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Subject:
From:
Debra Swank <[log in to unmask]>
Reply To:
Lactation Information and Discussion <[log in to unmask]>
Date:
Thu, 11 Feb 2021 05:24:52 -0500
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Greetings All,

New study with a press release (December 2020) in ScienceDaily:

Title:  Maternal diet alters human milk oligosaccharide composition with implications for the milk metagenome.  

In:  Scientific Reports 2020; 10 (1) DOI: 10.1038/s41598-020-79022-6

Authors:  Maxim D. Seferovic, Mahmoud Mohammad, Ryan M. Pace, Melinda Engevik, James Versalovic, Lars Bode, Morey Haymond, Kjersti M. Aagaard. 

Abstract: "Human milk is the optimal nutrition source for infants, and oligosaccharides represent the third most abundant component in milk after lactose and fat. Human milk oligosaccharides (HMO) are favorable macromolecules which are, interestingly, indigestible by the infant but serve as substrates for bacteria. Hypothesizing that the maternal diet itself might influence HMO composition, we sought to directly determine the effect of maternal diet on HMO and the milk bacteria. Employing a human cross-over study design, we demonstrate that distinct maternal dietary carbohydrate and energy sources preferentially alter milk concentrations of HMO, including fucosylated species. We find significant associations between the concentration of HMO-bound fucose and the abundance of fucosidase (a bacterial gene that digests fucose moieties) harbored by milk bacteria. These studies reveal a successive mechanism by which the maternal diet during lactation alters milk HMO composition, which in turn shapes the functional milk microbiome prior to infant ingestion."

The ScienceDaily news release is also worth reading in its entirety, including the unusual commentary on mastitis near the end of the press release: 

"'One other exciting aspect of our study is the suggestion that HMOs seem to preferentially affect the growth potential of microbes that may also impart health risk or benefit for the mother. For instance, by shaping the community of microbes in the milk in ways that may favor the growth of certain beneficial microbes via the simultaneous exclusion of those that cause mastitis during breastfeeding,' Aagaard said."  

"If not treated with antibiotics, mastitis, or the painful inflammation of breast tissue that typically involves an infection, prevents breastfeeding and can become a serious condition."

The above odd statement on the management of mastitis may have been provided by a ScienceDaily writer, rather than the authors of the study.  That above statement infers that the foremost and only appropriate treatment of mastitis is with antibiotics, and says nothing about the long-recommended approaches of breastfeeding more often or otherwise draining the breast more often, rest, compresses, etc. that often resolves mastitis without antibiotics, as opposed to "mastitis preventing breastfeeding."                                                                                                                                                             
                                                                                                                                                                                                                                  
The following is from the discussion section of the authors' study:

"We speculate the significance of HMO-driven proliferation of Streptococcus spp. may be twofold: firstly, this may be of maternal benefit and function to help prevent mastitis by allowing Streptococcus spp. to outcompete potential pathobionts such as Staphylococcus aureus, a common causative pathogen of mastitis. Since mastitis is known to be associated with a loss of diversity in the milk microbiome, we speculate that HMO may serve to prevent sparsity and dysbiosis by favoring proliferation of multiple Streptococcus spp., thus increasing the bacterial diversity of the milk microbiome to 'crowd out' pathogens. Second, HMO may serve to promote growth of commensal Streptococcus spp. in the infant digestive tract, in particular the oral microbiome where Streptococcus spp. predominate and are crucial for the establishment of complex commensal communities. We speculate the net effect of both mechanisms would be the minimization of mastitis pathobionts in both the maternal milk and the infant mouth (e.g., Staphylococcus aureus); this concept is consistent with the ecologic principle of colonization resistance. On a global scale as great as 20–30% of all breastfeeding women have at least one occurrence of postpartum mastitis, and while modern medicine in the developed world generally regards mastitis as being self-limiting or readily treatable with a short course of dicloxacillin or cephalexin, community acquired methicillin-resistant S. aureus (CA-MRSA) breast infections have been increasing. Approximately 10% of cases result in breast abscess formation, and in under resourced settings with scant availability of both antibiotics and readily accessible care, mastitis increases the risk of transmission of HIV through breastfeeding. A promising route of future investigation will be to explore the use of maternal dietary modification and optimization for the prevention of postpartum or puerperal mastitis; such approaches could reduce the prevalence of mastitis resulting in less antibiotic use and diminished prevalence of resistant organisms, particularly CA-MRSA, alongside an anticipated risk reduction of postpartum mother-to-child transmission of HIV."

Open access:  https://www.nature.com/articles/s41598-020-79022-6#Sec7


With best regards,

Debbie

Debra Swank, RN BSN IBCLC
Program Director
More Than Reflexes Education
Elkins, West Virginia USA
http://www.MoreThanReflexes.org

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