Hector's objections to adaptation

I’ve found that most of those adaptations have been due to epigenetic regulation. Very often amino acid substitutions are results of RNA editing. This means the true list representing beneficial DNA mutations in human genome is very short. Especially compared to those 1,132,942 disease-related harmful mutations (DisGeNet).

Please post references to that data so we can read about it. Thanks.

1 Like

If you want to discuss scientific mechanisms that explain variation, that could be fun, but your post is full of “evolution believers” and outrageous charges of “pseudoscience,” and you’ll have to find someone else to talk to if that’s your stance.


@Hector64, your post above is a copy paste of the following: Modern Science refutes the Evolutionary theory: Random beneficial DNA mutations? Forget them.

You are allowed to share blog posts, but please do not copy paste material from them in this forum. Explain and contextualize for this discussion.


They have the gene-sequences buddy, that means heritable mutations.

This is a common refrain among creationists, because for some reason some of you reeeeally don’t want to admit that mutations can be beneficial, but even a cursory glance at the paper is enough to see the problem with the claim.
The claim is that methylation levels, NOT genetic mutations, are responsible for lactase persistence, but the very paper you cited shows that the methylation levels are directly linked to the mutations in question.
A few quotes:

methylation levels are associated with the genotype at −13910C > T

The association between DNA methylation at the lactase enhancer and lactase enzymatic activity is largely attributable to the −13910C > T genotype

These results suggest that most of the DNA methylation variation at the LCT enhancer is explained by the genotype at rs4988235 alone.

I don’t see how it’s possible to read the paper and miss these kinds of statements, not to mention figures 3, 4, and 5. The point is that the genotype is what results in the differential methylation that drives the differential enzymatic activity that drives the phenotype. It’s not an either/or situation - the genetic mutation and epigenetics are involved.


Methylation levels of the LCT enhancer result in a typical C>T change due to lack of a repair mechanism. These have been found at least ten different in human ethnic groups all over the world.


“However, an epigenome-wide approach using the Illumina Infinium HM450 bead chip identified a differentially methylated position in the LCT promoter where methylation levels are associated with the genotype at −13910C > T, the persistence/non-persistence phenotype and lactase enzymatic activity. DNA methylation levels at this promoter site and CpGs in the LCT enhancer are associated with genotype. Indeed, taken together they have a higher power to predict lactase phenotypes than the genotype alone.”

A change from C to T is a transition mutation, and mutations are heritable. So it’s a beneficial heritable genetic mutation.

1 Like

What do you mean “lack of a repair mechanism”? When 5-methylcytosine is deaminated into uracil, this error can be corrected by base-excision repair, before or after the uracil gets replaced with a thymine, so the G-U or G-T pair is fixed back to a G-C pair.

All of this is besides the point though, because regardless of how the mutation in the LCT enhancer may have been caused, it’s still a genetic mutation that results in differential methylation that results in the lactase persistence phenotype. Shouting “epigenetics” doesn’t change that.

1 Like

Epigenetics is one of the more widely misunderstood concepts and mechanisms in this debate. Some people try to act as if epigenetics is completely divorced from gene sequence, but it isn’t. For example, a mutation from a CpG to a TpG will result in one fewer target for methylation, and it can result in an increase in expression of the gene downstream of the DNA mutation.

At least in vertebrates, almost all methylation patterns are wiped out during the production of gametes. Methylation patterns emerge during embryonic development and throughout life. There are very, very few instances of transgenerational epigenetic inheritance among vertebrates, certainly not enough to account for variation in the vertebrate phylum.

Can the environment influence epigenetics? Absolutely. However, it is the DNA sequence of the genome that determines how the environment influences epigenetics. The environment doesn’t directly methylate DNA, nor does it directly participate in histone ubiquitination. All of those processes are carried out by gene products, and the are heavily influenced by the DNA sequence of those genes and their targets. Lactose tolerance is a beautiful example where a mutation inherited from your parents can change your epigenetic profile.


You have that backwards. The repair mechanisms missed a C>T transition mutation in DNA that was used to produce sperm or eggs. That mutation was inherited by the offspring from that sperm or egg. The result is a change in epigenetics because of that mutation. The mutation precedes the change in epigenetics.

1 Like

The way I understand the lactose intolerance study, DNA methylation seemed to explain some of the phenotypic variability (intolerant or not) in heterozygotes for a particular C->T change in the enhancer of the gene. But the mutation was still important, indeed necessary. Variation in homozygous individuals was explained just fine by the sequence (C or T) at the relevant position.

I don’t see how this supports @Hector64’s position.

1 Like

Just a general question: What explains the love affair creationists have with what they call “epigenetics”? It’s not like DNA methylation is some supernatural miraculous process that points to a god.

Evolutionary biologists don’t like it, and that’s good enough for them. Sal likes it because it makes gene regulation seem more complicated, and as we know, complicated = Jesus. Finally, it seems more plausible to them that methylation patterns are a built-in, designed mechanism for variation, while mutation seems too random. Thus we escape the law of higgledy-piggledy.


This is overstated. I’m an evolutionary biologist, and I “like” (for lack of a better word) epigenetics. In fact, most of the evolutionary biologists I know think it’s an interesting topic. Some of them are studying it.

If by “epigenetics” you’re referring to the bizarre creationist misunderstandings demonstrated in this thread, then sure, I’m right there with you. But epigenetics as understood and practiced by actual biologists is a perfectly cromulent field of study.

1 Like

I refer to epigenetic inheritance as a carrier of information across generations at evolutionary time scales, i.e. the sort of thing Hector is claiming, in which a heritable adaptation depends solely on methylation patterns.

1 Like

Thanks for the clarification.

Unfortunately, that’s what “epigenetics” means, not just to creationists, but in the press. It used to refer to the physical processes of development, but now it just means non-genetic inheritance and neo-Lamarckian evolution.

Doesn’t it mean any type of inheritance that is not genetic?

No. Epigenetics also includes transient modification of genetic material that is not inherited, such as transient methylation of CpG’s, transient histone modifications, and transient microRNA expression. There are some who would also include protein phosphorylation, glycosylation, and a whole host of other DNA, RNA, and protein modifications, none of which are inherited.

There can be transgenerational epigenetic inheritance in some lineages, such as in Arabidopsis and nematodes. However, these are special cases under the larger epigenetic umbrella.