Category Archives: physiology

What’s the deal with A2 milk?

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So what’s all this business about A2 milk?  How is it different from A1 milk?  Is it hooey?  What do these codes refer to anyway?

Starting with the last question first, A1 and A2 refer to “versions” of the beta-casein gene. In this case, the gene in question encodes the protein beta-casein, one of three casein proteins, which is, of course, a key component of cheese. The A2 version of this protein varies just a little bit in its structure from the A1 version. An individual cow’s genotype could be A1A1, A2A2, or A1A2 for the beta-casein gene; her milk would then contain whichever protein versions her genes dictate.

The a2 Milk Company claims that A2-only milk is easier on digestion. A recent study has suggested that in milk-sensitive individuals, milk containing A1 protein may be associated with symptoms of discomfort after milk consumption, and with strictly A2 milk those symptoms may be lessened. Also, gastrointestinal transit time appears to be slower with A1 milk consumption but, contrarily, yielding softer stools. Additional studies to provide replication of these findings are needed. Early studies on A1 and A2 milk that suggested a link between A1 milk and several diseases have been unsupported by subsequent investigations. That is, there is no evidence that consuming milk containing A1 protein carries any disease risk.

So, should breeding decisions be made on the basis of beta-casein genotype? Or perhaps the question is, is A2 milk a fad or a legitimate, long-term slice of the market? Does A1 vs. A2 matter for yogurt or cheese making? There is a lot we still don’t know about the biology of milk. However, there would seem to be little risk in choosing A2A2 bulls. There are quite of few of them out there, although the number varies by breed. The most comprehensive and recent documentation of beta-casein genotype by breed has been compiled by the Canadian Dairy Network (see table).

Available data from U.S. cattle are more limited in number and over 20 years old. Interestingly, Zebu- or Brahman-type cattle have a very high frequency of A2A2.

Bottom line, don’t compromise your primary genetic objectives for your herd just to chase an A2A2 genotype, but there’s likely no harm in moving that direction if it makes sense for your market of the future.

For a deeper dive into the biology of A1 and A2, read on.

A1 and A2 refer to types of gene variants of the beta-casein gene. A gene variant (an allele, for those who remember their biology) is when we have a difference in the DNA sequence for a particular gene. The A2 gene variant encodes a proline (a particular amino acid; you’ll recall that amino acids are the building blocks of proteins) at position 67 in the 209-amino acid chain that forms beta-casein (see figure below). The A1 gene variant encodes a histidine at position 67.

The A1 beta-casein protein is thought likely to be cleaved (cut) during gastrointestinal digestion at the position 67 histidine, while A2 beta-caseins are less likely to be cleaved there. Cleavage at amino acid 67 generates a short protein (a peptide) called beta-casomorphin-7 (abbreviated BCM7). BCM7 has opioid properties. Now, no need for concern. We all know that while milk is tasty, it is not a very effective painkiller nor brain manipulator. It is possible though, that BCM7 may have some effect on processes in the gut, such as slowing the rate of passage. Also, all milk contains additional types of opioid peptides. Other foods (from animals and plants) do as well.

 

Diagram shows cartoon of regions of beta-casein protein with variable amino acid indicated.
The region of the beta-casein protein where A1 and A2 vary.

OSU Research: Predicting post-calving clinical mastitis in dry cows via serum profile

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Researchers from Oregon State University investigated the blood serum profiles of Holstein cows before and after calving and compared those that developed clinical mastitis with those that did not. To do so, they used ultra-performance liquid chromatography high resolution mass spectrometry plus statistics to identify differences in concentration of metabolites, lipids, minerals, and inflammatory markers in blood serum. It’s OK if you read that last sentence and went, “Huh?”  The short version is that they ran blood serum samples from dry cows through some fancy laboratory equipment to see if there were any indicators associated with developing clinical mastitis after calving. And yes, there are!

For example, alpha-tocopherol (a form of vitamin E) levels were significantly higher in the blood of cows that did not develop clinical mastitis compared to those that did (Figure 1). Another difference was in the overall profile of metabolites (molecules that participate in or are produced during metabolism); they were quite different for cows that remained healthy and those with post-calving mastitis (Figure 2).

Figure 1. Control animals (no mastitis; open bars) had significantly more alpha-tocopherol (vitamin E) in their blood than cows that developed mastitis (shaded bars). From Figure 4 from Zandkarimi et al. 2018.
The figure shows self-organizing map of metabolomic data.
Figure 2. See the starkly different profiles in serum metabolite concentration between cows that developed mastitis post-calving (CMP) and those that did not (Control)? The metabolites are grouped by metabolite family, e.g., carnitines. The more red colors indicate higher concentrations, while blue indicates lower. From Figure 5 from Zandkarimi et al. 2018.

 

 

 

 

 

 

 

 

 

 

 

 

 

 

While no dairies have liquid chromatography mass spec technology in their on-farm lab, these results may lead the way to identifying one or two highly reliable blood markers that could be easily measured on the dairy. And forewarned is forearmed, right? Knowing which cows were likely to develop mastitis could allow proactive treatment to prevent the more expensive and damaging clinical mastitis.

The paper: F. Zandkarimi, J. Vanegas, X. Fern, C.S. Maier, G. Bobe. Metabotypes with elevated protein and lipid catabolism and inflammation precede clinical mastitis in prepartal transition dairy cows. Journal of Dairy Science, June 2018, 101:5531–5548

How do cows digest all that feed they eat?

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Lactating cows can eat upwards of 55 pounds of feed a day on a dry matter basis. How do they do that?  Ruminants produce large quantities of saliva every day. Estimates for adult cows are in the range of 25 to 38 gallons of saliva per day. Aside from its lubricating qualities, saliva serves at least two additional very important functions in the ruminant. It plays a major role in buffering the pH in the foregut and provides fluid for the fermentation activities in the rumen. Boluses of preliminarily chewed forage are regurgitated from the reticulorumen and re-chewed: the process we refer to as rumination or cud chewing. The grinding action of the teeth mechanically breaks down the plant fibers into smaller particles, providing additional surface area for digestive enzymes to “attack”. Animals on pasture or range typically graze for around 8 hours a day, providing a steady stream of feedstuffs to the reticulorumen. Contractions mix the feed around and between the rumen and reticulum. See Figure 1 for a diagram of a typical ruminant digestive tract.

outline of a cow with detailed labeling of the digestive tract: mouth, esophagus, reticulum, rumen, omasum, abomasum, small intestine, large intestine
Figure 1 – Illustration of the digestive system in a cow.

The rumen is essentially a fermentation vat. We have often heard cows have four parts to their stomach, the rumen in the largest section in this stomach series and tend to get most the attention because of its unique capabilities. It provides an anaerobic environment, constant temperature and pH, and thorough mixing that allow the microbes to digest forages. Bacteria, protozoa, and fungi are the three major types of microbes. Figure 2 illustrates the types and approximate numbers of microbe types in a rumen (and the number of humans on Earth, just for comparison). Mammals don’t produce enzymes that can digest plant fibers like cellulose. Cattle and other herbivores rely on the digestive enzymes produced by their gut microbes in order to get the majority of nutrients out of forages.

bar graph showing numbers of bacteria, protisis, fungi, mycoplasma, and viruses in a rumen. Also shown is the number of humans on earth for comparison. Data courtesy of Mel Yokoyana, Michigan State University.
Figure 2 – Illustration of microbe populations typically found in the rumen. The scale on the left is logarithmic.

The rate of flow of solid material through the rumen is quite slow and dependent on feedstuff size and density. However, water flows through the rumen rapidly and appears to be critical in flushing particulate matter downstream. As fermentation proceeds, feedstuffs are reduced to smaller and smaller sizes and microbes constantly proliferate. Ruminal contractions constantly flush lighter solids back around the reticulorumen while denser particles (feedstuffs that have been there longer) proceed to the omasum.

The function of the omasum is rather poorly understood. It may function to absorb residual volatile fatty acids and bicarbonate. The tendency is for fluid to pass rapidly through the omasal canal, but for particulate matter to be retained between the omasal leaves. Periodic contractions of the omasum knock flakes of material out of the leaves for passage into the abomasum.

The abomasum is a true, glandular stomach which secretes acid (significantly lowering the pH) and otherwise functions very similarly to the stomach of a monogastric. One fascinating specialization of this organ relates to its ability to process large masses of bacteria. In contrast to the stomachs of non-ruminants, the abomasum secretes lysozyme, an enzyme that efficiently breaks down bacterial cell walls. Much of the protein need of the ruminant is actually satisfied by digesting bacteria that have traveled from the rumen.