2023/07/20

A good example of how people have been misled by stories about random mutations

The theory of random mutations and selection is going down in history



Excerpt: "A genetic mutation that occurred thousands of years ago might be the answer to how early humans were able to move from central Africa and across the continent in what has been called "the great expansion," according to new research from Wake Forest Baptist Medical Center.

By analyzing genetic sequence variation patterns in different populations around the world, three teams of scientists from Wake Forest Baptist, Johns Hopkins University School of Medicine and the University of Washington School of Medicine, Seattle, demonstrated that a critical genetic variant arose in a key gene cluster on chromosome 11, known as the fatty acid desaturase cluster or FADS, more than 85,000 years ago. This variation would have allowed early humans to convert plant-based polyunsaturated fatty acids (PUFAs) to brain PUFAs necessary for increased brain size, complexity and function. The FADS cluster plays a critical role in determining how effectively medium-chain PUFAs found in plants are converted to the long-chain PUFAs found in the brain.

Archeological and genetic studies suggest that homo sapiens appeared approximately 180,000 years ago, but stayed in one location around bodies of water in central Africa for almost 100,000 years. Senior author Floyd H. "Ski" Chilton, Ph.D., professor of physiology and pharmacology and director of the Center for Botanical Lipids and Inflammatory Disease Prevention at Wake Forest Baptist, and others have hypothesized that this location was critical, in part, because early humans needed large amounts of the long-chain PUFA docosahexaenoic acid (DHA), which is found in shellfish and fish, to support complex brain function.

"This may have kept early humans tethered to the water in central Africa where there was a constant food source of DHA," Chilton said. "There has been considerable debate on how early humans were able to obtain sufficient DHA necessary to maintain brain size and complexity. It's amazing to think we may have uncovered the region of genetic variation that arose about the time that early humans moved out of this central region in what has been called the 'great expansion.'"

Once this trait arose, the study shows that it was under intense selective pressure and thus rapidly spread throughout the population of the entire African continent. "The power of genetics continually impresses me, and I find it remarkable that we can make inferences about things that happened tens of thousands of years ago by studying patterns of genetic variation that exist in contemporary populations," said Joshua M. Akey, Ph.D., lead scientist at the University of Washington.

This conversion meant that early humans didn't have to rely on just one food source, fish, for brain growth and development. This may have been particularly important because the genetic variant arose before organized hunting and fishing could have provided more reliable sources of long-chain PUFAs, Akey said."'

My comment: That's quite a story! Now let's walkthrough for this study. First, we have to check the methods they have used for sequencing the samples. First of all, they used '1000 genomes project' data for making their conclusions. That SNP data bank has been evaluated to be very unreliable:

https://bmcgenomics.biomedcentral.com/articles/10.1186/s12864-019-5957-x

"We observe that phasing and imputation for rare variants are unreliable, which likely reflects the limited sample size of the 1000 Genomes project data. Further, it appears that using a population specific reference panel does not improve the accuracy of imputation over using the entire 1000 Genomes data set as a reference panel. We also note that the error rates and trends depend on the choice of definition of error, and hence any error reporting needs to take these definitions into account."

Older studies, especially before the year 2015, used mRNA/cDNA samples for data analysis. cDNA samples can't be used as reference material for genomic DNA, because mRNAs may have gone through several modification procedures.

Modern research has revealed that adaptation to fatty acids is based on a built-in mechanism, alternative splicing. It means that the cell is able to modify pre-mRNA molecule in order to produce required mRNA for protein production. No changes in DNA are needed. Converting plant-based polyunsaturated fatty acids (PUFAs) to long chain PUFAs is an essential metabolic mechanism in almost all kind of animals in nature. Finding similar solutions in different kind of organisms is not an evidence for evolution. Here's a few study revealing that alternative splicing is used for making different protein isoforms by reading only one FADS gene:

So, the fairytales of FADS gene mutations and evolution are wrong. However, these stories still hang in 'science' magazines and journals giving people false information of how cellular mechanisms work. This is how evolution indoctrination works.

Evolution believers also claim that FADS genes are results of duplications. But they don't know that if you remove just one of those necessary genes, then there will be serious problems in reproduction:

https://www.sciencedirect.com/science/article/pii/S0022227520307392

Mutations in FADS2 gene result in metabolic syndrome:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9228863/

There are numerous examples of claimed mutation driven evolution. I have studied almost all of them. Here's the results:

- CCR5 is based on 32 bp DELETION. No information increase.
- APO-Ai has not been verified as a beneficial mutation. Read more about it from here:
- LRP5 mutation is a genetic disorder, No information increase.
- SOST mutation is a genetic disorder, No information increase.
- HbC mutation is a genetic disorder that shortens life span. No information increase.
- Tetrachromatic vision? People don't know that some people still have even pentachromatic vision. We are losing information, not gaining of it. Read more from here:


- Adaptation to cold with fewer sweat glands. This is epigenetic regulation.
- EPAS1 - High altitude adaptation. Pure epigenetics.
- G127V - Immunity to brain disease. False information:
- Rh-null blood type, a splice variant caused by epigenetic regulation. No information increase.
- DEC2 mutation disturbs your circadian rhythm causing metabolic syndromes and cancer. Not so beneficial.
- MC1R mutation - A broken gene.
- Lactose Tolerance - Pure epigenetics resulting in a broken gene.
- OCA2 Blue eyes - Pigment differences are results of transcript variants, epigenetic regulation.
-  Factor V Leiden is an inherited genetic disorder
- In humans, the MYH16 gene has a mutation that causes the protein not to function.
- Osteocrin - hypothetical mutation, not observed
- SLC30A8 - Correct information can be read from here:
- ABCC11 - An example of a knockout gene, loss of information
- VMAT2 - Another example of a knockout gene
- HAR1 - This gene is associated with brain development
- OCA2 - Pigment differences are results of transcript variants, epigenetic regulation. Keywords: OCA2 ensembl
- MC1R a gene located on chromosome 16, Red hair - Caused by a broken gene.
- FOXP2 is a transcription factor and its loss is associated with speech ability.
- ACTN3 and the super-sprinter variant - Splice variants, pure epigenetics
- hDEC2 mutation disturbs your circadian rhythm causing metabolic syndromes and cancer. Not so beneficial.
- TAS2R38 and the supertaster variant - This is a transcript variant caused by epigenetic regulation
- LRP5 mutation is a genetic disorder, No information increase.
- CETP - A splice variant caused by epigenetic regulation

The theory of evolution is the most dangerous heresy of our time.


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