Outbreeding depression

There need to be more studies on this but I know scientists are busy with buttered toast experiments and rating their own farts.

This is the genetic thing you never hear about, despite everyone and their purebred* dog knowing about inbreeding depression.
Hybrid vigour doesn’t even apply to modern wheat.

And hybrid is misused.

I saw this explanation:

A hybrid is a cross between two closely related strains such as an Arab and a Jew or a Swede and a Spaniard. A mongrel is a cross between different races such as a Mulatto, a Mestizo, a Eurasian, etc.

https://www.sciencedirect.com/science/article/pii/B9780123847195000733

Positive outbreeding studies are conducted on flies.
https://link.springer.com/article/10.1023/A:1024081416729

…I don’t even, insects are already heavily inbred by default so outbreeding isn’t really possible.

Outbreeding depression is more of an issue than inbreeding (some inbreeding is good for a gene pool, the most fertile and healthy couple combinations and normal historically), which is fixed by breaking the pattern for a few generations. However, you cannot undo outbreeding depression in part due to its novelty. It’s easy to add, impossible to take away.
http://www.vortex10.org/Lacy/Reprints/FrankhamConsBiol2011.pdf

Actually it’s the combination of genes that makes the organism unfit.
(The fact of lower parental singular quality aside, two mutts won’t make a prize dog).

Its ideal environment doesn’t exist. In any other environment, it’s defective.
In the race for life, they’re disabled. It’s like mixing wines, they lose their distinctive character but other examples haven’t. In a competition…

Easy example:

One nose selection gene for cold weather, one selection for hot.
Result: poorly adapted child for either.

*They care about the dog’s bloodline more than their grandkids, who will hate their guts.

Human taxonomic diversity paper

https://lesacreduprintemps19.files.wordpress.com/2011/06/woodley-2009-is-homo-sapiens-polytypic-human-taxonomic-diversity-and-its-implications.pdf

Is Homo sapiens polytypic? Human taxonomic diversity and its implications

The term race is a traditional synonym for subspecies, however it is frequently asserted that Homo sapiens is monotypic and that what are termed races are nothing more than biological illusions. In this manuscript a case is made for the hypothesis that H. sapiens is polytypic, and in this way is no different from other species exhibiting similar levels of genetic and morphological diversity. First it is demonstrated that the four major definitions of race/subspecies can be shown to be synonymous within the context of the framework of race as a correlation structure of traits. Next the issue of taxonomic classification is considered where it is demonstrated that H. sapiens possesses high levels morphological diversity, genetic heterozygosity and differentiation (FST) compared to many species that are acknowledged to be polytypic with respect to subspecies. Racial variation is then evaluated in light of the phylogenetic species concept, where it is suggested that the least inclusive monophyletic units exist below the level of species within H. sapiens indicating the existence of a number of potential human phylogenetic species; and the biological species concept, where it is determined that racial variation is too small to represent differentiation at the level of biological species. Finally the implications of this are discussed in the context of anthropology where an accurate picture of the sequence and timing of events during the evolution of human taxa are required for a complete picture of human evolution, and medicine, where a greater appreciation of the role played by human taxonomic differences in disease susceptibility and treatment responsiveness will save lives in the future.

Humans are a species, deal with it.

I don’t care if I’ve posted this before, I’ll post it a hundred times if it’s true.

https://disenchantedscholar.wordpress.com/2015/07/14/a-reply-to-common-race-denial-claims/

Paper: Race: A social destruction of a biological concept

https://www.researchgate.net/publication/225799711_Race_A_Social_Destruction_of_a_Biological_Concept

It is nowadays a dominant opinion in a number of disciplines (anthropology,
genetics, psychology, philosophy of science) that the taxonomy of human
races does not make much biological sense. My aim is to challenge the arguments
that are usually thought to invalidate the biological concept of race. I will try to
show that the way ‘‘race’’ was defined by biologists several decades ago (by
Dobzhansky and others) is in no way discredited by conceptual criticisms that are
now fashionable and widely regarded as cogent. These criticisms often arbitrarily
burden the biological category of race with some implausible connotations, which
then opens the path for a quick eliminative move. However, when properly
understood, the biological notion of race proves remarkably resistant to these
deconstructive attempts. Moreover, by analyzing statements of some leading contemporary
scholars who support social constructivism about race, I hope to demonstrate
that their eliminativist views are actually in conflict with what the best
contemporary science tells us about human genetic variation.

mentioned here

https://disenchantedscholar.wordpress.com/2014/12/31/three-race-realism-papers-for-some-reason/

Gene for nose shape found

http://www.ucl.ac.uk/news/news-articles/0516/190516-nose-shape

Figured I’d remind you this exists in light of  How To Judge People By What They Look Like’s detractors.

The four genes mainly affect the width and ‘pointiness’ of noses which vary greatly between different populations.

Populations = races

Pic or it didn’t happen

Compare to Marquardt’s work, which should be compared to character traits and faults in a meta-analysis.

Are people who fit this mask just good-looking or good people, period?

The researchers identified five genes which play a role in controlling the shape of specific facial features. DCHS2, RUNX2, GLI3 and PAX1 affect the width and pointiness of the nose and another gene – EDAR – affects chin protrusion.

See attractiveness tag.
Perception is invaluable.

“Few studies have looked at how normal facial features develop and those that have only looked at European populations, which show less diversity than the group we studied. What we’ve found are specific genes which influence the shape and size of individual features, which hasn’t been seen before.

try looking

“Finding out the role each gene plays helps us to piece together the evolutionary path from Neanderthal to modern humans. It brings us closer to understanding how genes influence the way we look, which is important for forensics applications,” said the first author of the report, Dr Kaustubh Adhikari, (UCL Cell & Developmental Biology).

Isn’t it a little superficial to assume the genes just code for appearance of the face and not the brain behind it? What about forehead size and brain size?

https://www.theguardian.com/uk/2003/sep/28/research.health

The study identified genes that are involved in bone and cartilage growth and the development of the face. GLI3, DCHS2 and PAX1 are all genes known to drive cartilage growth – GLI3 gave the strongest signal for controlling the breadth of nostrils, DCHS2 was found to control nose ‘pointiness’ and PAX1 also influences nostril breadth. RUNX2 which drives bone growth was seen to control nose bridge width.

hooks?

The genes GLI3, DCHS2 and RUNX2 are known to show strong signals of recent selection in modern humans compared to archaic humans such as Neanderthals and Denisovans; GLI3 in particular undergoing rapid evolution.

You should be forced to disclose any and all plastic surgeries before marriage, with photos of the real face. Otherwise it’s genetic fraud.

Guardian quote

Proper nourishment in early life and providing a stimulating intellectual environment are vital for achieving good brain growth and development and this lasts through life. In other words, brain growth in childhood is important not only in determining how bright you become but how bright you stay,‘ said Martyn.

‘That is the real message from this study: that we have to ensure infants and children are brought up in conditions that optimise brain growth – partly to provide us with lots of bright young adults but also to reduce risk of decline in higher mental function in old age.’

When I object to poverty, I see the long-time consequences.

https://disenchantedscholar.wordpress.com/2018/04/08/but-foreign-aid-is-important/

Lower national IQ. We’re sending all those nutrients overseas.

https://disenchantedscholar.wordpress.com/2018/01/07/population-r-selection-food-supply-and-famine/

Literally.

Gen Z grew up with organic food. Coincidence?

Alcohol, DNA mutation and evolution

https://www.cancer.gov/about-cancer/causes-prevention/risk/alcohol/alcohol-fact-sheet

Michael Douglas’ cancer was probably caused by alcohol.

All alcohol causes permanent DNA mutation. Over time it builds up.

Researchers have identified multiple ways that alcohol may increase the risk of cancer, including:

Alcoholic beverages may also contain a variety of carcinogenic contaminants that are introduced during fermentation and production, such as nitrosaminesasbestos fibers, phenols, and hydrocarbons.

Is there a racial difference?

You bet.

Can a person’s genes affect their risk of alcohol-related cancers?

A person’s risk of alcohol-related cancers is influenced by their genes, specifically the genes that encode enzymes involved in metabolizing (breaking down) alcohol (13).

For example, one way the body metabolizes alcohol is through the activity of an enzyme called alcohol dehydrogenase, or ADH. Many individuals of Chinese, Korean, and especially Japanese descent carry a version of the gene for ADH that codes for a “superactive” form of the enzyme. This superactive ADH enzyme speeds the conversion of alcohol (ethanol) to toxic acetaldehyde. As a result, when people who have the superactive enzyme drink alcohol, acetaldehyde builds up. Among people of Japanese descent, those who have this superactive ADH have a higher risk of pancreatic cancer than those with the more common form of ADH (14).

Another enzyme, called aldehyde dehydrogenase 2 (ALDH2), metabolizes toxic acetaldehyde to non-toxic substances. Some people, particularly those of East Asian descent, carry a variant of the gene for ALDH2 that codes for a defective form of the enzyme. In people who have the defective enzyme, acetaldehyde builds up when they drink alcohol. The accumulation of acetaldehyde has such unpleasant effects (including facial flushing and heart palpitations) that most people who have inherited the ALDH2 variant are unable to consume large amounts of alcohol. Therefore, most people with the defective form of ALDH2 have a low risk of developing alcohol-related cancers.

However, some individuals with the defective form of ALDH2 can become tolerant to the unpleasant effects of acetaldehyde and consume large amounts of alcohol. Epidemiologic studies have shown that such individuals have a higher risk of alcohol-related esophageal cancer, as well as of head and neck cancers, than individuals with the fully active enzyme who drink comparable amounts of alcohol (15). These increased risks are seen only among people who carry the ALDH2 variant and drink alcohol—they are not observed in people who carry the variant but do not drink alcohol.

Few epidemiologic studies have looked specifically at the association between red wine consumption and cancer risk in humans.