Idle Rambling On A Saturday Morning -- August 29, 2020

First thing that appeared in my 'in-box" this morning, from SeekingAlpha: the US is going into hyperinflation. We won't know for many years, of course, but I expect to see some scholarly articles on this very phenomenon: to what extent national debt drives inflation. Whether that linked article has validity or not, it lost all credibility when near the end it turned out to be nothing but another "gold" article. The contributor noted Warren Buffett added "gold" to his portfolio. Did Buffett add "gold" to his portfolio or did he add miners or did he add both? It makes a huge difference.

For ordinary folks not interested in gold, would the next best hedge against inflation be buying a home? Based on top stories of the week, it certainly seems a lot of folks are doing just that, buying new homes, although the real reason, I assume: the low interest rates, not as a hedge against inflation.

However.

I doubt anyone wakes up on a Saturday morning and says, "hey, mortgage rates are really, really low. Maybe I need to buy a house."

I think it works the other way around. Folks have a reason (other than mortgage rates) to buy a house. The ultimate decision to buy, after considering the other 37 reasons to buy or not buy, is the the monthly cash flow. And maybe the down payment. 

Could the surge in home buying have less to do with low interest rates and more to do with folks fleeing New York, Seattle, San Francisco, and Chicago? One thing I've noted after ten years of blogging: it doesn't take much to move the needle sometimes. I really have trouble imagining rural Americans buying houses moving that needle. If there is a surge in house buying, it has to be coming from the major population centers. And that means high-income families, or at least families paying taxes.

Why did Willie Sutton rob banks? That's where the money was. Why are home sales surging? Fleeing high-tax states, flee Antifa, and fleeing mostly peaceful riots.

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What Causes Inflation

See this article. See this post.

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What Causes Color Blindness?

I find these articles incredibly interesting considering that much of this was only "discovered" after 1986.

PCM, April 13, 2012:

In 1986, Nathans and colleagues isolated and sequenced the genes encoding the human long wavelength (L), middle wavelength (M) and short wavelength (S) cone opsins and took the first steps toward testing the long-held, two-part hypothesis that (1) variation in the amino acid sequences of the cone opsins are responsible for the spectral differences among the photopigments that all share the same 11-cis retinal chromophore, and (2) alterations in the cone opsin genes underlie inherited color vision deficiencies. 

Findings from these studies both confirmed what previous genetic studies had suggested, and they produced several surprises. As predicted by inheritance patterns of red-green and blue-yellow color vision deficiencies, the genes for human long-wavelength (L) and middle-wavelength (M) cone opsins were localized to the X-chromosome at Xq28, and the gene for the short-wavelength (S) cone opsin to an autosome, chromosome 7 at 7q32 . 

The official genetic designations for the L, M and S opsin genes are OPN1LW, OPN1MW, and OPN1SW, respectively. 

OPN1LW and OPN1MW are arranged in a tandem array. Among individuals with normal color vision there is variability in the number of OPN1LW and OPN1MW genes per X-chromosome array, with more variability in the number of OPN1MW than in OPN1LW genes; thus, contrary to expectation, most people with normal color vision do not have just one L and one M gene. 

OPN1LW and OPN1MW are nearly identical to one another, sharing more than 98% nucleotide sequence identity, whereas they share only about 40% nucleotide sequence identity with OPN1SW, indicating that OPN1LW and OPN1MW arose via a relatively recent gene duplication. 

Because of their similarity, the L and M opsin genes are prone to unequal homologous recombination, which has profound implications for visual function.

NIH, August 17, 2020: color vision deficiency.

Lyonization, NIH: 

Lyonization is commonly known as X-inactivation. In mammals, males receive one copy of the X chromosome while females receive two copies. To prevent female cells from having twice as many gene products from the X chromosomes as males, one copy of the X chromosome in each female cell is inactivated. In placental mammals, the choice of which X chromosome is inactivated is random, whereas in marsupials it is always the paternal copy that is inactivated.

Dinosaurs, monkeys, and humans, from Richard Dawkins' The Ancestor's Tale:

During their formative megayears, mammals were creatures of the night. The day belonged to dinosaurs, who probably, if their modern relatives (birds) are any guide, had superb colour vision. So, we may plausibly imagine, did the mammals' remote ancestors, the mammal-like repties, who filled the days before the rise of the dinosaurs. 

But during the mammals' long nocturnal exile, their eyes needed to snap up whatever photons were available, regardless of color. Not surprisingly, colour discrimination degenerated. 

To this day most mammals, even those who have returned to live in the daylight, have rather  poor colour vision (deer hunters use that to their advantage in the US) with only a two-colour system ("dicrhomatic"). This refers to the number of different classes of colour-sensitive cells -- "cones" -- in the retina.

Humans and Old World monkeys have three: red, green, and blue, and are therefore trichromatic, but the evidence suggests that we regained a third class of cone, after our nocturnal ancestors lost it.

Most other vertebrates, such as fish and reptiles but not mammals, have three-cone ("trichromatic") or four-cone ("tetrachromatic) vision, and birds and turtles can be even more sophisticated. 

Now, the New World monkeys:

Again, the "blue gene" sits on an autosome in both males and females, present in all individuals, but the red and green genes sit on the "X" chromosome, the female sex chromosome. 

The red and green genes, on the X chromosome, are more complicated. Each X chromosome has only one locus where a red or a green allele might sit.

Since a female has two X chromosomes, the has two opportunities for a red or green gene. But a male, with only one X chromosome, has either a red or a green gene but not both. (Again, we are talking about New World monkeys, not humans.)

So a typical male New World monkey has to be dicrhomatic. He has only two kinds of cones: blue plus either red or green. By our standards, all male New World monkeys are colourblind, but they are colourblind in two different ways: some males within a population lack green opsins, others lack red opsins. All have blue.

Females are potentially more fortunate. Having two X chromosomes, they could be lucky enough to have a red gene on one and a green gene on the other (plus the blue which again goes without saying). 

Such a female would be a trichromat. But an unlucky female might have two reds, or two greens, and would therefore be a dichromate. By our standards, such females would be colourblind, and in two ways, just like males.

By the way, humans are more closely related to Old World monkeys (Africa) than New World monkeys (South America). Humans are more closely related to apes, than to monkeys, and there are those who say Old World monkeys are "apes with tales" whereas New World monkeys are "true" monkeys.