Ah yes, lactose intolerance…that seminal occurrence of stomach rumbling, gaseous bloat and odoriferous farts strong enough to make a dog vacate the room and that can, with little forewarning, transform into a Rorshach-inspired shart in one’s undergarments or sheets.
Magic, pure utter magic!
Lactose intolerance is defined by the Mayo Clinic this way:
“People with lactose intolerance are unable to fully digest the sugar (lactose) in milk. As a result, they have diarrhea, gas and bloating after eating or drinking dairy products. The condition, which is also called lactose malabsorption, is usually harmless, but its symptoms can be uncomfortable.
A deficiency of lactase — an enzyme produced in your small intestine — is usually responsible for lactose intolerance. Many people have low levels of lactase but are able to digest milk products without problems. If you’re actually lactose intolerant, though, your lactase deficiency leads to symptoms after you eat dairy foods.”
Ask most doctors, registered dietitians and nutritionists what causes intolerance to dairy and 9 times out of 10 they will regurgitate a very similar explanation. But there’s a wee bit of a problem with this unproven hypothesis. Not everyone who eats dairy experiences these symptoms, and if they do not always in a consistent manner.
As I’ve suspected for quite some time, this disorder has less to do with the presence of dietary lactose coupled with nonexistent endogenous lactase production and much more to do with the type of dairy consumed. So today’s post will summarize a very well designed study out of China that looked at differences in self-reported lactose intolerance in subjects when drinking milk containing either A1 or A2 casein protein. (1)
To refresh your memory on these protein differences, here’s what I wrote in part two of my GERD series:
“This is an illustration of one section of the milk protein casein found in two different types of dairy. The casein at the top is derived from A2 dairy. The milk protein below from A1 dairy.
Each of these circles represents the different amino acids that make up this protein. Both are identical except for position 67. In A2 dairy, this position is occupied by the amino acid proline. In A1 dairy, this position is occupied by the amino acid histidine.
As humans, we are quite adept at producing enzymes capable of breaking apart or cleaving histidine bonds. Not so proline, which is why gluten, being very rich in this amino acid, is so difficult for us to digest into harmless peptides or individual amino acids.
The seven amino acid structure formed by the cleaving of the histidine bond in A1 dairy forms an opioid by the name of beta-casomorphin-7 (BCM7). The number seven refers to the number of amino acids in this peptide.
Just as gluten opioid peptides would be expected to have an effect on gastrointestinal function, including stomach emptying, so too BCM7. A1 dairy is derived from the milk of cows that originated in Europe. Although it contains the number 1 in its name, it’s actually a more recent evolutionary variant of older A2 cattle.
A1 dairy comes from the milk of Holstein and Frisian cows. These are the predominant dairy animals found in North America. A2 dairy is derived from Jersey cows, Asian and African cattle, goats and sheep. Milk and milk byproducts from A2 dairy sources do not form opioids.”
So to review, it’s the formation of beta-casomorphin-7 peptide or BCM7 that distinguishes the two types of dairy from each other. And it is this opioid the researchers of this paper sought to investigate.
A total of 45 ethnic Han Chinese subjects (21 males and 24 females) with self-reported intolerance to cow’s milk were enrolled in this randomized, double-blind crossover trial. A crossover study involves both randomized groups undergoing the same intervention after a set non-intervention period known as the washout.
All subjects were between the ages of 25 and 68 and drank milk infrequently because of reported gastrointestinal discomfort including gas, bloating, flatulence, stomach rumbling and diarrhea. All were screened to be free from irritable bowel syndrome, constipation or untreated inflammatory bowel disease before enrollment.
Subjects were divided into two groups: one composed of 22 people (10 males, 12 females) and another of 23 people (11 males, 12 females). One group was instructed to consume approximately a cup of commonly available milk containing both A1 and A2 casein after two meals daily for a total of two cups per day for 14 days. The other group was similarly instructed but they consumed only A2 casein cow’s milk.
After the initial 14 day period, all participants were instructed to refrain from drinking any cow’s milk for two weeks during the washout period. Milk type was then switched for each group during the second 14-day study period. Neither the participants nor the researchers knew which group drank which type of milk during the length of the trial.
At the start and end of both 14-day study arms, every person was administered what is known as a Subtle Cognitive Impairment Test (SCIT). This test measures the speed and effectiveness of information processing. The test consists of sitting in front of a computer screen while you’re shown a series of parallel lines and you quickly have to select which line is shorter by pressing either the left or right mouse button. The more mentally impaired you are the more wrong answers you’ll record.
On the 14th day of each study arm, forty participants were given a smart pill to swallow. These swallowable gadgets accurately measure transit time through the gastrointestinal tract. They can also assess the presence of both stomach and small intestinal inflammation.
OK, enough with the preliminaries. What were the results?
Well for one, those consuming A1 dairy complained of all the symptoms typically reported by those suffering from lactose intolerance: abdominal pain, bloating, flatulence, stomach rumbling and diarrhea. However, when these same people were consuming A2 milk, none of these symptoms appeared even though both kinds of milk contain the same quantity of lactose. So much for the lactose/lactase hypothesis! The issue with most commercially available dairy is with the formation of BCM7 opioid peptides, not lactose sugar.
It should come as no surprise that given the general gut-paralyzing effects of opioids, participants consuming A1 milk experienced increased intestinal transit time as opposed to when they were consuming A2 dairy. This explains the stomach and intestinal bloating.
In the stomach, opioids temporarily paralyze the pyloric sphincter that sits at the base of that organ delaying stomach emptying into the duodenum thereby increasing the risk of acid reflux and burping as I explained in my acid reflux series. In the intestine, slowed transit time increases the period digested food is subjected to fermentation by gut bacteria leading to uncomfortable intestinal bloat.
Now, this doesn’t mean lactose is entirely blameless. Any ingested substance that is not fully digested in the small intestine via enzymatic breakdown reaches the colon where it is set upon by gut bacteria and fermented, which is also true for all soluble and insoluble fiber. However, fermentation in the absence of a GI tract paralyzed by opioids results in most gas being absorbed back into the body through the gut wall or expelled as harmless farts.
But any concurrent consumption of gluten grains, which themselves precipitate into six known opioid peptides upon proteolysis, only compounds the problem. Add in dietary fiber from vegetables, legumes and fruit, and you now have copious amounts of substrate available for colonic gut flora to ferment. Also, if the person happens to suffer from untreated small intestinal fungal and bacterial overgrowth (SIFBO), this fermentation will occur twice in both the small and large intestine resulting in an agony I was all too familiar with back in the day.
Recall that slowed transit time is THE major risk factor for developing SIFBO. It is also a significant risk factor for causing a bloom of pathogenic gut critters in the colon. And the reason for this is that those involuntary muscle contractions along the entire length of the intestinal tract (peristalsis) have a dual housekeeping function: 1) to prevent colonic gut flora from migrating upwards to the small intestine where they do not belong and 2) prevent pathogens from adhering to the gut wall in both the small and large intestine. Opioids, including those derived from the dietary metabolism of both A1 dairy and gluten grains, inhibit peristalsis. And once pathogens take root, the curtain will soon rise on the Inflammatory-Cortisol Ballet.
But how does this increased transit time square with the noted increase in reported diarrhea in certain study participants and many others with so-called lactose intolerance? I suspect that many people who experience diarrhea when consuming A1 dairy (not to mention gluten) do so because they are actually constipated. I realize this sounds paradoxical so let me explain.
The longer feces remain in the colon, the drier they become because water is being continually drawn out of them. That is why dry, hard to pass stools are always indicative of constipation.
Now, if you have dried feces partially blocking your colon because of delayed intestinal transit, liquid and other matter will begin to pool behind this partial obstruction, especially if tight junctions in the gut become leaky causing water to escape the body by entering the intestinal lumen. Some of this liquid will detour around the partial impaction and be experienced as watery diarrhea. However, after a certain amount of time and fecal buildup, an “explosive” evacuation will inevitably take place making a toilet brush your new best friend.
This alternation between constipation and diarrhea is not uncommon in those complaining of GI disorders, including lactose intolerance or irritable bowel syndrome. So I suspect that those in this study who had an increase in diarrhea were actually experiencing the effects of this paradox.
But as with all uncomfortable gastrointestinal symptoms, there was something more ominous afoot. Those consuming A1 dairy also showed an increase in inflammatory markers like interleukin 4, which was especially noticeable in the small intestine.
These inflammatory markers have also been observed in a rodent study when mice were fed A1 casein. (2) In that study, BCM7 was seen to activate the Th2 immune pathway. This particular arm of the immune system is involved in several disease states including histamine reactions, asthma, allergies and eczema. In another animal study conducted with rabbits, A1 casein was shown to increase fatty streaks on aortic surfaces in comparison to A2 fed rabbits suggesting that A1 casein may promote the development of arterial heart disease. (3)
Another disturbing finding was that when participants were consuming milk that formed BCM7, their levels of short-chain fatty acids (SCFAs) decreased. Recall that SCFAs are the metabolic fermentation byproducts of beneficial gut flora. These SCFAs are produced when ingesting prebiotics either through food or supplements. Beneficial gut flora absolutely love prebiotics because the more they get, the more rapid their communities grow. And the more rapid their growth, the fewer nutrients and space available for competing pathogenic organisms. This is why I refer to prebiotics as grade-A fertilizer for beneficial gut flora.
SCFAs like butyrate, propionate and acetate all serve critical metabolic functions. For example, butyrate is essential for the structural health of the enterocytes lining both the gut wall and the blood-brain barrier. Reduce levels of butyrate production by decreasing beneficial gut flora populations, and I can assure you that a leaky gut and blood-brain barrier will follow like regret follows a debt-fueled shopping binge.
The fact that SCFA production declined in those consuming A1 casein dairy is a sure sign that this opioid peptide had adverse effects on beneficial gut flora and given BCM7’s deadening effects on intestinal peristalsis, how could it not? Remember, whenever beneficial bacteria is diminished, you can be guaranteed that opportunistic pathogens will quickly fill their vacated ecological niche much like rabbits and rats.
And now for the final negative outcome found in those consuming A1 dairy for 14 days. Remember the Subtle Cognitive Impairment Test (SCIT) that each study participant was given at the beginning and end of the 14-day study period? Well, those who consumed the A1 containing milk did worse on the second test than they did on the first while no difference was noted in those consuming A2 dairy. Imagine that.
I’m impressed that these researchers included this test in their study as it shows a keen understanding of how the gut-brain axis impacts brain health and functioning. As I’ve written before, whenever there is inflammation caused by gut dysbiosis, there will always be a negative impact on brain function. And this impact is not only confined to information processing as it was here.
Both depression and anxiety are now recognized as inflammatory disorders whose genesis is intestinal inflammation as I have written here and here. So too Parkinson’s. Excessive aggression in both men and women is also being recognized as an immune response to lipopolysaccharides. (4) (5) As I wrote in this post, endotoxemia directly affects the hypothalamic-pituitary-adrenal axis. Furthermore, pathogenic metabolites can directly affect the brain via the vagus nerve. (6)
There has been much written about the apparent healthfulness of the Mediterranean diet in recent years, but little focus has been given to the type of dairy consumed in that part of the world in contrast to the dairy that is typically consumed in Northern Europe, North America and Australia. I believe one key to this puzzle is due partly to the A2 dairy sources ingested there: goat and sheep’s milk being the two common dairy types found in that region. And as recent research has revealed, oligosaccharides naturally found in goat’s milk have been discovered to feed and enhance populations of beneficial bacteria in the gut. (7)
So I would encourage all my readers and clients who consume A1 dairy to switch over to 100% A2 dairy sources. In the United States, A2 branded milk has become readily available in supermarkets over the past few years and I assume this milk brand is also available in other developed nations. If not, there is always sheep or goat’s milk as an alternative.
And what is true of milk is also valid for cheese made from that milk, although butter being mainly fat is not a concern. As the dose makes the poison, I would caution against consuming A1 dairy in appreciable quantities if keeping gut dysbiosis, inflammation and the symptoms associated with so-called lactose intolerance at bay.
That said, you would be kidding yourself if you believe that BCM7 is the only dietary opioid you need to concern yourself with. As I’ve repeatedly written, opioid peptides derived from gluten grains also have adverse effects not only on gastric emptying and intestinal peristalsis but also on the integrity of tight junctions sealing both the gut wall and blood-brain barrier via zonulin upregulation as well as on DNA methylation. Given the ridiculous quantities of wheat eaten around the world, often accompanied by A1 dairy (a heaping bowl of Wheaties anyone?), the gut-disrupting aftereffects of these opioid peptides will continue to guarantee copious profits for pharmaceutical and medical interests for years and years to come.
Until next time!