How is evolution happening? I can't observe it

No evolution but extremely rapid human genetic degradation

The number of harmful mutations in human genome worldwide nearly doubled in 16 months

In last January I estimated that the next DisGeNet (DisGeNET - a database of gene-disease associations) update will raise the number of harmful mutations in human genome to over a million. The latest update has been released a couple of days ago and the number of disease-causing mutations is today even 1,134,942. The number almost doubled from the previous update (Jan 2019). Even if it is partly a matter of advance in research, such a rapid doubling of mutations indicates that the human genome is currently deteriorating very rapidly. It is because the phenomenon accelerates itself; the more genetic defects, the weaker the repair systems work, again resulting in more genetic defects, etc.

The current version of DisGeNET (v7.0) contains 1,134,942 gene-disease associations (GDAs)

Another interesting database that gives important information regarding human germ line mutations is the Human Mutation Database:

There are two versions available of this database; a free public version which is three years old and an up to date version which you have to pay for. The free version lists 275,716 harmful germline mutations in human genome at population level.

Where are all positive mutations? I can’t see evolution happening anywhere. Seems that humans are experiencing rapid genetic decay.

What if it’s entirely a matter of advance in research? How does that affect your conclusion? Hey, GenBank is also experiencing rapid increase in data, which I suppose means that new genes and species are constantly evolving. You’re welcome.

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What do you mean at the population level? How large a population?

Suppose you don’t feel ill, are you likely to go to the doctor so he can set you down a path to look for the causes of your not having health-problems, such as your beneficial mutations? No, that generally doesn’t happen. So there’s an inherent systematic bias in medicine to look for and discover harmful or disease-causing mutations.

Despite this, of course many positive mutations are known, that contribute positively to everything from athletic performance, alchohol and lactose tolerance, increased resistance to diabetes, obesity, and heart disease, high altitude living, diving ability, to some measures of cognitive performance etc. etc.


//athletic performance, alchohol and lactose tolerance, increased resistance to diabetes, obesity, and heart disease, high altitude living, diving ability, to some measures of cognitive performance etc. etc.//

Those are not based on mutations but epigenetic regulation.

No, they’re mutations.


The figure of 1,134,942 isn’t the number of harmful mutations in the human genome, it’s the number of gene-disease associations (GDAs). In other words, there are 1,134,942 instances where a particular gene can be linked to a particular disease in some way.
What kind of way? Well, one obvious one is mutation - disease X is correlated with Y mutation in gene Z. In can be the opposite though, like associations where reduction in the expression of a particular genes protects against a particular pathology (e.g. the link between the VWF gene and liver cirrhosis, citing Joshi et al. 2017). They can also be associations where a mutation mediates the side-effects of a particular treatment of a particular disease (e.g. the second COMT gene association with bipolar disorder).

Looking at the curated GDA database of 84,038 GDAs, supported by 151,277 individual lines of evidence, 115,331 of those lines of evidence are listed as “biomarker” type associations - in other words, the gene in question can be used in some way to assay for a particular disease. That doesn’t indicate that gene is actually causative in the disease, or that it’s the result of a mutation. An example would be the VWF gene and the specific entry of an association with liver cirrhosis (experimental) I mentioned earlier. VWF is a biomarker for cirrhosis because it seems to be upregulated in diseased livers and plays a role in the pathology. That has nothing to do with mutations to VWF.

There are all sorts of these different categories of associations, and the only ones really relevant to the idea of genetic entropy would be the gremlin causative mutations, that sort of thing. Somatic mutations leading to things like cancer are completely irrelevant.

Suffice it to say, the phrase “gene-disease associations”, is not synonymous with “harmful mutations”. This is apparent anyone that bothers to take a cursory glance at the database itself, not just its homepage. “Associations” really means “associations”, who’d of thought?

Even the term “disease” is used quite loosely. To quote the authors in Piñero et al. 2019:

Note that the term ‘disease’ refers to a wide range of phenotypes relevant in human genomics: actual diseases, disease symptoms and abnormal phenotypes that are observed as disease manifestations, as well as normal traits and phenotypes that are currently explored in large scale Genome Wide Association studies (GWAs)

What evidence do you have that this is anything other than the result of advances in research? Do you really think that the number of harmful mutations in the human adult population (given that they are the ones the majority of research is being done on) spontaneously doubled in the last year? That doesn’t make any sense at all.


According to the original definition by de Vries, mutations are random changes. C>T alterations are no random events. When a methylated cytosine is deaminated, the repair mechanism (glycosylase) will not repair that alteration. This the most significant reason why genomes are decaying. In human genome, there are 32,000 C>T alterations that scientists want to repair.


C <> T is a transition mutation. Case closed.

You haven’t established anything is “decaying” as opposed to merely mutating.

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Mutations result in broken genes and genetic entropy. Scientists try to repair these damaged genes caused by C>T transitions:

Excerpt: “Other scientists at Harvard and the Broad Institute have been working on an even more daring tweak to the Crispr system: editing individual base pairs, one at a time. To do so, they had to design a brand-new enzyme—one not found in nature—that could chemically convert an A-T nucleotide pairing to a G-C one. It’s a small change with potentially huge implications. David Liu, the Harvard chemist whose lab did the work, estimates that about half of the 32,000 known pathogenic point mutations in humans could be fixed by that single swap.”

If new species are evolving then name three with thier new species names.
A reason evolution can’t seen could also be it never happens by the way old scholl evolutionism teaches.

Speciation might happen just in two generations due to alternative epigenetic programming. There’s no need for DNA changes in order to get new species. Instead, speciation often results in genetic errors and loss of information.

Is this common knowledge or am I supposed to just take your word for this? I think you need to substantiate your statement here.


speciation might happen in just two generations …

They key word there is might.

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Chimps and humans are different species.

Why do chimps and humans look different from one another? Is it because of the DNA sequence differences between their genomes?

If changes to the DNA sequences of genomes will only cause damage, then what of the ~40 million changes that separate the human and chimp genomes? Do they all result in broken genes and diseases?

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How are you supposed to see something that ordinarily takes so long to happen?

But here’s a treat for you … here is some INSTANT evolutionary progress!

One-Celled Protists Swallow Algae - - that refuse to die!

I think this is a pretty important finding … buried within one of the hundreds of YouTube videos on Evolution !

Protists that fed on algae cells swallowed some that would not be digested and did not die… and they were lucky they did! Those algae cells helped the Protists survive starvation.

Link to YouTube video: