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Let’s Talk About Milk

What if we found the milk we are drinking is linked to Diabetes, Autism, Heart Disease, Schizophrenia, Prostate & Ovarian Cancer and is not that all that is cracked up to be after all? I don’t know about you, but I was brought up to believe wholeheartedly that milk (by which I mean cow, sheep or goat’s milk) is good for us, indeed, that we need milk in our diet for optimal health. We are told that it will help us grow, strengthen our bones, prevent fractures, and provide useful protein, vitamins and minerals.

 

Firstly, it is important to say that this is an emerging field of research, which means that finding high quality studies can be quite a challenge! Whilst researching this post, it was frustrating to see just how many of the studies in favour of milk, whilst although seeming reliable at first, then turned out to be supported by one dairy board or another. Although I don’t want to fall into the trap of ‘us vs. big food business’, I couldn’t help but feel that there may well be a stronger marketing force at play here than feels completely comfortable. If you want to understand what is at play here in the milks on offer, please watch these two videos from Sean at Underground Wellness after he read the Devil In The Milk, the book by Professor Keith Woodford. (see it below).

 

 

 

The Devil In The Milk

This groundbreaking work is the first internationally published book to examine the link between a protein in the milk we drink and a range of serious illnesses, including heart disease, Type 1 diabetes, autism, and schizophrenia.

 
These health problems are linked to a tiny protein fragment that is formed when we digest A1 beta-casein, a milk protein produced by many cows in the United States and northern European countries. Milk that contains A1 beta-casein is commonly known as A1 milk; milk that does not is called A2. All milk was once A2, until a genetic mutation occurred some thousands of years ago in some European cattle. A2 milk remains high in herds in much of Asia, Africa, and parts of Southern Europe. A1 milk is common in the United States, New Zealand, Australia, and Europe.

 
 

Download Study (PDF): Ischaemic heart disease, Type 1 diabetes, and cow milk A1 beta-casein by Murray Laugesen, and Robert B Elliott.
Read: The importance of Indian breed of cow’s milk (Desi)

 
In Devil in the Milk, Keith Woodford brings together the evidence published in more than 100 scientific papers. He examines the population studies that look at the link between consumption of A1 milk and the incidence of heart disease and Type 1 diabetes; he explains the science that underpins the A1/A2 hypothesis; and he examines the research undertaken with animals and humans. The evidence is compelling: We should be switching to A2 milk.

 
A2 milk from selected cows is now marketed in parts of the U.S., and it is possible to convert a herd of cows producing A1 milk to cows producing A2 milk.

 
This is an amazing story, one that is not just about the health issues surrounding A1 milk, but also about how scientific evidence can be molded and withheld by vested interests, and how consumer choices are influenced by the interests of corporate business.

 

What is good about milk then?

Well, it contains many of the essential nutrients we need everyday, from the well-known calcium, to dietary vitamin D, phosphorus, potassium, iodine, B vitamins and much more. It is also a good source of protein, a thirst-quenching, low-sugar drink, and is cheap and readily available.

 
That sounds pretty good, really! So what are the concerns?

 
A1 beta – casein and A2 beta – casein are components of the protein in milk. The book and various independent researchers have extensively shown the various characteristics of all the components of this protein, including A1 and A2 beta-casein. Just to explain things in a better manner, the mass-produced commercial milk has A1 beta-casein, it is, in turn, converted into beta casomorphin-7 (BCM-7).

Image result for devil in the milk

 
It is this BCM-7 that ultimately has been known to cause many health issues. Majorly, A1 milk’s consumption since childhood has been shown to increase the risk of diabetes, heart ailments, sudden infant death syndrome (in milk consuming children), autism (when consumed by mother over a long time, before and during pregnancy), digestive intolerance and cancer. It also has been known to cause bloating, which ultimately makes an individual lazy and hence is indirectly responsible for a lot of lifestyle diseases.

 
On the contrary, A2 milk is totally free of A1-beta casein. It has been known through studies that Indian & African Desi cow breeds (Zebu/Bos Indicus/Humped Cow) & (Guernsey, Jersey, French Charolais/ Limousin breeds) are quite capable of producing A2 milk. This A2 milk is not only safe but has been shown to add valuable health benefits to the consumer.

 
Nowadays, it is a hot topic of discussion amongst scholars and a lot needs to be brought out into the light. But the eye-opening efforts of Keith Woodford is just the beginning.

 

Lactose intolerance

Intolerance to milk-containing foods is common, and increases with age. This is thought to be because as we get older, our need to digest milk declines (which we would originally have only consumed from our mother’s breast). The majority of the world’s population starts to decrease their ability to digest milk by the age of 3-5 years. This trend then continues as we get even older; in one study, around half of adults over 50 were lactose intolerant, and around a quarter were under the age of 50, although this does vary between ethnic groups, and Northern Europeans in fact seem to have one of the highest lactose tolerances (1) (2).

 
Milk intolerance is caused by low levels of the enzyme ‘lactase’ which breaks down the milk sugar known as ‘lactose’. This is usually due to a genetic trait, which means that we don’t produce enough of the lactase enzyme anymore (2).

 
This matters because lactose sugar needs to be broken down into two smaller sugars, known as glucose and galactose, before it can be absorbed as energy;

 
If this breakdown doesn’t happen, then the lactose travels onwards from the small bowel into the large bowel, or colon. In those who don’t have good lactase enzyme activity, around 75% of the unabsorbed lactose sugar will pass into the large bowel (2).

 
Unfortunately, when unabsorbed lactose sugar reaches the colon it is fermented by the gut bacteria, producing a gas. This can distend and stretch the bowel walls, leading to discomfort and bloating, two of the classical signs of lactose intolerance. The higher sugar load of the large bowel also draws water into the gut, which can lead to loose stools or diarrhea (2).

 
The symptoms of lactose intolerance may include (noticed after eating at least two servings of dairy / day)*

 
Long-term problems with diarrhoea
Abdominal pain or discomfort
Bloating
Flatulence

*Note: These symptoms are very non-specific, so if you are suffering from any of the above, or are worried you might have lactose intolerance, do see your GP to just check there is nothing else that might be going on. This is especially important in children.

 

Galactose

Studies have shown that a high intake of one of the milk sugars we’ve looked at above, galactose, may not be all that beneficial to our health. Long-term exposure, particularly to high amounts of galactose, has been shown to hasten biological aging in animal models (in this instance, in mice).
 

D-galactose forms advanced glycation end products (AGEs) in vivo, and a comparison of D-galactose-aged and AGEs-aged mice demonstrated that both models resembled aged mice, suggesting that advanced glycation may be part of the
D-galactose aging mechanism (14).  
These changes include damage from oxygen radicals (known as oxidative stress), chronic inflammation, degeneration of the nervous system (including the brain), reduced immune function and changes in the way that genes are read and copied (which is potentially a risk factor for cancer development) (3) (4) (5). Such effects have been estimated to potentially affect humans with milk consumption of just 1-2 glasses per day (6).

 
Now, it is important to point out that there are obviously big differences between studies in mice, and what this would mean for humans, but this initial research offers us a warning shot as to why milk might not turn out to be quite so great for us afterall. A study of over 100,000 people, published in the British Medical Journal in 2014, showed that drinking milk was shown to increase levels of certain inflammation markers in both men and women (6).

 
There is a glimmer of good news for dairy lovers though. It is thought that cheese and fermented dairy products (such as kefir or yoghurt) would have less of these effects, because of their lower lactose sugar, and therefore galactose, content. In fact, a high intake of fermented milk products has been associated with a decreased risk of heart disease, as well as reducing the markers of oxidative stress and inflammation (6).

 
Galactose sugar is present in other foods, mainly cereals, vegetables, and fruits, but the amount is very small compared to that found in milk (7).

 

Dr Alex Richardson, a Senior Research Fellow, University of Oxford; had this to say about the book; “Woodford’s book reviewed the significant body of evidence that had already accumulated on the podevil-in-the-milk-booktential implications of A1 vs A2 beta casein for human health. This has increased considerably since then, and it strongly suggests that A2 milk may have advantages over A1 for prevention or amelioration of symptoms in a wide range of health conditions, including Type 1 diabetes and other auto-immune disorders; cardiovascular disease; some respiratory problems (including apnoea and sudden infant death syndrome in infants); atopic conditions such as eczema and asthma; and some developmental and mental health conditions, including autism and schizophrenia.

 

For most of these conditions, conclusive evidence of causal links with A1 consumption – i.e. evidence from randomised controlled trials in humans – remains lacking. However, just as with the link between smoking and lung cancer (which was never ‘proven’ in human clinical trials), in relation to many of these conditions, such trials simply cannot be conducted for practical and/or ethical reasons. Current evidence for potential health benefits from A2 vs A1 milk therefore mainly involves mechanisms and associations observed in human clinical and population studies, together with findings from animal studies and ‘in vitro’ research involving human cells or tissue.

 
With respect to theory and mechanisms, A1 and A2 beta-casein differ by just one amino acid from the 209 that make up this major milk protein (the A1 mutation leads to a histidine rather than a proline at position 67). However, this affects how the beta-casein is broken down during digestion, such that A1 beta-casein gives rise to a peptide (protein fragment) called beta-casomorphin-7 (BCM-7), while A2 does not.

 
As its name suggests, BCM-7 activates opioid receptors – which have multiple potential effects on health and behaviour. BCM-7 is known to stimulate mucus production; and animal studies show not only that consumption of A1 vs A2 beta-casein promotes gut inflammation, but that this is mediated by opioid mechanisms. Recent studies further show that in human brain cells, BCM-7 reduces production of glutathione (a key antioxidant), while also modifying the expression of many other genes.
Such ‘epigenetic’ effects have potential relevance to some developmental disorders (e.g. increased vulnerability to ‘oxidative stress’ has long been implicated in both autism and schizophrenia). However, the sheer complexity of brain development, and the innumerable mechanisms as well as the timescales involved, again make definitive evidence of causality difficult or impossible to obtain.

 
In my experience, many people with no classical allergy to cows’ milk protein (assessed via IgE responses) find that standard cow’s milk doesn’t “agree with them” – giving them physical symptoms such as digestive problems (constipation, diarrhoea or irritable bowel syndrome), excessive mucous production (sinusitis, ‘stuffy nose’ or wheezing), otherwise inexplicable aches and pains; and sometimes mental symptoms, including mood swings and/or attentional and cognitive problems typically described as like “brain fog”. Anyone with clinical experience of autism, ADHD, schizophrenia and related conditions knows that many people with these conditions (as well as many without) show strong ‘cravings’ for milk and dairy products. These could plausibly reflect opioid mechanisms triggered by BCM-7 from A1 beta-casein – as could similar cravings for foods containing gluten (also common in people with autism), because gluten digestion also gives rise to peptides with opioid activity.

 
Some of the digestive complaints associated with milk and dairy products (particularly bloating, constipation or stomach pain) may simply reflect intolerance to lactose – the sugar in milk. However, testing shows that lactose intolerance actually affects only around 5% of the UK population – so this cannot explain the much larger proportion (around 20%) who report intolerance to cows’ milk products, but have no classic allergy to cows’ milk protein. Similarly, many of the other physical and mental symptoms reported following consumption of standard cows’ milk products are not easily explicable in terms of low lactase production, but would plausibly follow from sensitivity to the opioid peptide BCM-7, produced from A1 beta-casein.

 
Clearly, many people can consume standard A1 cows’ milk without obvious ill effects, so more research is still needed into individual differences in sensitivity to BCM-7. One aspect of vulnerability already under study concerns the efficiency of the enzyme DPP-IV, which breaks down BCM-7. Other differences in gut and immune function also merit further investigation. Animal studies clearly show that A1 vs A2 beta-casein promotes gut inflammation. Furthermore, the first randomised controlled trial in humans to compare the two also found differences in digestive function favouring A2. More such trials are urgently needed to replicate this and identify susceptible people.

 
Meanwhile, A2 beta casein is the original form of beta-casein, so human milk is A2, as is milk from goats, sheep, buffalo, donkey, camel and other mammals. Some people find these milks easier to tolerate than standard A1 cows’ milk, although they are not to everyone’s taste – hence the growing interest in A2 cows’ milk. Importantly, these other animal milks still contain lactose, so are not suitable for the 5% of people with definite lactose intolerance. Most importantly, no animal milks are suitable for those with classic cows’ milk protein allergy, owing to the potential for cross-reactivity. However, some people with otherwise inexplicable ‘intolerance’ to standard cows’ milk find the A2 form perfectly acceptable.”

 

Milk quality

Organic milk has been found to contain more of the healthy omega-3 fats (although less of the essential minerals iodine and selenium) than non-organic milk (8). Unfortunately, we don’t yet know what the overall effect of any residual chemicals (such as antibiotics, pesticides etc.) and hormones found in milk has on the human body.

 

A1 vs. A2

A major source of the protein found in milk is called Beta-casein, of which there are two subtypes – named A1 and A2. It is now possible to buy milk that has only the less common A2 protein (99% of supermarket milk is A1). You may have seen some adverts for this on the television or in magazines.

 
Some studies have found that, in people who have milk intolerance, A2 milk may give them fewer gastrointestinal symptoms (such as bloating or pain), compared to regular milk. This suggests that there may be some people who, instead of being intolerant to the lactose sugar, are in fact intolerant to the A1 milk protein casein (9), (10) (11). However, these studies have been rather small, and have generally been funded by the A2 industry, so to be certain of the effects, a larger, independent study is certainly needed.

 
There is also still rather a lot of uncertainty about the potential effects, good or bad, of A1 vs. A2 milk (12) (13), but research is still going on to try to unpick the facts to help guide our decision of the future.

 

The bottom line?

If you do choose to reduce the amount of milk that you are consuming, it is really important to make sure that you have plenty of other sources of the essential nutrients that milk provides in your diet – particularly calcium, iodine and B-vitamins. Thankfully, there are lots of non-dairy sources of these out there!

 
If you think that you might be lactose intolerant, do consult with your healthcare provider, as the symptoms are rather non-specific and it is important to ensure that you are not missing another diagnosis.

 
Perhaps the health claims of milk are not quite what we have believed for all these years. Although there clearly needs to be lots more research until we know for sure what exactly is going on, there are some emerging studies that have questioned the links with bone health in particular. Do note, however, that these are studies in adults, and therefore should not be relied upon in children.

 

References:

(1) Rao, D.R., Bello, H., Warren, A.P. and Brown, G.E. (1994) ‘Prevalence of lactose maldigestion’, Digestive Diseases and Sciences, 39(7), pp. 1519–1524.

(2) Montgomery, R., Grand, R. and Buller, H. (2015) Lactose intolerance: Clinical manifestations, diagnosis, and management. Available at: UpToDate (Accessed: 4 April 2016).

(3) Cui, X., Wang, L., Zuo, P., Han, Z., Fang, Z., Li, W. and Liu, J. (2004) ‘D-Galactose-caused life shortening in Drosophila melanogaster and Musca domestica is associated with oxidative stress’, Biogerontology, 5(5), pp. 317–326.

(4) Cui, X., Zuo, P., Zhang, Q., Li, X., Hu, Y., Long, J., Packer, L. and Liu, J. (2006) ‘Chronic systemic D-galactose exposure induces memory loss, neurodegeneration, and oxidative damage in mice: Protective effects of R-a-lipoic acid’, Journal of Neuroscience Research, 83(8), pp. 1584–1590. doi: 10.1002/jnr.20845.

(5) Hao, L., Huang, H., Gao, J., Marshall, C., Chen, Y. and Xiao, M. (2014) ‘The influence of gender, age and treatment time on brain oxidative stress and memory impairment induced by d-galactose in mice’,Neuroscience Letters, 571, pp. 45–49.

(6) Michaelsson, K., Wolk, A., Langenskiold, S., Basu, S., Warensjo Lemming, E., Melhus, H. and Byberg, L. (2014) ‘Milk intake and risk of mortality and fractures in women and men: Cohort studies’, BMJ, 349(oct27 1), pp. g6015–g6015.

(7) Gross, K.C. and Acosta, P.B. (1991) ‘Fruits and vegetables are a source of galactose: Implications in planning the diets of patients with Galactosaemia’, Journal of Inherited Metabolic Disease, 14(2), pp. 253–258.

(8) Srednicka-Tober, D., Baranski, M., Seal, C.J., Sanderson, R., Benbrook, C. and Steinshamn, H. (2016) ‘Higher PUFA and n-3 PUFA, conjugated linoleic acid, a-tocopherol and iron, but lower iodine and selenium concentrations in organic milk: A systematic literature review and meta- and redundancy analyses’, British Journal of Nutrition, 115(06), pp. 1043–1060.

(9) Ho, S., Woodford, K., Kukuljan, S. and 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, 68(9), pp. 994–1000.

(10) Jianqin, S., Leiming, X., Lu, X., Yellend, G., Ni, J. and Clarke, A. (2016) ‘Effects of milk containing only A2 beta casein versus milk containing both A1 and A2 beta casein proteins on gastrointestinal physiology, symptoms of discomfort, and cognitive behavior of people with self-reported intolerance to traditional cows’ mi’, Nutrition Journal (pending publication)

(11) Pal, S., Woodford, K., Kukuljan, S. and Ho, S. (2015) ‘Milk intolerance, beta-casein and Lactose’, Nutrients, 7(9), pp. 7285–7297.

(12) Allison, A.J. and Clarke, A.J. (2005) ‘Further research for consideration in “the A2 milk case”’, European Journal of Clinical Nutrition, 60(7), pp. 921–924.

(13) Truswell, A.S. (2005) ‘The A2 milk case: A critical review’, European Journal of Clinical Nutrition, 59(5), pp. 623–631.

(14) Song X, Bao M, Li D and Li YM: Advanced glycation in D-galactose induced mouse aging model. Mech Ageing Dev 108:
239-251, 1999.