1. Lactase persistence

Lactase persistence is the continued activity of the lactase enzyme in adulthood, allowing the digestion of lactose in milk. According to Wikipedia, only a small proportion of human mammals keep the ability to digest lactose when reaching adulthood:

In most mammals, the activity of the enzyme is dramatically reduced after weaning. In some human populations though, lactase persistence has recently evolved as an adaptation to the consumption of nonhuman milk and dairy products beyond infancy. (...) Worldwide, most people are lactase non-persistent, and are affected by varying degrees of lactose intolerance as adults.

The scientific consensus is that the enzyme lactase is encoded by the mammalian lactase gene (LCT), and that Hypolactasia is known to be recessively and autosomally inherited. Most mammals lose the ability to digest lactose once they are old enough to find their own source of nourishment away from their mothers, and there is still debate about the selection mechanism which yield the human excepcion: Lactose malabsorption is typical for adult mammals, and lactase persistence is a phenomenon likely linked to human interactions in the form of dairying.

2. Gut Flora inheritance

Our understanding of the gut microbiota has recently evolved (the study of gut flora began in 1995): the digestive tracts hosts a whole population of microbiotes, each with their own DNA, playing active (positive and negative) roles in the digestion process and co-evolving with their host. The composition of human gut microbiota changes over time, when the diet changes, and as overall health changes.

The gut flora are believed to be inherited, in particular from the mother and from people living around the infant:

During birth and rapidly thereafter, bacteria from the mother and the surrounding environment colonize the infant's gut. The exact sources of bacteria are not fully understood, but may include the birth canal, other people (parents, siblings, hospital workers), breastmilk, food, and the general environment with which the infant interacts. (Wikipedia)


Could an environment selecting for lactase persistence phenotypes select both human and gut flora genotypes in paralel, so that the survival or disappearance of gut flora able to hydrolyse lactose to glucose and galactose play as important a role in the ability of selected humans to digest or not fresh milk as the various genes previously identified?


I wonder if these hypothesis have been previously ignored because the gut was considered "neutral" rather than "active" in the digestive process (the alternative being that theses hypothesis have been already proven wrong beyond questioning, which I am curious to learn about).

I understand that this is not the scientific consensus, and I am not claiming that the scientific consensus is wrong. But the scientific consensus was once that the earth was flat, or that the sun was rotating around the earth, and it evolved. I am wondering if there is place for doubt in the current scientific consensus about the genetic causes of the ability or inability to digest lactose in human adults (from a scientific point of view).

  • $\begingroup$ What brings you to the conclusion that this is not (as it is the fact) caused by our genetics? $\endgroup$
    – Chris
    Oct 24, 2023 at 12:28
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    $\begingroup$ Just a thought, but try looking up the LCT gene. It's a human one, producing lactase. I'm not sure how your experiment tests the hypothesis - wouldn't that work equally well if the enzyme continued to be produced by the growing organism because of continued milk intake due to something in the milk interacting with the organism directly? Do you mean to suggest that the LCT gene expression is regulated in some way that's mediated by gut flora? $\endgroup$ Oct 24, 2023 at 12:29
  • $\begingroup$ @Chris: The intestinal flora has genetics (distinct of our own), is transmitted from parents to children (as our genetics) and evolve under the same selection mechanism as our genetics. I am aware that the current state of scientific knowledge is that the ability to digest lactose is based on genetic, but I wonder if an alternative or complementary theory based on the genetics of the microbiome could also explain the ability and inability to digest lactose in adult mammals. (Sun and stars rotating around the earth used to be a scientific fact too!) $\endgroup$
    – J..y B..y
    Oct 24, 2023 at 13:32
  • $\begingroup$ Scientifically spoken, tt was not a fact - it was a hypothesis. Which was proven wrong. Besides this the mutation which leads to persistent expression of lactase nicely explains the mechanism. $\endgroup$
    – Chris
    Oct 24, 2023 at 13:46
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    $\begingroup$ I suggest reading this paper: "Human adaptation, demography and cattle domestication: an overview of the complexity of lactase persistence in Africa". $\endgroup$
    – mgkrebbs
    Oct 24, 2023 at 16:44

1 Answer 1



The original version of this question has been edited, so the first part of my answer, which addressed certain arguments and proposed experiments has now been removed. The question now incorporates material accepting the role of the enzyme lactase in determining whether humans can continue to digest milk after weaning, but I retain the section I wrote on that point, as it presents some precise genetic evidence and points to a useful review. In my update in response to the changes in the question I have extended my consideration of the role of gut bacteria.

The mechanism of lactase persistence has been established to be genetic

A recent (2017) review in Annual Review of Genomics and Human Genetics covers the topic in detail. There are five separate genetic variants and details of one of these are:

In 2002, a study of Finnish families by Enattah et al. (30) identified the first mutation associated with the LP [lactase persistence] phenotype: −13.910:C>T (rs4988235).

A further study showed that the −13.910:T variant creates a new binding site for octamer-binding protein 1 (Oct-1), a transcription factor that interacts with human hepatocyte nuclear factor 1α (HNF1α) to bind to the LCT [lactase] promoter (77). This allele therefore leads to an alternative path for LCT expression that is not downregulated, as the original path is.

There are questions about lactase persistence that still have not been answered — primarily why it arose in some human populations, but not others. However experimental evidence and scientific logic lead to the conclusion that cessation of expression of the gene for lactase ([lactase non-persistence) results in loss of ability to metabolize lactose. Any “scientific consensus” rests on this experimental and logical basis and the absence of any experimental evidence for a different or additional explanation.

Intestinal flora and lactose tolerance

The poster now accepts the role of genetics, but posits that the microbiome might be an additional factor in lactose tolerance. I shall now consider studies in this area.


The review already quoted does provide some information on Bifidobacterium, a bacterial constituent of human microbiota able to metabolize lactose:

Interestingly, although most of the focus has been on the cost of drinking milk for LNP [lactase non-persistent] individuals, arguments can also be made that consuming milk or dairy also has advantages for these individuals. Indeed, recent studies have shown that the gut microbiota of LNP individuals differ from those of LP individuals from the same population in that they have a higher prevalence of Bifidobacterium (11, 15, 47), which is explained by the larger amounts of lactose available for bacterial fermentation. In fact, this represents one of the strongest associations to date between genetic variants and variation in gut microbiome composition (11, 15, 47).

Thus, humans who for genetic reasons do not expresses lactase (a trait that correlates with the inability to digest lactose) have a larger intestinal population of lactose-metabolizing bacteria. This is consistent with their having unabsorbed lactose in the gut. However it provides no evidence in support of an additional role of such bacteria in lactase persistent individuals, even assuming that there was a mechanism by which these bacteria could contribute to lactose tolerance. (This latter point will be considered next.)


The implicit assumption — now made explicit in the title of the question — is that bacteria possessing a lactase (generally known as β-galactosidase in bacteria) could or would supply the products of lactose hydrolysis (glucose and galactose) to the human host. This is by analogy with ruminant bacteria, and perhaps the supply of vitamins by human bacteria. Unfortunately there is no evidence to support this idea. It has been demonstrated that bifidobacteria take up and utilize lactose for their own growth, employing the (anaerobic) fermentation pathway known as the bifid shunt, which also involves glucose. The products of this are lactate, acetate and ethanol.


It is worth recalling that lactose intolerance can be a pathological condition if the subject consumes dairy products. This is not my area of expertise, but it would appear that this results from the fermentation of lactose by bacteria other than bifodobacteria, with the formation of different products — fatty acids, hydrogen, methane and carbon dioxide. The gas produced causes various problems (flatulence, bloating etc.), and the acidification of the intestinal contents can cause diarrhoea — a major problem in this condition.

It should be noted that bifidobacteria are regarded as beneficial (‘probiotic’) in lactose intolerant individuals, although the basis of this is not known. (Perhaps they compete for the lactose with the bacteria whose metabolism produces more harmful products.)

  • $\begingroup$ I am confused: you seem to equal "Lactase non persistent" humans and "humans who cannot digest lactose", when my understanding (from your own quotes) is that humans with a higher prevalence of Bifidobacterium do indeed digest lactose without producing lactase? $\endgroup$
    – J..y B..y
    Nov 8, 2023 at 8:54
  • $\begingroup$ Thanks a lot for the pointer to the survey! I am sorry if my question seemed unscientific to you: if no biologist, I am nevertheless a scientist, and a "believer" that science progresses by asking the right questions (and that stack exchange is a good engine to make science progress). I am not sure than mine are the right ones to progress, but at least they are the right ones for me (and others) to learn! $\endgroup$
    – J..y B..y
    Nov 8, 2023 at 9:00
  • $\begingroup$ @J..y B..y — I have now modified my answer. I did not read your original point properly. "when my understanding (from your own quotes) is that humans with a higher prevalence of Bifidobacterium do indeed digest lactose without producing lactase". The quote says nothing about digesting lactose only "beneficial effects" which may be due to the protein or fat content of the milk. All this implies is that they tolerate some milk — i.e. don't show the lactose intolerant pathology. As I mentioned in my wild speculation, the bifidobacteria may outcompete those responsible for the pathology $\endgroup$
    – David
    Nov 11, 2023 at 9:05

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