Getting drunk on people

Extended quote from http://agentyduck.blogspot.com/2017/06/tasting-godhood.html

"In early college, when I drank wine for the first time outside of Mass, my experience was very different. I was mainly concerned with whether I could tolerate the taste long enough to get drunk.

My brain is programmed to efficiently assess whether food is safe to eat, and whether it is calorically rich. Chefs, winemakers, and other culinary artists are doing their own thing, which is almost orthogonal to the goals (so to speak) of biological evolution. So, if I want to know what a carefully crafted food actually tastes like, then I have to do something weird with my mind. I have to be an epicure, which I would not do by default, because it’s not part of a human mind’s factory settings.

This is, of course, a metaphor for rationality in general. But I’m going to apply it a bit more precisely than that.

When I struggle to empathize with someone (which is pretty much every time I try, in my case), the main obstacle is the very same thing that originally prevented me from tasting wine.

By default, I’m only perceiving a few blunt fragments of info about how they relate to my goals and values. Are they smart? Do they signal like my in-group? Are they easy to talk to? Do they enjoy the same things as me? Can I tolerate this wine long enough to get drunk?

And I’m filtering the info so quickly that I’m not even aware it’s happening, unless I’m looking right at the process. The thing that makes it to consciousness and feels like “my perception of the person” actually contains more of my song than theirs. I’ve discarded most of their personhood."

Economics Charts

Source:  https://politicalcalculations.blogspot.com/2018/03/january-2018-median-household-income.html#.Wp2kEGrwaUk






Source:  https://politicalcalculations.blogspot.com/2018/02/spring-2018-snapshot-of-expected-future.html#.Wp2kNWrwaUk

Is Capitalism the real Superintelligent AI?

All quotes are from SlateStarCodex:

Value misalignment results in perverse incentives and therefore (unintended?) negative outcomes. But this is a problem with any economic system, and almost certainly worse with the systems that are a little freer with the use of state force.

Unregulated capitalism gets humans to act for the human goals signaled by the prices people are willing to pay for things they buy, the amount people charge for the labor they sell, the amount people are willing to accept in exchange for postponing consumption in order to invest instead, and the like. It does its maximization by getting firms and individuals to respond to those signals.

These arguments behind capitalism suffer neglect, causing Chiang to fall into a fallacy of composition: Capitalists optimize only for money, therefore capitalism optimizes only for money.

Capitalists optimize for profits, seeking for the highest-profit opportunities (at least theoretically – it gets complicated). But a working capitalist market economy acts to shrink profits over time, something even the Marxists identify (with their talk of the “falling rate of profit” and such).

Capitalism optimizes allocation of scarce resources. Profits is what happens when somebody discovers and remedies suboptimal resource allocation. In a perfect market, there are no profits. Profit is just a symptom, a fever indicating that something was wrong with the market, but that it is now getting better.

Chiang is more wrong about capitalism than he is about AI. Markets are not a simple optimization around money, they are distributed preference valuation processes that incorporate flexible human values of labor and possessions. If a free market is producing too many paperclips, the price drops until there is no value in producing them at their underlying costs and the relevant resources are employed towards other tasks where there is value. The simplistic AI risk runaway scenarios have a simple, unchanging value function for which they optimize, so there is no correction for the change in human preferences to indicate we already have plenty of paperclips. Perhaps a better argument would be that applying market forces to AI value functions would constrain simplistic runaway AIs, much like market forces constrain his simplistic version of capitalism.

Chiang spends the entire essay detailing how capitalism already operates as an obsessively optimized entity while these AI risks are still hypothetical. That's silly, because the problem with the Paperclip Maximizer is there’s no feedback mechanism to tell the Paperclip Maximizer “we don’t need no more stinking paperclips.” But capitalism has such a feedback mechanism built right in: no paperclip manufacturer is ever going to grey goo the world to make more paperclips because once the supply of paperclips outstrips the demand for paperclips the profit derived from manufacturing paperclips drops to zero, and so paperclip production halts.

Runaway AI is scary precisely because it lacks the feedback mechanisms inherent in the capitalist marketplace.

Does truth exist in analogies?

"Truth is not revealed; it is discovered. And in this process, anything goes."

We use observations to shape or formulate a concept; while on the other hand, we use a concept to shape the nature of future inquiries or observations of reality. Under these circumstances, a concept must be incomplete since we depend upon an ever-changing array of observations to shape or formulate it. Likewise, our observations of reality must be incomplete since we depend upon a changing concept to shape or formulate the nature of new inquiries and observations.

“If one’s understanding is always imperfect, it cannot be committed to print because revision is imminent”. The accurateness of one’s storytelling becomes less important that the purpose of the story itself: moving forward in the infinite and mutually influencing loop of observation and conceptualization.

CF: https://www.ribbonfarm.com/2018/01/18/the-unapologetic-case-for-bullshit/

Natural Resource Management Stories

Conservation - Collaboration Success Story: Nature Conservancy and Nutrient Stewardship Council in Western Lake Eire Watershed.  Accreditation of fertilizer merchants (term?) to educate farmers in the 4Rs:   Right amount, right time, right place, right ....  These are complicated decisions; fertilizer reps and farmers understand better all of the details of each decision, while scientists and Nature Conservancy have ideas about solutions.  By working together (also motivated by Ohio Law) they are innovating solutions, like using liquid fertilizer to furrow-apply salt-free fertilizer directly on seeds of side-dressing or foliar applications

Monarch voluntary conservation agreements.  Monarch butterfly has been in steep decline and the iconic insect is the subject of a successful citizen science campaign to document migration patterns and encourage milkweed host plant cultivation.  Now Monarch is being considered for listing as endangered species. Voluntary conservation agreements and memorandum of understanding between the USFWS and private companies and individuals are being encouraged as a way to avoid ESA listing.

The recent decision to de-list the lesser prairie chicken was based on the existence of a voluntary conservation agreement whose possible beneficial effects on the species were not considered by USFWS.

Now power companies and Midwestern farmers seem to think a voluntary conservation agreement is a good insurance policy against a possible listing decision.  If the monarch is listed, the government could require landowners across the country to be pollinator friendly.  Monarchs need us to manage for milkweeds.

Don't mess with Iowa.  Agricultural misperceptions of the 2015 proposed Clean Water Act rule led to lawsuits that forced the EPA and Army Corps to halt the implementation of the rule.  Coal states were able to obtain a supreme court ruling halting implementation of the 2015 CO2 rule for the "Clean Air Act".  And now Iowa (and other midwestern farmers) are against the EPA's proposed strengthened standards for atrazine, a popular herbicide.  Midwestern farmers argue that lowering the allowed concentration of the popular herbicide would impair their ability to grow food for the country.  Farmers also point out that the proposed standards might lead to more water pollution, not less, due to the reliance of no-till farmers on broad-spectrum "burn down" herbicides to clear the fields for planting.  Without these herbicides, farmers would be forced to go back to tilling their land in order to mechanically disrupt existing weeds.  

Albuquerque 2016 Monsoon Season

From the ABQ NWS Homepage.

The monsoon began early in Albuquerque this year, with a week of good moisture at the end of June. But then June high pressure returned and most of July was hot and dry.  It wasn't until the beginning of June that the rains reliably returned.  Overall, the monsoon wasn't bad, but the hiccup in the beginning ended up dooming most annual plants.  Only perennials managed to reap the rewards of the late-breaking monsoon moisture.  Now, at the end of September, many monsoonal plants are still trying to finish flowering and set seed.  Many plant species are flowering late and show signs of stunted growth.

Atherosclerosis

Pathogenesis of atherosclerosis. (a) In the first stage, low density lipoprotein-cholesterol (LDL) is deposited in the endothelium and undergoes oxidative modification, resulting in oxidized LDL (oxLDL). OxLDL stimulates endothelial cells to express adhesion molecules (vascular cell adhesion molecule-1 (VCAM-1), P-Selectin) and various chemokines (e.g., Monocyte Chemoattractant Protein-1 (MCP-1), Interleukin 8 (IL-8)). This leads to a recruitment of monocytes, which transmigrate into the intima and differentiate to pro-atherogenic macrophages; (b) Macrophages harvest residual oxLDL via their scavenger receptors and add to the endothelial activation and, subsequently, leukocyte recruitment with the secretion of Tumor Necrosis Factor α (TNF-α) and IL-6; (c) The increasing plaque volume promotes neovascularization. Proliferating smooth muscle cells (SMCs) stabilize the nascent fibrous plaque. With deposition of fibrin and activated platelets on the dysfunctional endothelium that expresses tissue factor (TF) and von Willebrand factor (vWF), a pro-thrombotic milieu is formed; (d) Foam cells can undergo apoptosis and release cell-debris and lipids, which will result in the formation of a necrotic core. In addition, proteases secreted from foam cells can destabilize the plaque. This can lead to plaque rupture, in which case extracellular matrix molecules (e.g., collagens, elastin, TF, vWF) catalyze thrombotic events.
(PMC full text: Int J Mol Sci. 2015 May; 16(5): 9749–9769. Published online 2015 )

The Problem with Nutrigenomics

"Personalized nutritional counseling is a burgeoning field. Several companies, including Vitagene, Nutrigenomix and DNAFit, are already offering individualized dietary counseling.  Their efforts are based mostly on genetic testing, but scientists have only just begun to explore the links between DNA and good nutrition. “I think companies offering personalized dietary advice are probably running ahead of the evidence,” said John Mathers, director of the Human Nutrition Research Center at Newcastle University in Britain." [NYTimes Blog]

Introduction

Science skeptics have recently reviewed these services, and found plenty of quackery. [Science Based Medicine] [Skeptical Raptor]

However, there is some research to back up the idea that genetic testing can provide insights into metabolic disorders.  There may be as many as 200 SNPs for which there are proven metabolic effects, and only a subset of these alter nutrient requirements in a significant portion of the population [e.g., the rs1801133 MTHFR SNP and folate requirement in 15–30% of the population (Solis et al., 2008) and the rs12325817 PEMT SNP and choline requirement in 20–45% of the population (da Costa et al., 2006)].

What do genetic testing services measure?

The human genome consists of about 3 billion nuceleotide bases, each of which is either A,C, T, or G.  A reference genome based on the similarities of all genotyped humans has been assembled, along with a corresponding reference database of all of the point "mutations" where individuals differ from that baseline.  So far, scientists have documented about 150 million of these single nucleotide polymorphisms, called SNPs.  The average person doesn't have all of these differences, however; most people have about 3 millions SNPs that differentiate them from the reference human genome.   Since 3 million is about 0.1% of the 3 billion base pairs, most humans differ from each other by about 0.1% of our DNA. Ancestry genomic testing services like 23andme test for a few hundred thousand SNPs for $100-$200.  For $1000-10,000 a complete genomic sequence can be obtained.  (there are about 3 billion bases total.  

Examples: MTHFR – metabolic pathways and nutrigenomics

In humans, SNPs in the gene MTHFD1 increase the demand for betaine as a methyl-donor, thereby increasing the dietary requirement for choline. Another SNP in the gene PEMT prevents the activation of this gene by estrogen, thereby decreasing endogenous production of phosphatidylcholine (a source of choline) in the liver and increasing the dietary requirement for choline. [Choline: Critical Role During Fetal Development and Dietary Requirements in Adults. Ziesel]

But note that it is not so simple.  There are several forms of the MTHFD1 gene, for example MTHFD1L and MTHFD2. If MTHFD1 is commonly mutated, it may be a pseudogene.

Complexities interpreting SNPs

No simple test can unravel the intricacies of the human genome, and consumers should be suspicious of anyone claiming to be able to interpret measurements of tens of thousands of genes, with millions of genetic variations, some of which have effects on hundreds or thousands of the small molecules of metabolism (and perhaps on thousands of peptides or proteins involved in metabolism).

[A grand challenge for nutrigenomics.  Steven Zeisel. 2010.]

Mistakes in genomics data

Note that 23andme data, like any large genome scan, can have mistakes in it.  For example, the Enlis genomics blog found more than 500 likely mistakes in a sample of 23andme raw data!  (Enlis)

Furthermore, many important nutritional SNPs are not testing by 23andme.

Solution: Metabolic Testing
There is a genetic test for MTHFR variations. But there’s also a cheaper and more accurate way to test for whetherMTHFR variations are causing disease. We simply check the levels of homocysteine in the blood...In other words, the homocysteine levels determine our actions, not the MTHFR test results.[Cleveland Clinic]

Portable Real-Time Measurement of Air Quality

I recently purchased a Uni-Trend Air Quality Meter.

It measures VOCs (both natural and man-made), PM2.5, and temperature and humidity.

Coarse particles (PM10) have a diameter of between 10 micrometers and 2.5 micrometers and settle relatively quickly whereas fine (PM2.5) (0.1 to 2.5 micrometers in diameter) particles remain in suspension for longer. To put things into perspective, human hair has a diameter of 50-70 micrometers and a grain of sand has a diameter of 90 micrometers.



Sources of fine particles include all types of combustion activities (motor vehicles, power plants, wood burning, etc.) and certain industrial processes.  Sources of coarse particles include crushing or grinding operations, and dust from paved or unpaved roads.

PM2.5 is made up of sulfates, nitrates, carbon, and soil.


Albuquerque reports the Air Quality Index for daily pollen and Fine/Coarse Particulates:



 But these numbers are reported as "Index" values, and have to be converted to ug/m3 to compare to measured values:

Over the last week, Albuquerque has reported AQI for PM2.5 of almost 50, which should be about 15 micrograms per square meter, whereas my unit typically reports 30-50 micrograms per square meter, indoors and outdoors.  It is possible that ABQ measures air quality higher from the ground than my unit, or that PM2.5 is lower during the night when I don't check it.

Here is an excellent resource for more information.  Most of the graphics on this page are from this source.

Metabolic Pathways

Say you want to know what the possible effects of taking a supplement might be.  You could research the supplement on the two high-quality websites that report supplement interactions based on human trials:

Examine.com

The Mayo Clinic - not as many supplements covered.

It would be great if there were reliable "trip reports" from patients on the effects and side-effects of drugs, but unfortunately side-effects are not reliably reported.

If you wanted more basic information, you could consult a metabolic pathway interaction diagram.  Note that the study of genetics and proteomics still has a long way to go:  we don't know what most of the essential genes even do, nor do we know the function of xx% of all genes.  No network diagram is complete....

SigmaAldrich offers a searchable poster:



According to this, NAC can increase glutathione, but also homocysteine. Important information from the network!




Biochemical-pathways.com has even more information.  Note that because the network diagram is again a poster, single compounds (e.g. cysteine) can occur in different places on the diagram.




Metacyc is the most detailed, but only shows one "pathway" at a time.


KEGG is another very good resource with drop-down menus to explore individual pathways.

A long list of other resources.