Why is it assumed that the absence of lactase is the ancestral state?, why is lactase persistence not the ancestral state, then a mutation occurred that reduced its production after weaning?
In no mammal species do they breastfeed into adulthood? Over your life-history you begin by getting milk from your mother, as you are an infant. But as you grow up you stop breastfeeding. Since milk would no longer be a staple in your diet(prior to domestication of species we obtain milk from), there’s no reason for you to keep producing enzymes that break down lactose. For millions of years our ancestors did not have domesticated goats and cows to harvest milk from, so when you grew up you stopped getting milk in your diet relatively early.
All our closest relatives do not breastfeed into adulthood, and none of them have domesticated cows or goats. That implies the ancestral state is that lactase production is eventually turned off as you grow up. Then eventually on the human lineage we domesticated cows and goats and could get milk in our diets well into adulthood. It then became advantageous to keep the gene turned on for your entire life. That’s why it’s a derived instead of ancestral trait.
So you see, it’s not an assumption. It’s an inference from the evidence.
Just to clear up a few terms, nearly all humans produce lactase as children. If we didn’t then we couldn’t use the lactose in milk.
The phenotype you are referring to is lactase persistence, the ability to keep producing lactase throughout one’s life. This is due to mutations upstream of the coding region of lactase which alters its expression through life.
@Rumraket does a good job of explaining the ecological reasons why lactase persistence would be a more recent adaptation with the ancestral state being lactase expression just in childhood.
The genetics kind of seal the deal.
All of this comes with the caveat of “if I am understanding the paper and concepts correctly”.
First, there are many different alleles for lactase persistence, and they are geographically distributed. This would indicate that the alleles originated in these populations after migration out of Africa. This would mean the lactase persistence allele is not the ancestral state. Also mentioned in the paper is the sequencing of ancient DNA in which the lactase persistence allele only appears recently (<5,000 years ago in some cases).
Second, the sequence surrounding the mutations responsible for lactase persistence is also very similar between those with the same allele. This would indicate a recent selective sweep that has not allowed time for the accumulation of other mutations in the surrounding sequence. However, there are differences in recombination rates that may cloud these findings.
However, this is not evidence that the absence of lactase was also the case for our human ancestors. I believe the strongest evidence would be to examine the DNA of as many ancient humans as possible and demonstrate that they lacked the lactase persistence mutation.
Since we know our ancestors did not have domesticated animals that produced milk, and none of our closely related cousin species have domesticated animals that produce milk, and since we all (both we and all our closest relatives) stop breastfeeding early and a subpopulation of humans is the only outlier, that is in fact evidence that lactase persistence is a derived trait that evolved in the human lineage.
thank you @T_aquaticus , the presence of SNPs (single nucleotide polymorphisms) in the lactase gene, along with the absence of mutations in the DNA of ancient humans, strongly suggests that the ability to digest lactose as an adult is a relatively recent human adaptation. The ancestral condition, therefore, is the absence of lactase persistence, which means that lactose was likely not a significant part of the diet for early humans.
I understood. The presence of agriculture led to the selection of this trait and therefore it spread
Thank you, and you’re welcome!
Given that the presence of the mutations that confer lactase persistence doesn’t seem to correlate with milk consumption, your simple scenario probably doesn’t reflect the reality.
The ENV article gets this very wrong:
This is false. The mutations result in a new binding site for a transcription factor:
This is a new positive function, not a loss of function as claimed at ENV.
Assuming that statement is correct(massive grain of salt for anything written on EN&V), it still straightforwardly doesn’t follow that what I describe is incorrect. It is not required that today the geographical areas where the mutations are most prevalent, should also correlate with today’s degree of milk consumption.
I’m curious if all people will be able to digest milk if they can drink milk from animals that eat nutritious food, and the milk they drink from animals hasn’t been processed, and the fat and other nutrients in the milk aid in digestion for all adults. As a result, all adults can digest milk.
If cows farts stink up an entire town, how can that cow, who can’t even digest an unhealthy way of eating, produce milk that some adults can’t digest?
Regarding the molecular mechanism underlying the lactase persistence phenotype in human, the paper you point to is old (2005) and not very convincing. In fact, nearly 2 decades later, the situation remains unclear. But the think to bear in mind is that the expression of the LPH enzyme is tightly regulated in mammals, being silenced after weaning. How this timely silencing system operates is not really understood, but one thing seems clear, the lactate persistence phenotype is more likely to result from the destruction of some element of the silencing system than from the creation of a new function.
But, for your scenario to be correct, it is required that a correlation exists
between milk consumption in antiquity and the presence of the lactase mutation in a region But according to the study Behe refers to, it doesn’t seem to be the case.
Why is it not convincing? Be specific.
It is as clear as day in the paper I supplied.
I already supplied evidence to the contrary.
It has to do with the presence of lactose that hasn’t been broken down. The correlation between lactose intolerance and the mutations is pretty tight.
I’m going to have to second this. Why would the papers date be relevant at all (is there something wrong with the assays done in 2005), and how do these assays fail to demonstrate a binding interaction?
Apparently, @Giltil would have fully accepted the paper in 2006, kind of liked it in 2012, but totally rejects the paper now, even though not a word or number in the paper has changed. Quite funny, actually.
Nah, he’d have rejected it in 2006 too. He’d simply have omitted the comment about its age, giving instead some other equally ridiculous excuse.