I wonder about the title of a new nature medicine editorial
Breathing easier with breast milk
It is not so much the unwanted analogy to aspiration; the paper simply hasnÂ´t to do anything with breathing. It is a poor narrative of a concomittant NM article repeating many of its prejudices. Although the authors would like to let you belief that they have discovered allergen transfer into breast milk, this is known for at least 25 years. There is also a lot of literature of beneficial TGFß effects in breast milk unfortunately some human studies (not mentioned) arrive at an opposite conclusion
Infants receiving breast milk with low levels of TGF-beta2 were less likely to become sensitized during their first 2 yr of life.
I guess that the authors have also never looked at current epidemiological research; they would have discovered that we certainly have differentiated non-allergic and allergic mothers when looking at breast feeding effects.
The illustrating figure is rather nonsense as there is no anatomical correlate of allergens going from the trachea to the right breast while the depicted T cell should even show its CD4 receptor – even worse that CD4+ T cells are constitutively inhibited by TGFß. The whole thing becomes dangerous when the authors advocate the supersizing (!) of breast milk (as if the supersizing strategy would not have done enough harm). More of their own words
it seems probable that breastfeeding provides the right context – TGFß and perhaps other breast milk factors, such as vitamin A – to induce protective immunity to maternal inhaled antigens in neonates.
Maybe the authors should have checked a recent mouse studies on vitamin A
VA/retinyl palmitate supplementation during lactation and after weaning … significantly enhanced IL-4 production and OVA-specific IgE after sensitisation. In contrast, mice fed VA-elimination diet displayed no significant alteration … Our results showed that a single allergen injection during postnatal development induces allergic sensitisation whose degree is modified by the VA content of the maternal diet during lactation…
or another study with the same message
We used the OVA exposure mouse model to determine the contributions of vitamin A-deficient, control (4IU/g), and high-level vitamin A (250-IU/g) diets to the development of allergic airway inflammation and hyperresponsiveness. VAD reduced serum IgE and IgG1 responses, pulmonary eosinophilia, and the levels of IL-4 and IL-5 in bronchoalveolar lavage specimens, whereas the 250-IU/g diet increased serum IgE.
Somewhat unusual also their world-embracing statement
Therefore, in addition to the need to resolve major outstanding questions regarding regulatory T cell development and function in adults and neonates, it will be important in the future to answer fundamental questions about the cellular, molecular, and anatomical determinants of immunological outcome poerating in early life
which would be better suitable for a presidential address.