Mitochondria and chloroplasts as the original sites of melatonin synthesis: a hypothesis related to melatonin's primary function and evolution in eukaryotes. , J. Pineal. Res 54(2), 127-38.
  1. 32.Manchester L C, Coto-Montes A, Boga J A, Andersen L P, Zhou Z. (2015) Melatonin: an ancient molecule that makes oxygen metabolically tolerable. , J. Pineal. Res 59(4), 403-19.
  1. 33.Erren T C, Reiter R J. (2015) Melatonin: a universal time messenger. , Neuroendocrinol Lett 36(3), 187-192.
  1. 34.Reiter R J, Tan D X, Rosales-Corral S A, Manchester L C. (2013) The universal nature, unequal distribution and antioxidant functions of melatonin and its derivatives. , Mini. Rev. Med. Chem 13(3), 373-384.
  1. 35.Lanoix D, Guérin P, Vaillancourt C. (2012) Placental melatonin production and melatonin receptor expression are altered in preeclampsia: new insights into the role of this hormone in pregnancy. , J. Pineal. Res 53(4), 417-25.
  1. 36.Huether G. (1993) The contribution of extrapineal sites of melatonin synthesis to circulating melatonin levels in higher vertebrates. , Experientia 49(8), 665-670.
  1. 37.Reiter R J, Tan D X, Galano A. (2014) Melatonin: exceeding expectations. , Physiology. (Bethesda) 29(5), 325-333.
  1. 38.Anderson G, Maes M. (2016) Melatoninergic Pathways in Alzheimer's Disease. Chapter In book: Frontiers in Clinical Drug Research-Alzheimer Disorder. Ed: Atta-Ur-RahmanrBentham Press e-books.
  1. 39.Martín M, Macías M, León J, Escames G, Khaldy H. (2002) Melatonin increases the activity of the oxidative phosphorylation enzymes and the production of ATP in rat brain and liver mitochondria. , Int. J. Biochem. Cell. Biol 34(4), 348-57.
  1. 40.Rodriguez C, J C Mayo, R M Sainz, Antolin I, Herrera F. (2004) Regulation of antioxidant enzymes: a significant role for melatonin. , J. Pineal. Res 36(1), 1-9.
  1. 41.Hardeland R, D P Cardinali, Srinivasan V, D W Spence, G M Brown. (2011) Melatonin--a pleiotropic, orchestrating regulator molecule. , Prog. Neurobiol 93(3), 350-84.
  1. 42.Alvarez-Diduk R, Galano A, D X Tan, R J. (2015) N-acetylserotonin and 6-hydroxymelatonin against oxidative stress: implications for the overall protection exerted by melatonin. , J. Phys. Chem. B 119(27), 8535-8543.
  1. 43.S W Jang, Liu X, Pradoldej S, Tosini G, Chang Q. (2010) N-acetylserotonin activates TrkB receptor in a circadian rhythm. , Proc. Natl. Acad. Sci. U S A 107(8), 3876-81.
  1. 44.J H Stehle, Saade A, Rawashdeh O, Ackermann K, Jilg A. (2011) A survey of molecular details in the human pineal gland in the light of phylogeny, structure, function and chronobiological diseases. , J. Pineal. Res 51(1), 17-43.
  1. 45.Reiter R J, Tan D X, Manchester L C, Terron M P, Flores L J. (2007) Medical implications of melatonin: receptor-mediated and receptor-independent actions. , Adv. Med. Sci 52, 11-28.
  1. 46.Anderson G, Maes M. (2014) Local melatonin regulates inflammation resolution: a common factor in neurodegenerative, psychiatric and systemic inflammatory disorders. , CNS. Neurol. Disord. Drug. Targets 13(5), 817-27.
  1. 47.Sagrillo-Fagundes L, Salustiano Assuncao, E M Yen, P W Soliman, A et al. (2016) . Melatonin in Pregnancy: Effects on Brain Development and CNS Programming Disorders. Curr. Pharm. Des 22(8), 978-86.
  1. 48.Gałecki P, Szemraj J, Bartosz G, Bieńkiewicz M, Gałecka E.Single-nucleotide polymorphisms and mRNA expression for melatonin synthesis rate-limiting enzyme in recurrent depressive disorder. , J. Pineal. Res 48(4), 311-7.
  1. 49.S L Deming, Lu W, Beeghly-Fadiel A, Zheng Y, Cai Q. (2012) Melatonin pathway genes and breast cancer risk among Chinese women. , Breast. Cancer. Res. Treat 132(2), 693-9.
  1. 50.Xin Z, Jiang S, Jiang P, Yan X, Fan C. (2015) Melatonin as a treatment for gastrointestinal cancer: a review. , J. Pineal. Res 58(4), 375-387.
  1. 51.Natarajan R, Einarsdottir E, Riutta A, Hagman S, Raunio M. (2012) Melatonin pathway genes are associated with progressive subtypes and disability status in multiple sclerosis among Finnish patients. , J. Neuroimmunol.250(1-2): 106-10.
  1. 52.Lopez-Gonzalez A, Alvarez-Sanchez N, P J Lardone, Cruz-Chamorro I, Martinez-Lopez A. (2015) Melatonin treatment improves primary progressive multiple sclerosis: a case report. , J. Pineal. Res 58(2), 173-177.
  1. 53.Etain B, Dumaine A, Bellivier F, Pagan C, Francelle L. (2012) Genetic and functional abnormalities of the melatonin biosynthesis pathway in patients with bipolar disorder. , Hum. Mol. Genet 21(18), 4030-7.
  1. 54.Naveen S, Siddalingaswamy M, Singsit D, Khanum F. (2013) Anti-depressive effect of polyphenols and omega-3 fatty acid from pomegranate peel and flax seed in mice exposed to chronic mild stress. , Psychiatry. Clin. Neurosci 67(7), 501-8.
  1. 55.Anderson G, Maes M. (2015) Pharmaceutical and nutrition benefits in Alzheimer’s disease via convergence on the Melatoninergic Pathways. In book: Frontiers in Clinical Drug Research-Alzheimer Disorder.Ed:Atta-Ur-Rahmanr.Bentham Press e-books.Chap3 78, 50-127.
  1. 56.Beijers R, J M Riksen-Walraven, C de Weerth. (2013) Cortisol regulation in 12-month-old human infants: associations with the infants' early history of breastfeeding and co-sleeping. , Stress 16(3), 267-77.
  1. 57.Lanoix D, Beghdadi H, Lafond J, Vaillancourt C. (2008) Human placental trophoblasts synthesize melatonin and express its receptors. , J. Pineal. Res 45(1), 50-60.
  1. 58.Sagrillo-Fagundes L, Soliman A, Vaillancourt C. (2014) Maternal and placental melatonin: actions and implication for successful pregnancies. , Minerva. Ginecol 66(3), 251-66.
  1. 59.Gitto E, Karbownik M, Reiter R J, Tan D X, Cuzzocrea S. (2001) Effects of melatonin treatment in septic newborns. , Pediatr. Res 50(6), 756-760.
  1. 60.ElFrargy M, El-Sharkawy H M, Attia G F. (2015) Use of melatonin as an adjuvant therapy in neonatal sepsis. , J. Neonatal. Perinatal. Med 8(3), 227-32.
  1. 61.Fulia F, Gitto E, Cuzzocrea S, Reiter R J, Dugo L. (2001) Increased levels of malondialdehyde and nitrite/nitrate in the blood of asphyxiated newborns: reduction by melatonin. , J. Pineal. Res 31(4), 343-349.
  1. 62.Aly H, Elmahdy H, El-Dib M, Rowisha M, Awny M. (2015) Melatonin use for neuroprotection in perinatal asphyxia: a randomized controlled pilot study. , J. Perinatol 35(3), 186-91.
  1. 63.Katzer D, Mueller A, Welzing L, Reutter H, Reinsberg J. (2015) Antioxidative status and oxidative stress in the fetal circulation at birth: the effects of time of delivery and presence of labor. , Early. Hum. Dev 91(2), 119-24.
  1. 64.Katzer D, Pauli L, Mueller A, Reutter H, Reinsberg J.(In press) Melatonin Concentrations and Antioxidative Capacity of Human Breast Milk According to Gestational Age and the Time of Day. , J. Hum. Lact
  1. 65.Wang M, Monaco M H, Donovan S M.(In press) Impact of early gut microbiota on immune and metabolic development and function. , Semin. Fetal. Neonatal. Med
  1. 66.Labrecque N, Cermakian N. (2015) Circadian Clocks in the Immune System. , J. Biol. Rhythms 30(4), 277-90.
  1. 67.Anderson G, Maes M. (2014) Reconceptualizing adult neurogenesis: role for sphingosine-1-phosphate and fibroblast growth factor-1 in co-ordinating astrocyte-neuronal precursor interactions. , CNS. Neurol. Disord. Drug. Targets 13(1), 126-36.
  1. 68.J L Luby, A C Belden, Whalen D, M P Harms, D M Barch. (2016) Breastfeeding and Childhood IQ: The Mediating Role of Gray Matter Volume. , J. Am. Acad. Child. Adolesc. Psychiatry 55(5), 367-75.
  1. 69.Vriend J, Reiter R J. (2016) Melatonin, bone regulation and the ubiquitin-proteasome connection: A review. , Life. Sci 145, 152-60.
  1. 70.Qian J, F A Scheer. (2016) Circadian System and Glucose Metabolism: Implications for Physiology and Disease. , Trends. Endocrinol. Metab 27(5), 282-93.
  1. 71.G C Brainard, J P Hanifin, Warfield B, M K Stone, M E James. (2015) Short-wavelength enrichment of polychromatic light enhances human melatonin suppression potency. , J. Pineal. Res 58(3), 352-361.
  1. 72.Groer M, Duffy A, Morse S, Kane B, Zaritt J. (2014) Cytokines, Chemokines, and Growth Factors in Banked Human Donor Milk for Preterm Infants. , J. Hum. Lact 30(3), 317-323.
  1. 73.Rahman S A, Castanon-Cervantes O, Scheer F A, Shea S A, Czeisler C A. (2015) Endogenous circadian regulation of pro-inflammatory cytokines and chemokines in the presence of bacterial lipopolysaccharide in humans. , Brain. Behav. Immun 47, 4-13.
  1. 74.Thibeau S, D’Apolito K, A F Minnick, M S Dietrich, Kane B. (2016) . , Relationships of Maternal Stress with Milk Immune Components in African American Mothers of Healthy Term Infants. Breastfeed. Med 11, 6-14.
  1. 75.Rochow N, Fusch G, Choi A, Chessell L, Elliott L. (2013) Target fortification of breast milk with fat, protein, and carbohydrates for preterm infants. , J. Pediatr 163(4), 1001-7.
  1. 76.M W Groer, K E Gregory, Louis-Jacques A, Thibeau S, Walker W A. (2015) The very low birth weight infant microbiome and childhood health. , Birth. Defects. Res. C. Embryo. Today 105(4), 252-64.
  1. 77.H Y Chang, Y L Tain. (2016) Postnatal dexamethasone-induced programmed hypertension is related to the regulation of melatonin and its receptors. , Steroids 108, 1-6.
  1. 78.Bertagnolli M, T M Luu, A J Lewandowski, Leeson P, A M Nuyt. (2016) Preterm Birth and Hypertension: Is There a Link?. , Curr. Hypertens. Rep 18(4), 28.
  1. 79.Ringholm L, J A Damm, Vestgaard M, Damm P, E R Mathiesen. (2016) Diabetic Nephropathy in Women With Preexisting Diabetes: From Pregnancy Planning to Breastfeeding. , Curr. Diab. Rep 16(2), 12.
  1. 80.Liu Q, Huang Z, Li H, Bai J, Liu X.(In press) Relationship between melatonin receptor 1B (rs10830963 and rs1387153) with gestational diabetes mellitus: a case-control study and meta-analysis. , Arch. Gynecol. Obstet
  1. 81.Liu S, Guo Y, Yuan Q, Pan Y, Wang L. (2015) Melatonin prevents neural tube defects in the offspring of diabetic pregnancy. , J. Pineal. Res 59(4), 508-17.
  1. 82.Reiter R J, Tamura H, Tan D X, Xu X Y. (2014) Melatonin and the circadian system: contributions to successful female reproduction. , Fertil. Steril 102(2), 321-328.
  1. 83.H R Svendby, B F Løland, Omtvedt M, S T Holmsen, Lagerløv P. (2016) Norwegian general practitioners' knowledge and beliefs about breastfeeding, and their self-rated ability as breastfeeding counsellor. , Scand. J. Prim. Health. Care 18, 1-8.
  1. 84.Paradies G, Paradies V, F M Ruggiero, Petrosillo G. (2015) Protective role of melatonin in mitochondrial dysfunction and related disorders. , Arch. Toxicol 89(6), 923-939.
  1. 85.H K Erdemli, Akyol S, Armutcu F, M A Gulec, Canbal M. (2016) Melatonin and caffeic acid phenethyl ester in the regulation of mitochondrial function and apoptosis: The basis for future medical approaches. , Life. Sci 148, 305-12.
  1. 86.Hardeland R, D P Cardinali, G M Brown, S R Pandi-Perumal. (2015) Melatonin and brain inflammaging. , Prog. Neurobiol 127, 46-63.
  1. 87.E L Mills, O’Neill L A. (2016) Reprogramming mitochondrial metabolism in macrophages as an anti-inflammatory signal. , Eur. J. Immunol 46(1), 13-21.
  1. 88.S R Marder.(In press) Alpha-7 nicotinic agonist improves cognition in schizophrenia. , Evid. Based. Ment. Health
  1. 89.H O Kalkman, Feuerbach D.(In press) Modulatory effects of α7 nAChRs on the immune system and its relevance for CNS disorders. , Cell. Mol. Life. Sci
  1. 90.Gergalova G, Lykhmus O, Kalashnyk O, Koval L, Chernyshov V. (2012) Mitochondria express α7 nicotinic acetylcholine receptors to regulate Ca2+ accumulation and cytochrome c release: study on isolated mitochondria. , PloS. One 7(2), 31361.
  1. 91.T W Costantini, Krzyzaniak M, G A Cheadle, J G Putnam, A M Hageny. (2012) Targeting α-7 nicotinic acetylcholine receptor in the enteric nervous system: a cholinergic agonist prevents gut barrier failure after severe burn injury. , Am. J. Pathol 181(2), 478-86.
  1. 92.D A Gidrewicz, T R Fenton. (2014) A systematic review and meta-analysis of the nutrient content of preterm and term breast milk. , BMC. Pediatr 14, 216.
  1. 93.Pontes G N, Cardoso E C, Carneiro-Sampaio M M, Markus R P. (2007) Pineal melatonin and the innate immune response: the TNF-alpha increase after cesarean section suppresses nocturnal melatonin production. , J. Pineal. Res 43(4), 365-71.
  1. 94.D J Kennaway. (2000) Melatonin and development: physiology and pharmacology. , Semin. Perintol 24(4), 258-266.
  1. 95.Joseph D, N W Chong, M E Shanks, Rosato E, N A Taub. (2015) Getting rhythm: how do babies do it?. , Arch. Dis. Child. Fetal. Neonatal. Ed 100(1), 50-4.
  1. 96.Alm B, Wennergren G, Möllborg P, Lagercrantz H. (2016) Breastfeeding and dummy use have a protective effect on sudden infant death syndrome. , Acta. Paediatr 105(1), 31-8.
  1. 97.F R Hauck, J M Thompson, K O Tanabe, R Y Moon, Vennemann M M. (2011) Breastfeeding and reduced risk of sudden infant death syndrome:Ameta-analysis.Pediatrics. 128(1), 103-10.
  1. 98.K E McIsaac, Moineddin R, F I Matheson. (2015) Breastfeeding as a means to prevent infant morbidity and mortality in Aboriginal Canadians: A population prevented fraction analysis. , Can. J. Public. Health 106(4), 217-22.
  1. 99.Anderson G. (2016) Editorial: The Kynurenine and Melatonergic Pathways in Psychiatric. , and CNS Disorders. Curr. Pharm. Des 22(8), 947-948.
  1. 100.Elmahallawy E K, Luque J O, Aloweidi A S, Gutiérrez-Fernández J, Sampedro-Martínez A. (2015) Potential Relevance of Melatonin Against Some Infectious Agents: A Review and Assessment of Recent Research. , Curr. Med. Chem 22(33), 3848-61.
  1. 101.Kurcer Z, Iraz M, Kelesyilmaz N, Kilic N, Olmez E. (2006) Beneficial effects of melatonin on diaphragmatic contractility and fatigability in Escherichia coli endotoxemic rats. , Arzneimittelforschung 56(2), 90-5.
  1. 102.Dick A, Ford R. (2009) Cholinergic and oxidative stress mechanisms in sudden infant death syndrome.Acta. , Paediatr 98(11), 1768-75.
  1. 103.P M Siren, M J Siren. (2011) Critical diaphragm failure in sudden infant death syndrome. , Ups. J. Med. Sci 116(2), 115-23.
  1. 104.R A Chalmers, C A Stanley, English N, J S Wigglesworth. (1997) Mitochondrial carnitine-acylcarnitine translocase deficiency presenting as sudden neonatal death. , J. Pediatr 131(2), 220-5.
  1. 105.Törő K, Vörös K, Mészner Z, Váradi-T A, Tóth A. (2015) Evidence for Infection and Inflammation in Infant Deaths in a Country with Historically Low Incidences of Sudden Infant Death Syndrome. , Front. Immunol 6, 389.
  1. 106.A R Highet, A M Berry, K A Bettelheim, P N Goldwater. (2014) Gut microbiome in sudden infant death syndrome (SIDS) differs from that in healthy comparison babies and offers an explanation for the risk factor of prone position. , Int. J. Med. Microbiol.304(5-6) 735-41.
  1. 107.Cerpa V J, Aylwin Mde L, Beltrán-Castillo S, Bravo E U, Llona I R. (2015) The Alteration of Neonatal Raphe Neurons by Prenatal-Perinatal Nicotine. Meaning for Sudden Infant Death Syndrome. , Am. J. Respir. Cell. Mol Biol 53(4), 489-99.
  1. 108.P M MacFarlane, C A Mayer, D G Litvin.(In press) Microglia modulate brainstem serotonergic expression following neonatal sustained hypoxia exposure: implications for Sudden Infant Death Syndrome. , J. Physiol
  1. 109.N J Robertson, Faulkner S, Fleiss B, Bainbridge A, Andorka C. (2013) Melatonin augments hypothermic neuroprotection in a perinatal asphyxia model. Brain.136(Pt1) 90-105.

Cited by (16)

  1. 1.Mirza‐Aghazadeh‐Attari Mohammad, Mohammadzadeh Amir, Mostavafi Soroush, Mihanfar Aynaz, Ghazizadeh Saber, et al, 2020, Melatonin: An important anticancer agent in colorectal cancer, Journal of Cellular Physiology, 235(2), 804, 10.1002/jcp.29049
  1. 2.Booker Lauren A., Fitzgibbon Cheree, Spong Jo, Deacon-Crouch Melissa, Wilson Danielle L., et al, 2023, Rapid Versus Slow Cooling Pasteurization of Donor Breast Milk: Does the Cooling Rate Effect Melatonin Reduction?, Breastfeeding Medicine, 18(12), 951, 10.1089/bfm.2023.0244
  1. 3.Anderson George, Vaillancourt Cathy, Maes Michael, Reiter Russel J., 2017, Breastfeeding and the gut-brain axis: is there a role for melatonin?, Biomolecular Concepts, 8(3-4), 185, 10.1515/bmc-2017-0009
  1. 4.Lewicka Małgorzata, Zawadzka Magdalena, Henrykowska Gabriela, Rutkowski Maciej, Buczyński Andrzej, 2021, The antioxidant effects of melatonin in blood platelets during exposure to electromagnetic radiation – an in vitro study, Postępy Higieny i Medycyny Doświadczalnej, 75(1), 889, 10.2478/ahem-2021-0026
  1. 5.Bonmatí-Carrión María-Ángeles, Rol Maria-Angeles, 2023, Melatonin as a Mediator of the Gut Microbiota–Host Interaction: Implications for Health and Disease, Antioxidants, 13(1), 34, 10.3390/antiox13010034
  1. 6.Anderson George, 2018, Linking the biological underpinnings of depression: Role of mitochondria interactions with melatonin, inflammation, sirtuins, tryptophan catabolites, DNA repair and oxidative and nitrosative stress, with consequences for classification and cognition, Progress in Neuro-Psychopharmacology and Biological Psychiatry, 80(), 255, 10.1016/j.pnpbp.2017.04.022
  1. 7.Song Minyu, Park Won Seo, Yoo Jayeon, Ham Jun-Sang, 2018, Breastfeeding and Melatonin, Journal of Milk Science and Biotechnology, 36(3), 133, 10.22424/jmsb.2018.36.3.133
  1. 8.Ivanov Dmitry O., Evsyukova Inna I., Mazzoccoli Gianluigi, Anderson George, Polyakova Victoria O., et al, 2020, The Role of Prenatal Melatonin in the Regulation of Childhood Obesity, Biology, 9(4), 72, 10.3390/biology9040072
  1. 9.Cosemans Charlotte, Nawrot Tim S., Janssen Bram G., Vriens Annette, Smeets Karen, et al, 2020, Breastfeeding predicts blood mitochondrial DNA content in adolescents, Scientific Reports, 10(1), 10.1038/s41598-019-57276-z
  1. 10.Booker Lauren A., Spong Jo, Deacon-Crouch Melissa, Skinner Timothy C., 2022, Preliminary Exploration into the Impact of Mistimed Expressed Breast Milk Feeding on Infant Sleep Outcomes, Compared to Other Feeding Patterns, Breastfeeding Medicine, (), 10.1089/bfm.2022.0125
  1. 11.Gombert Marie, Codoñer-Franch Pilar, 2021, Melatonin in Early Nutrition: Long-Term Effects on Cardiovascular System, International Journal of Molecular Sciences, 22(13), 6809, 10.3390/ijms22136809
  1. 12.Booker Lauren A., Lenz Katrin E., Spong Jo, Deacon-Crouch Melissa, Wilson Danielle L., et al, 2023, High-Temperature Pasteurization Used at Donor Breast Milk Banks Reduces Melatonin Levels in Breast Milk, Breastfeeding Medicine, 18(7), 549, 10.1089/bfm.2023.0068
  1. 13.Verteramo Rosita, Pierdomenico Matteo, Greco Pantaleo, Milano Carmelia, 2022, The Role of Melatonin in Pregnancy and the Health Benefits for the Newborn, Biomedicines, 10(12), 3252, 10.3390/biomedicines10123252
  1. 14.Catale Clarissa, Gironda Stephen, Lo Iacono Luisa, Carola Valeria, 2020, Microglial Function in the Effects of Early-Life Stress on Brain and Behavioral Development, Journal of Clinical Medicine, 9(2), 468, 10.3390/jcm9020468
  1. 15.Bērziņš Kārlis, Harrison Samuel D.L., Leong Claudia, Fraser-Miller Sara J., Harper Michelle J., et al, 2021, Qualitative and quantitative vibrational spectroscopic analysis of macronutrients in breast milk, Spectrochimica Acta Part A: Molecular and Biomolecular Spectroscopy, 246(), 118982, 10.1016/j.saa.2020.118982
  1. 16.Booker Lauren A., Wilson Danielle, Spong Jo, Fitzgibbon Cheree, Deacon-Crouch Melissa, et al, 2024, Maternal Circadian Disruption from Shift Work and the Impact on the Concentration of Melatonin in Breast Milk, Breastfeeding Medicine, 19(1), 33, 10.1089/bfm.2023.0252