I want to talk about
the findings from Ho and colleagues [1] today, and in particular their observation of: "
differences in gastrointestinal responses in some adult humans consuming milk containing beta-casein of either the A1 or the A2 beta-casein type". If you're wondering why such a paper finds it's way on to a blog predominantly about autism research, well stay with me on this rather long blogging entry...
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Before progressing, I am going to put a sort of
COI (conflict of interest) statement into this blog post. As part of my day job, I have, down the years, been party to some conversations on
A2 milk and how one might scientifically test some of the claims / assumptions made about this milk with specific populations in mind. That also our lab has been looking at
analytical ways of differentiating A1 and A2 milk from each other is another COI, allowing for the fact that I am neither a consumer of, nor advocate for, anything to do with any of the white stuff.
In case you're not up to speed with A1 and A2 milk, well, it all boils down to type of cow and type of milk produced. Anyone with a handle on autism research history will have probably heard about
the opioid-excess hypothesis [2]. The long-and-short-of-it is that
casein, the protein found in milk and dairy products, is eventually metabolised into it's constituent
amino acids. Along the way, short chains of amino acids called
peptides are formed. Some of these peptides look (chemically) similar to compounds like
morphine and are hence referred to as the
casomorphins (casein derived morphine-like). The opioid-excess hypothesis suggested that these exogenously derived peptides mimic some of our own naturally occurring
morphine-like compounds that we all have, and disrupt typical functioning in this area to such an extent that it may correlate with some of the signs and symptoms called autism.
I talked about something similar quite recently.
Granted, such a model looks a little simplistic these days knowing what we think we know about
the very plural autisms and
the ESSENCE of cormorbidity. Still, such a hypothesis did seem to fit in well with
the suggested effectiveness of a casein-free (and gluten-free) diet for
some on the autism spectrum, and also some work looking at the opioid receptor blocker that is naltrexone (
see here) and autism. It is with the structure of those peptides in mind that we come to the differences suggested for A1 and A2 milk. Y'see not every cow or other mammal
produces the same kind of casein protein in their milk and hence peptide formulations can vary also. For A2 casein, the idea is that beta-casomorphin fragment 1-7 (BC 1-7), a peptide formed during digestion is not the same as the BC1-7 from A1 milk (
see here) particularly when
it comes to a single amino acid change (proline over histidine) [3].
After such a long-winded explanation, we come back to the Ho paper and some interesting findings...
- First things first, this was a double-blind, randomised cross-over study looking at "gastrointestinal effects" in adults under conditions of either A1 or A2 milk consumption. Two weeks of either A1 or A2 milk consumption (with an appropriate washout period in between) were completed.
- The very informative Bristol Stool Chart was used to grade poop (stool) consistency alongside other more physiological measures such as faecal calprotectin.
- Results: "The A1 beta-casein milk led to significantly higher stool consistency values". That and a correlation between stool consistency and reports of abdominal pain for participants when on the A1 milk compared with when on A2 milk. Ergo, it didn't seem that A2 milk did anything over and above A1 milk, rather that consumption didn't seem to be linked to the symptoms noted when drinking A1 milk.
Appreciating the authors' call for further study in this area, I was intrigued by these results. Not so many moons ago, I came across
the paper by Barnett and colleagues [4] talking about greater gastrointestinal (GI) transit time in rats fed A1 milk over A2 milk (
see here for some additional commentary from one of the study authors). One might very well overlap those rodent reports with the more recent Ho results in terms of how longer transit time from A1 milk might mean greater discomfort bearing in mind some of the literature on
longer transit time and "pain and distension" [5] in certain conditions. Interestingly, the authors ask that research not only focus on confirmation of their results but: "
confirmation in a larger study of participants with perceived intolerance to ordinary A1 beta-casein-containing milk" which begs the question: who and what ailments are being reported?
That all being said, not all the literature on A2 milk is so directional. Take for example
the paper by Crowley and colleagues [6] (open-access) looking at the question of milk consumption correlating with the functional bowel issue constipation. They concluded that: "
that removal of CMP [cow's milk protein]
from the diet of children with CFC [chronic functional constipation]
significantly increased the number of bowel motions and improved constipation". Their results however did not show any significant effect based on casein type when looking at A1 and A2 milk. Constipation, by the way, is also something talked about with some autism in mind (
see here) and particularly
the findings from Afzal and colleagues [7] which concluded: "
Multivariate regression analysis showed consumption of milk to be the strongest predictor of constipation in the autistic group".
I am quite interested in this whole area of different milks from different animals potentially possessing different qualities which might impact on physiology particularly
if eventually applied to conditions like autism, or at least some comorbidity. I think back to the post I did on milk derived opioid peptides and methylation status (
see here) as also being important, as might be the work on something like the use of camel milk (
see here) bearing in mind
the adverse publicity our humped friends have received recently. As per my previous caveat, I don't think we are in a position yet to advocate changes in milk drinking practices for specific groups based on the available literature, but there might be quite a bit more research to do in this important area...
To close, I know this might sound a little odd but am I the only father with young children
who know Barry Scott on sight?
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[1] Ho S.
et al. Comparative effects of A1 versus A2 beta-casein on gastrointestinal measures: a blinded randomised cross-over pilot study.
Eur J Clin Nutr. 2014 Jul 2.
[2] Shattock P. & Whiteley P. Biochemical aspects in autism spectrum disorders: updating the opioid-excess theory and presenting new opportunities for biomedical intervention.
Expert Opin Ther Targets. 2002 Apr;6(2):175-83.
[3] Truswell AS. The A2 milk case: a critical review.
Eur J Clin Nutr. 2005 May;59(5):623-31.
[4] Barnett MP.
et al. Dietary A1 β-casein affects gastrointestinal transit time, dipeptidyl peptidase-4 activity, and inflammatory status relative to A2 β-casein in Wistar rats.
Int J Food Sci Nutr. 2014 Mar 20.
[5] Cann PA.
et al. Irritable bowel syndrome: relationship of disorders in the transit of a single solid meal to symptom patterns.
Gut. May 1983; 24(5): 405–411.
[6] Crowley ET.
et al. Does Milk Cause Constipation? A Crossover Dietary Trial.
Nutrients 2013; 5: 253-266
[7] Afzal N.
et al. Constipation with acquired megarectum in children with autism.
Pediatrics. 2003 Oct;112(4):939-42.
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Ho, S., Woodford, K., Kukuljan, S., & Pal, S. (2014). Comparative effects of A1 versus A2 beta-casein on gastrointestinal measures: a blinded randomised cross-over pilot study European Journal of Clinical Nutrition DOI: 10.1038/ejcn.2014.127
So: "we have concluded that milk-derived opioid peptides and DPPIV [dipeptidyl peptidase-4 (DPPIV)] are potentially factors in determining the pathogenesis of autism."
