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S M Montgomery, A Ehlin, and A Sacker
Breast feeding and resilience against psychosocial stress
Arch Dis Child 2006; 91: 990-994 [Abstract] [Full text] [PDF]
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Electronic letters published:

[Read eLetter] Breast feeding, resilience against psychosocial stress, and polyunsaturated fatty acids
Undurti N Das   (11 August 2006)
[Read eLetter] Is it in the milk or in the genes?
Mats Reimer   (22 November 2006)
[Read eLetter] Is it in the milk or in the genes: why focus on milk?
Scott M Montgomery   (28 November 2006)

Breast feeding, resilience against psychosocial stress, and polyunsaturated fatty acids 11 August 2006
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Undurti N Das,
Physician/Scientist
UND LIfe Sciences

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Re: Breast feeding, resilience against psychosocial stress, and polyunsaturated fatty acids

undurti{at}hotmail.com Undurti N Das

Dear Editor,

The observation that breast feeding is associated with resilience against the psychosocial stress linked with parental divorce/separation is interesting and suggests that breast milk could contain nutrients or molecules that influence neurotransmitter function in the brain. I propose that polyunsaturated fatty acids (PUFAs) present in human breast milk is responsible for this beneficial action.

It was reported that behavioral variables associated with academic test anxiety such as appetite, mood, mental concentration, fatigue, academic organisation and poor sleep as well as elevated cortisol level could be improved by the admnistration of a mixture of omega-3 and -6 fatty acids (1). Hamazaki et al (2) showed that psychosocial stress associated behavioral change is less in those who took docosahexaenoic acid (DHA) supplementation compared to control. The ratio of plasma epinephrine to norepinephrine concentrations was significantly increased in the DHA group, whereas it did not chnage in the control group. Subchronic intracerebroventricular administration of interleukin (IL)- 1beta-induced stress/anxiety behavior of rats was attenuated by ethyl- eicosapentaenoic acid (ethyl-EPA). Ethyl-EPA also reduced the rise in serum corticosterone induced by IL-1 and enhanced the production of anti- inflammatory cytokine IL-10 (3). In addition, erythrocyte concentrations of most n-3 PUFAs were lower in patients with social anxiety disorder (4). Since, human breast milk is rich in n-3 and n-6 fatty acids (5), these results imply that adequately breast fed children will be less prone to psychosocial stress.

In view of this, it will be interesting to study the plasma and RBC concentrations of various PUFAs, profile of plasma cytokines and cortisol levels in those who were breast fed and showed less psychosocial stress and compare them with non-breast-fed controls.

References:

1. Yehuda S, Rabinovitz S, Mostofsky DI. Mixture of essential fatty acids lowers test anxiety. Nutr Neurosci. 2005;8:265-267.

2. Hamazaki T, et al. Administration of docosahexaenoic acid influences behavior and plasma catecholamine levels at times of psychological stress. Lipids 1999;34 Suppl:S33-S37.

3. Song C, Li X, Leonard BE, Horrobin DF. Effects of dietary n-3 or n -6 fatty acids on interleukin-1beta-induced anxiety, stress, and inflammatory responses in rats.J Lipid Res 2003;44:1984-1991.

4. Green P, et al. Red cell membrane omega-3 fatty acids are decreased in nondepressed patients with social anxiety disorder. Eur Neuropsychopharmacol 2006;16:107-113.

5. Das UN. Essential fatty acids: biochemsitry, physiology and pathology. Biotech J 2006; 1: 420-439.

Is it in the milk or in the genes? 22 November 2006
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Mats Reimer,
Community pediatrician
Molnlycke Sweden

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Re: Is it in the milk or in the genes?

reimer{at}telia.com Mats Reimer

Dear Editor,

This paper has in my view several serious flaws, and the conclusions does not seem well supported. The effect of reduced anxiety is so small that it seems clinically irrelevant, and is seen only in the subgroup of children having experienced divorce. Anxiety is a hereditary trait, but adjustment has only been made for very serious mental illness (not just anxiety) in the mother, and no adjustment was done for any traits in the father. Anxiety in either parent could obviously have a strong influence on the sucess in breastfeeding, as well as on the risk of divorce. Finally, I would expect that had the paper found a 7% increase in anxiety in breastfed children it would not have been published at all; because we all want breast milk to be the best thing we are prone to both data trawling and publication bias.

Is it in the milk or in the genes: why focus on milk? 28 November 2006
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Scott M Montgomery,
Principal research fellow
Karolinska Institutet

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Re: Is it in the milk or in the genes: why focus on milk?

scott.montgomery{at}ki.se Scott M Montgomery

Dear Editor,

I would like to thank Dr Reimer for his interest in our work and reciprocate by correcting his flawed understanding of the paper. Perhaps it would be helpful to start by summarising the hypothesis, results and interpretation of the study. Our a priori hypothesis was that positive physical contact between mother and child in early life may result in enhanced control of the stress response as indicated by animal studies (1, 2). We could not test this directly, but used breast feeding as an indirect marker of close contact in early life. Among breast fed children there was no statistically significant or notable association of parental divorce with anxiety, but among bottle fed children the association was more pronounced and statistically significant. This does not prove that early physical contact associated with breast feeding confers resilience against psychosocial stress, but is consistent with the hypothesis. Further research should have a more detailed focus on mother-child interactions (not just breast feeding) during the first months of life. Our abstract concludes: ‘This could be because breast feeding is a marker of exposures related to maternal characteristics and parent-child interaction.’

This study forms part of a collaborative programme of work investigating the concept of resilience, which is defined as a factor that limits the damaging consequences of adverse exposures.(3) To investigate this concept using statistical effect modification, it is necessary to consider the difference in outcome between those with and without an adverse exposure and how this difference varies by presence of the putative resilience factor using interaction testing. Dr Reimer seems to misunderstand interaction testing when he complains that reduced anxiety is only observed among those who experienced divorce. We chose divorce as a marker of exposure to chronic psychosocial stress as we have evidence from earlier studies of its potentially profound effect on child development.(4) The hypothesis being tested concerned children’s anxiety following exposure to stress reflecting differences in reactivity of the stress response. A limitation of the study is that we did not have acute measures of exposure and response to stress and only a proxy measure of maternal contact in early life (breast feeding): use of such measures means that associations are likely to be conservative. In claiming that the differences in anxiety are ‘clinically irrelevant’ Dr Reimer misses the point: we were not suggesting breast feeding as an intervention for families at a high risk of divorce, but identifying associations that may provide information about processes relevant to resilience. We have identified a potentially useful indirect marker of resilience against some forms of psychosocial stress that should now be confirmed and elucidated by further investigation.

Dr Reimer claims that ‘adjustment has only been made for very serious mental illness,’ but reading the paper shows this statement to be entirely inaccurate. Multiple potential confounding factors were included in the multivariate analysis, including the Malaise Inventory, which is a 24-item measure of tendency to depression.(5, 6) We modelled this information both as a dichotomous variable and using all of the 24 items as separate variables (hardly measuring just serious mental illness) in an attempt to perform the most comprehensive adjustment possible for maternal characteristics. This measure of depression is likely to be strongly associated with anxiety. Other relevant measures include cigarette smoking during pregnancy, which is associated both with maternal personality characteristics and adverse outcomes in offspring. While we do not have perfect measures, if the observed effect modification was mediated exclusively through maternal anxiety then a greater reduction in magnitude of association might be expected following adjustment for the potential confounding factors. The concern that father’s characteristics influence both exposure and outcome differentially by early breast feeding is of course possible but less plausible as a major source of confounding.

Observational studies cannot prove causation. In contrast with Dr Reimer’s assertion that the paper is trying to show ‘breast milk to be the best thing,’ the paper outlines several potential explanations for the results that may not be mutually exclusive, including: the influence of early physical contact on neuro-endocrine mechanisms; maternal personality characteristics associated both with breast feeding and other aspects of mother-child interactions; breast feeding may indicate a non-causal association with parental attachment or may be implicated in the development of parental attachment.

References:

1. Sapolsky RM. The importance of a well-groomed child. Science 1997; 277:1620-1621.

2. Liu D, Diorio J, Tannenbaum B, Caldji C, Francis D, Freedman A et al. Maternal care, hippocampal glucocorticoid receptors, and hypothalamic- pituitary-adrenal responses to stress. Science 1997; 277:1659-1662.

3. Osika W, Ehlin A, Montgomery SM. Does height modify the risk of angina associated with economic adversity? Economics and Human Biology 2006; 4: 398-411.

4. Montgomery SM, Bartley MJ, Wilkinson RG. Family conflict and slow growth. Archives of Disease in Childhood 1997; 77: 326-330.

5. Rutter M, Graham P, Yule W. A neuropsychiatric study in childhood. London: Heinemann; 1970.

6. Grant G, Nolan M, Ellis N. A reappraisal of the Malaise Inventory. Social Psychiatry and Psychiatric Epidemiology 1990; 25:170-178.

 

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