Jack

What the California law is doing to freelancers isn't even the biggest problem with it.

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President Donald Trump is expected to sign a bill into law today that will bar the federal government and its contractors from asking about the criminal history of a job applicant prior to the extension of a conditional offer of employment.

The Fair Chance Act, which was tucked into the massive defense spending bill passed by Congress earlier this week, was part of a national campaign by criminal justice advocacy groups and like-minded lawmakers to "ban the box"—referring to the question on job applications about whether one has been convicted of a crime—and reduce barriers to employment for an estimated 70 million Americans with criminal records.

"After many fits and starts, we are finally about to give formerly incarcerated individuals a second chance by eliminating a major hurdle they face when job-searching," Sen. Cory Booker (D–N.J.), one of the bill's cosponsors, said in a press release. "This legislation will immediately change lives by allowing thousands of qualified people with criminal records to more meaningfully integrate into life outside prison walls."

The law was supported by a bipartisan group of criminal justice organizations. Holly Harris, the executive director of Justice Action Network, said it will open "tens of thousands of federal government and contracting jobs to people who have made mistakes, but just need a chance to get a foot in the door to present their skills and qualifications."

According to the National Employment Law Project, 35 states and more than 150 cities have passed similar legislation, including red states like Georgia, Kentucky, and Oklahoma. Thirteen states extend those hiring requirements to private businesses.

Of course, while government should set an example for hiring practices it wishes others to follow, coercing private businesses to do so is not the preferable solution. Several major companies have voluntarily instituted "fair-chance" hiring practices, such as Walmart, Target, Home Depot, and Koch Industries.

In a statement, Kanya Bennett, senior legislative counsel for the American Civil Liberties Union, said the passage of the Fair Chance Act eliminates "a significant obstacle to employment faced by those reentering society from our broken criminal legal system."

"More than 70 million people in the United States have an arrest or conviction record that shows up in a criminal background check," Bennett continued. "This forces one in three prospective employees to check the box when applying for jobs."

Home prices have recovered, but construction remains severely depressed. Why is that?

Let’s take Phoenix, which was the poster child for the 2006 housing bubble. Prices are not back at the peak, but they are well above 2003 levels, even in real terms:

Given the high prices, you might expect housing construction in Phoenix to be highly profitable.  Indeed, just looking at that price data I’d expect construction to be well above 2003 levels, assuming there were no factors depressing supply.  In fact, new construction in Phoenix is roughly half the level of 2003, at least for single-family homes:

Why do I focus on Phoenix? Recall that many articles pointed to Phoenix as the smoking gun behind the 2006 “housing bubble” hypothesis.  It was generally conceded that the price spikes in New York, Boston and California might have partly reflected building restrictions, the so-called NIMBY phenomenon.  But cities such as Phoenix and Las Vegas were seen as having almost unlimited land for development.  The price spike seemed irrational, as it was assumed that the high prices would lead to a surge in new construction, eventually bringing prices down to much lower levels.

But what if supply is also constrained in Phoenix and Las Vegas?  I don’t have any good explanation for what that might be so, but the data strongly suggests that there is some sort of supply problem.  The high prices are back, but construction remains severely depressed.  During the period from 1950 to 2006, the sort of prices we now see in Phoenix and Vegas would have led to a huge surge in housing construction.  For some reason we are not seeing that surge.  Thus the most powerful evidence in favor of a 2006 housing bubble—the anomalous rise in house prices in the inland Southwest—is no longer evidence for the existence of a housing bubble.

I have no idea why supply in these markets is so constrained.  I’ve read articles that make vague references to the cost of land and labor, but no real explanation of why things are so different from 2003.

Kevin Erdmann wrote by far the best account of what really happened during the housing bubble:

 

 

(27 COMMENTS)

While politicians search in vain for trade deals that will help blue-collar workers, the real problem is being ignored.

U.S. Steel Corp. plunged after delivering a barrage of harsh news, warning of a loss and announcing it will shut down most of its Great Lakes Works facility near Detroit, lay off workers and slash its dividend.

. . . The industrial icon plans to lay off as many as 1,545 workers from the Michigan plant, reduce its quarterly dividend to 1 cent from 5 cents, and prune capital expenditures.

U.S. steelmakers are facing slowing demand in the manufacturing sector, even though mills have enjoyed protection because of Trump administration tariffs. U.S. Steel has been a laggard in the domestic industry, with aging plants that are less efficient than rivals with newer technology.

Tariffs can’t save steel jobs, which are going the way of the dodo bird. And the effects of automation are not gradual; they come in big chunks as obsolete mills close down.

Mark Perry directed me to a couple of stories that illustrate the problem:

In the 1980s, American steelmakers needed 10.1 man-hours to produce a ton of steel; now they need 1.5 man-hours, says Joe Innace of S&P Global Platts.

Most American steel is now made at super-efficient mini mills, which use electric arc furnaces to turn scrap metal into steel. (Traditional integrated steel mills make steel from scratch, feeding iron ore and coking coal into blast furnaces.) Some mini-mills need just 0.5 man-hours to produce a ton of steel, Innace says.

Increased productivity means today’s steel mills don’t need as many workers. Steel industry employment peaked at 650,000 in 1953. By the start of this year, U.S. steelmakers employed just 143,000.

We still produce as much steel as in the 1950s, but with far fewer workers. And the problem is about to get much worse:

“So steel and aluminum will see a lot of good things happen. We’re going to have new jobs popping up,” Mr. Trump told steel and aluminum executives last Thursday at the White House as he announced his 25% and 10% tax on imports.

Someone should tell him about Voestalpine AG ’s steel plant in Austria, which reveals the reality of steel production and jobs. A Bloomberg News story from June 20, 2017 offered a fascinating look at how a modern plant can now produce high-quality steel with few workers.

The plant in Donawitz, a two-hour drive from Vienna, needs all of 14 employees to make 500,000 tons of steel wire a year. The same mill in the 1960s would have needed as many as 1,000 workers to produce a similar amount albeit of lesser quality.

Free traders like Paul Krugman claim that mercantilists don’t understand basic Ricardian trade theory. Mercantilists claim that neoliberals put too much weight on efficiency and don’t understand the pain inflicted on blue-collar workers by import competition. The fact that mercantilists are almost totally silent on automation is the “tell” that Krugman is right—they really are ignorant of the basic ideas of comparative advantage. If they weren’t they’d focus on automation, not trade.

In last night's Democratic presidential debate, Mayor Pete Buttigieg warned Sen. Elizabeth Warren (D–Mass.) against "issuing purity tests you cannot yourself pass." He was talking about the senator's millionaire status, but his statement applies just as much to her education plan. 

The plan, released on October 21, is radically anti-choice. It calls for ending federal funding for public charter schools, banning for-profit charter schools, increasing regulations for all charter schools, and making it more difficult to start new charter schools. Warren wants to stop private school choice programs such as vouchers or tuition tax credits.

At last night's debate, Warren declared her desire to "do even more for our public schools" with a "historic $800 billion investment." Though the phrases "charter school" and "school choice" did not come up on stage last night, Warren solidified her anti-choice stance in a previous debate when she said "money for public schools should stay in public schools, not go anywhere else." And she told the president of the National Education Association last month that families should stay put in their failing public schools.

That was a purity test that Warren and her family cannot pass. In October, I discovered that Warren sent her son to elite private schools starting in the fifth grade. Less than a month later, Warren was caught on video speaking misleadingly to a voter about her decision to send him to private schools.

The next generation of the candidate's family has continued to benefit from private education. Warren's three grandchildren attended last night's debate, and at least two of them attended an elite private school in Los Angeles. According to the school's online newspaper, Octavia Tyagi graduated from Harvard-Westlake School earlier this year. Lavinia Tyagi is currently a freshman at the same school. The tuition at Harvard-Westlake School is $39,700, so a full high school education at Harvard-Westlake costs over $158,000 in tuition alone. According to Niche, a website that grades schools, Harvard-Westlake School is the second-best private high school in the state and the sixth-best private high school in the nation. 

So Warren's daughter and son-in-law have chosen to send their kids to an elite private school, just as Warren chose to send her son to one. And that's fine! Parents should pursue what's best for their kids. If that means pulling them out of the public schools to get a better education elsewhere, they should have every right to do that.

The problem comes when politicians like Warren try to deny that opportunity to parents who do not have as much money as they do. All families, not just the rich and powerful, should be able to send their children to the schools of their choice.

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This graph caught my eye:

Notice that prior to 1980, the number of affluent people was growing rapidly, but the number of poor people was also increasing. After 1980, the number of affluent people rose even more rapidly, while poverty began declining.  I was in grad school in 1980, and I don’t recall very many people expecting such a dramatic turnaround in the number of poor people.  Many experts were predicting a global catastrophe, due to rapid population growth in poor countries.

So what changed in 1980?  The most likely explanation for the plunge in global poverty is the neoliberal revolution, which began around 1980.  Poverty fell especially rapidly in countries that adopted market reforms, such as Chile, Bangladesh, India and China.  Ironically, the media is now full of stories claiming that neoliberalism has failed.  My response is simple—compared to what?

(17 COMMENTS)

[This is an entry to the 2019 Adversarial Collaboration Contest by the delightfully-pseudonymous Adrian Liberman and Calvin Reese.]

About the Authors: Adrian Liberman is currently a PhD student in biology at a university in the mid-Atlantic. He previously worked at the National Institute of Aging and remains actively interested in gerontology and the biological study of aging. Calvin Reese is an author with a BS in Biology. He has always been interested in the possibility of life extension by calorie restriction. Recently, he has reexamined the subject after undertaking a series of intermittent fasts for weight loss reasons. Calvin believes CR extends life; Adrian has long been skeptical.

Introduction: Is food making us old?

We all agree that food is delicious, and we also all agree that too much food is bad for us, but exactly how bad is it? Various academics have proposed that too much food actually accelerates the aging process, and reducing our food intake via calorie restriction (CR) is one of the most accessible and available methods of extending human life. While billionaires pump vast fortunes into increasingly far-fetched stem cell treatments and consciousness transfers, CR advocates contend that they can get a 10-20% increase in their natural lifespans simply by eating a little less. If true, CR raises a question of enormous significance to gerontology and the science of aging: are our diets aging us one calorie at a time? And if so, can we stop it?

Calorie Restriction (CR) and Intermittent Fasting (IF) advocates generally claim that CR will extend your lifespan and prevent various diseases, and that IF is an effective form of CR. Evidencing these claims are animal studies in yeast, worms, flies, mice, and monkeys as well as indirect evidence from humans. A variety of biochemical studies have been performed, and a host of theoretical literature generally claims that the underlying mechanisms for the effect are the IGF axis affecting sugar metabolism, DNA damage mechanisms dealing with free radical formation, and inflammation modulation.

My position (Adrian) is that for the average individual reading this article, CR and IF are not generally worth the effort, because the individual will be exposed to non-trivial risks and the benefits will be minute.

My position (Calvin), is that there exists some amount of food, on average, that will produce an optimal human lifespan and that the average person could significantly extend their life by moderately reducing their calorie intake.

Calorie Restriction (CR) is a term coined to describe a series of experiments that have been conducted over the course of more than a century, demonstrating that various animals kept in laboratory conditions generally survive longer if fed diets that are ‘restricted’. This effect has been observed in bacteria, yeast, worms, fruit flies, mice, and arguably monkeys, so it appears to span every domain of life. (40)

On the other hand, population-level studies say that the lowest observed mortality in western populations occurs at a BMI of ~25. (4)(5) This appears to be a paradoxical result, since a BMI of 25 generally results from a diet that isn’t particularly “restricted”. Why would we observe a lower mortality in lab animals when they are undergoing perpetual mild starvation, but a higher mortality when this happens in humans?

And by extension, should you, the reader, adopt a calorie-restricted diet, or an NIH-approved 25 BMI diet?

Semantics: Calorie Restriction versus just not overeating

First things first. Let’s define some very strict terminology. This will become important later:

Kinds of diets:

• Ad libitum Diet (ad-lib) – at one’s pleasure, or as much food as you would like.

• Ad-lib Calorie Restriction (Ad-lib CR) – a diet that contains fewer (for example 30% fewer) calories than your diet would if you were eating an ad-libitum diet

• Normative Diet (ND) – a diet that is balanced and prevents the onset of obesity. The general analog to USDA’s 2000 calorie diet. (Our term and not in common usage)

• Normative Diet Calorie Restriction (nd CR) – a diet that is balanced, but contains fewer calories than a normative diet (for example 30% fewer)

Once we establish these definitions, the kinds of claims that proponents or opponents can make expand into the following:

Claim 0: You, the reader, should adopt an ad-lib diet
(Nobody claims this, put the chips down!) (null hypothesis)
Claim 1: You, the reader, should adopt an ad-lib CR diet
Claim 2: You, the reader, should adopt a Normative Diet
Claim 3: You, the reader, should adopt an nd-CR diet

For the purposes of this article, we’ll be assuming that you, the reader, are an average American of indeterminate sex.

First the claims of CR in detail:

Animal Studies and the NIA Interventions

CR relative to ad-lib leads to improved metabolic function in the animals studied, generally because they do not become obese. On the other hand CR relative to a normative diet leads to unfavorable/negative outcomes including a decrease in fertility, altered mental states, and muscle wasting, but also a significantly increased lifespan.

A Calorie Restriction experiment goes like this: Take some animals and first establish the amount of nutrients they consume “normally”, or under optimal growth conditions. After this, take half of those animals and provide them access to all the micronutrients and amino acids they want, but restrict their access to raw energy in the form of fats or carbohydrates to X% of their normal intake.

Where does this lead to increased lifespans? Let’s start at the beginning! The beginning of time:

CR dramatically extends the lifespan of yeast. (39) Yeast longevity is difficult to quantify, but experiments have suggested 75% CR in yeast (done by decreasing glucose concentrations in yeast media from 2% to 0.5%) extends yeast longevity by a factor of 3. (39)(40). Single-celled organism lifespan is a goofy term, but it can be measured both directly by looking under a microscope at cells and keeping track of when they kick it, and indirectly by comparing the steady population of cells to how often they divide.

Nematodes (worms) exposed to 50-75% CR experience a 2-3 fold increase in longevity. CR in Drosophila melanogaster produces between 30% and 100% increases in the observed lifespan of the flies. (40)(41) Many hypotheses have been proposed to explain why CR produces such marked increases in the lifespan of worms, flies, and yeast, but most notable is the behavior of the SIRT-family genes. (71) Unfortunately the SIRT mutation data is difficult to interpret due to the relatively central role SIRT genes tend to play to the functioning of a diverse array of cells, but some theories are more convincing than others. More on this later. Of course, in general, the problem with studies like these is that establishing what constitutes a normative diet in organisms like these is somewhat subjective. Is there such a thing as an obese yeast cell? On the other hand, a normative diet for rodents is pretty easy to establish.

Numerous studies and overwhelming evidence show that CR significantly extends the lifespan of rats. Rodent CR studies suggesting CR extends lifespan go back to the 1930s and 1940s (26) (30). The earliest rodent CR studies focused on longevity with modern approaches and methods were conducted in the 1980s. Pugh et. al in 1992 (27), Yu et. al in 1985 (28), and Weindruch and Walford in 1982 (29), all subjected rats to 40% CR diets compared to ad lib baselines and found between 10 and 20% increases in longevity as compared to normative diets. Similarly, 1986 Weindruch is a gold standard mouse CR study. Here we see that even fairly aggressive ndCR produces extended average and maximum lifespans, both relative to ad-lib and relative to a normative diet, with a normative diet extending lifespan 20% relative to ad-lib, and 40% ndCR extending lifespan another 30% on top of that. (Context: think big fat guy keeling over from a heart attack at 50, vs everyone’s stereotypical tiny Chinese grandma, who spends her 100th birthday stubbornly refusing to reveal the location of her phylactery)

Reported health benefits of CR in rodents include reduced cancer risk in p53-deficient mice (33), increased proteasome activity (34) in mice and rats, improved cognition (32)(35), reduced oxidative stress and NF-kB signaling (36), and various other health benefits. Several studies, including Park et. al. and Pires et. al. have observed dramatic changes in insulin signaling and serum glucose levels (32)(37)(38), which has been of particular interest to gerontology researchers. IGF signaling has been proposed as one of the mechanisms by which CR improves health outcomes (15).

So far this is a pretty strong story. What’s the sketch factor of this evidence? Well… Some rat and mouse strains responded to CR better than others and methodology varied widely between rodent trials, making them difficult to compare (32). The only study performed on wild-caught mice that aren’t buried under a mountain of genetic defects to shame the Habsburgs had a negative outcome. As a model for aging, mice are also slightly suspect because unlike most mammals, they are globally telomerase-positive, which means that the effects of mutational accumulation on their soma don’t directly translate to other mammals, since oxidative damage has a large interplay with telomeric senescence.

Overall, however, we agree that mouse lifespans are significantly extended by CR. But…

As the organism becomes larger and more complex, the beneficial effects of CR on lifespan appear to taper off (40). 25% nd CR extends dog lifespan 25% (66). Why isn’t more aggressive CR investigated in dogs? Larger animals don’t tolerate aggressive caloric restriction well, 40% caloric restriction would likely kill most dogs. It seems that brains are probably to blame, because the metabolic rate of the brain is generally not significantly regulated (70). If you run out of energy for running your brain cells, you’re done for. The larger the proportion of your metabolism dedicated to maintaining brain function, the less CR you can tolerate.

So, given that trend, the most relevant information for humans should probably come from monkeys. (#freescopes)

Unfortunately, monkeys live a long time, so studies of monkey aging are measured in many decades and cost millions and millions of dollars. The National Institute on Aging and the University of Wisconsin have taken on the task and subjected ~40 rhesus monkeys each to 30% CR. In the WNPRC study, CR was versus an ad lib baseline and in the NIA study CR was relative to a standardized diet designed to prevent obesity. (1) (3)

Rhesus monkeys have a maximum lifespan of ~40 years, and after 30, the WNPRC study reported only 13% of the CR group had died of age-related causes, whereas 37% of the control group had died. (1) The authors write “CR reduced the incidence of diabetes, cancer, cardiovascular disease, and brain atrophy.” (1) In 2017, 10 of the WNPRC CR group animals remained alive compared to 3 animals in the control group. (31) In a monument to absurd timelines, the WNPRC study is not yet over, as many CR monkeys survive in 2019. No mean lifespans are established.

Here we hit our first snag. In complete contrast to the WNPRC study, the NIA rhesus monkey study used a standardized diet designed to prevent obesity for the control group. The NIA study found no increase in survivability among the CR group. (3) What gives?

If we were being charitable, we would say that monkey studies are ridiculously hard to power properly. With only 86 monkeys present in the NIA study, the negative observation could easily have been a product of chance that was inadequately represented by the reported p-values, and we should defer to priors based on other mammals. Anecdotally, and though the NIA paper would never admit to this, the NIH sometimes staffs monkey studies of this kind with “leftover” monkeys from clinical trials that may have mysterious medical conditions that are not obvious to the naked eye but were caused by drug trials, experimental surgical procedures, etc.

If we wanted to be less charitable, we would look at the fact that the WNPRC study pulled shit like this:

…and point out that aging is almost by definition a process that impacts the survival rate relative to any injury, so trying to disentangle “age related” mortality from regular mortality is bad and wrong.

The most significant difference between these studies is the use of adCR (Wisconsin) vs ndCR (NIA). It’s no surprise that monkeys that are on a controlled diet are healthier and live longer than monkeys that are fed an ad-libitum diet. In mice, this is a commonly known problem for control populations, and monkeys are no different (72). The balance of evidence probably tilts against the idea that CR is effective in monkeys, however our priors that ndCR should be effective are fairly strong, so for now let’s assume that it is.

Adrian concedes that a 2017 statistical analysis of both studies by the University of Alabama at Birmingham in cooperation with the authors of the original studies determined that CR decreased mortality in rhesus monkeys (31), but the study is presented under protest because combining ndCR and adCR in the same analysis is inadvisable, disingenuous, probably illegal, and was the direct cause of the sinking of the Lusitania.

The gold standard of CR studies in animals with respect to human health would be studies that occur in higher animals (mice, dogs, monkeys) and perform CR relative to a normative diet. On the balance, evidence that ndCR extends lifespan in higher animals is fairly strong. The monkey problem, however, is pretty bad, and we remain skeptical of the strength of CR in humans.

Despite these objections, we agree that CR promotes longevity and reduces all-cause mortality of animal model organisms and that this finding supports the view that CR probably increases the lifespans of humans in an ideal scenario.

So… what’s up with that? Do the above findings mean that we need to radically reinterpret what being overweight or obese means? Are we just WILDLY overestimating the “healthy” weight for all these animals?

In a word, no. Animals are clearly not adapted to undergoing caloric restriction this severe. How do we know that? Easy. The animals in most of the experiments above, under fasting conditions, are driven sterile. From an evolutionary standpoint, it’s safe to assume that being sterile is not an adaptive trait, so clearly most animals have not evolved to operate at levels of caloric restriction this severe on a routine basis. That’s one of the simpler distinctions between a “healthy weight”, obesity, and being in a starvation regime. Still, clearly animals live longer when they are starving, so why?

Proposed Mechanism by Which Food Makes You Old (and how calorie restriction stops it)

First an interlude: aging is one of the last frontiers in biology where major theories still compete on an even footing to explain a basic and universal process. The simplest definition of aging is the observation that past a certain point in an animal’s life, the likelihood that it will die doubles every period X, where X is different for different species. This observation is stunningly universal. It’s also important to note that the likelihood of death from almost any type of injury increases over time, so aging is not just the idea that cancer is more frequent when you’re 50 than when you’re 20, but the idea that almost all diseases are more frequent in older individuals, and dying from almost any injury is more likely when you are old than young (78, Arkin).

Covering the slapfight over the specific mechanism involved fully is beyond the scope of this paper, especially because there are no conclusive answers to any of your questions, but briefly these are the major aspects of biology that change with age, drawing directly from “The Hallmarks of Aging” Lopez-Otin et al. (44).

1) genomic instability, such as replication errors, mutations, DS breaks, and crosslinking;
2) telomere attrition, including damage to the telomeres that does not result in telomere shortening;
3) epigenetic alterations, including changes in methylation patterns, histone modifications, and chromatin remodeling. This generally also leads to deregulated/erroneous gene expression;
4) loss of proteostasis, which is characterized by protein denaturation or unfolding and the accumulation of waste products your body cannot break down;
5) deregulated nutrient sensing, causing both the cell and the body to become less responsive to nutrients;
6) mitochondrial dysfunction, which is thought to be particularly central to the relationship between CR, obesity, and aging because mitochondria process glucose and create reactive oxidative species (ROS);
7) senescense or quiescence, the cessation of the cell cycle; and
8) stem cell exhaustion, which slows or halts renewal of virtually all tissues and cell types.

These are specific, measurable instances of the general breakdown we associate with aging chosen for their correlation with chronological and apparent age. None of them has been decisively established as the actual cause of aging as we understand it, though all are understood to contribute to aging at the cellular and tissue level, which is the general breakdown and cessation of cell functionality (44).

Gerontologists love to whip these hallmarks out, but in reality most of them are interrelated in some way, so establishing which ones of them are merely the byproducts of other is extremely difficult. Ex: mitochondrial dysfunction increases the rate at which oxygen radicals are produced leading to greater genome instability and telomere attrition. Stem cell exhaustion probably arises from genomic instability or nutrient sensing deregulation, but on the other hand it can lead to senescence in the tissues as replacement of dying cells slows down. It’s all an ouroborosian mess. (44)

Almost all of the hallmarks have been shown to be impacted by food intake. Obesity has been decisively implicated in causing genomic instability in model animals, but evidence is lacking in humans (45). Crucially, the CR-ROS hypothesis that excessive eating, causing both oxidative damage from digestion and metabolism of glucose and obesity – thus linking obesity and ROS damage together, remains poorly supported in humans (45)(46). Obese adult individuals suffer from greater telomere attrition than non-obese individuals and have shorter telomeres (47). Obese individuals have profoundly different epigenetics than non-obese individuals, which is not surprising, since insulin expression profiles and fat metabolism are well-established as being changed by, and changing, epigenetics (46)(48)(49). In fact, epigenetic changes in insulin expression due to a high-fat diet may be heritable (48). Obese individuals, and particularly diabetes patients, have markedly different DNA methylation patterns from non-obese persons and modified chromatin structure (49) Altered chromatin density due to obesity has been observed in rodents and implicated in the onset of dementia, which is commonly associated with old age (50)(51). Numerous proteasome dysfunctions and significant protein misfolding have been observed in obese rodent and human subjects (46). In addition to creating insulin resistance, human adipose tissue creates a pro-inflammatory environment and significantly alters cell response to NF-kB and inflammatory cytokines (52). Obesity has been specifically implicated in ROS damage to mitochondria, mitochondrial dysfunction, reduced mitochondrial fission, and further elevated ROS production by the Krebs cycle (53). Furthermore, adipose tissue and obesity apparently promote senescence (54). Obese mice exhibit dramatically increased rates of T-cell senescence (55). Finally, obesity results in far greater stem cell exhaustion and quiescence (56). Adipose tissue stem cells, hematopoetic stem cells (HSCs), bone marrow, and other stem cell reserviors have all demonstrated higher rates of quiescence in obese populations of rodents and humans (46).

So, we have covered all eight biomolecular cell and tissue-level hallmarks. Obesity does, in fact, make us older. And we are pretty sure CR makes most animals younger. That is an excellent clue as to how the two are related, and which of the mechanisms might be the most important.

Your body usually converts sugar into mechanical or chemical energy by using a complicated daisychain of a couple dozen proteins called the Electron Transport Chain (ETC). The ETC is so called because each protein in it contains an electrically charged amino acid that is highly reactive due to holding on to loose electrons that came from sugar. The ETC takes electrons obtained from sugar, and attempts to stick them onto molecules of oxygen, converting it into water. Unfortunately, this process occasionally fucks up, and instead of getting nice benign water, the oxygen becomes radicalized, gets an Al-Qaeda franchise, and becomes either Hydrogen Peroxide or the Superoxide anion. Both of these are comically reactive molecules, and if they happen to diffuse out of the mitochondrion, they can react with pretty much anything and cause damage. If they react with your DNA, you’re in trouble, because oxidative damage to your DNA produces mutations. Similarly, the oxidation of fats results in chemicals that cause inflammation, and the oxidation of proteins can result in byproducts that your body can’t break down.

From here comes the Rate of Living Theory: an animal can consume only a specific and finite number of calories in its lifetime, because after that point the damage induced by said calories becomes fatal.

Essentially, for a given cellular architecture, so many calories in results in so many molecules of peroxide and superoxide out, and so many mutation events in DNA, oxidized proteins, and rancid fats. Inside you there are populations of cells that can tolerate only a finite amount of oxidation events, namely heart muscle fiber nuclei, neurons, and long-term stem cells like marrow and fibroblast stem cells. For these tissues, the DNA you have is the DNA you get, and you can only expose it to so much chemical damage before it stops functioning. Similarly the accumulation of other byproducts would be fatal.

While there is some slight debate about this, the balance of evidence is that CR slows down the metabolism of most tissues relative to their quantity (74,75), so it should definitely allow you to stretch your “mutation budget” over a longer timeframe. This theory predicts that you can extend your remaining life by X% by cutting X% of calories out of your daily food intake. Napkin math tells us that this basically tracks with the results we saw above, and the limitation on this is obviously starving to death.

Hopefully at this point we have exhaustively convinced you that Calorie Restriction definitely works in small animals, probably due to inhibiting oxidant production, and it might work in humans, though the theoretical backing for this is dicier.

So we return to our claims. Should you eat an ndCR diet?

First we have to take care of Chesterton’s Fence.

Population Aging Studies and Human Trials

Why is it commonly recommended to consume ~2000 calories per day? And where does this number come from anyway?

Dietary guidelines approach the question of how much food you can eat epidemiologically, by asking what kinds of mortalities are associated with various food intakes.

A meta-analysis of large-scale population studies concludes that a BMI of roughly 24, considered to be “normal” weight, is associated with the minimum long-term all-cause mortality. (5) (4), and once BMI exceeds 30, all-cause mortality begins to sharply increase. (5) (4) A CDC estimate for the 2015-2016 period found that 39.8% of adults were obese, and it is not unreasonable to assume that the average American BMI is roughly 30 based on huge body of evidence. The interesting aspect of these studies lies in the fact that BMIs below 25 are likewise associated with increased mortality (5)(4). Direct observational data of western populations is nearly unanimous in showing that BMIs below 25 are correlated with bad health outcomes.

So here we meet the fundamental paradox: Why is it that we can observe lab animals living longer in the face of CR, but when we observe humans, we generally find an association between mortality and low body weight?

Epidemiologic studies on low BMIs in western populations become a little hazier. There is fairly wide agreement that BMIs below 25 correlate with lower survival, but not usually a clear claim as to why. BMIs below 25 generally appear to correlate with smoking. Excluding the effects of smoking, people with BMIs below 25 still appear to have increased all-cause mortality. This could be from correlations to weight loss from cancer and metabolic diseases, tuberculosis, or something similar. While the effects of obesity on risk of mortality are very clear, the effects of being underweight and starvation on health are obviously the source of our core paradox (4).

Even studies that attempt to exclude acute illnesses that commonly induce weightloss seem to find higher rates of death among men that are underweight across a wide range of causes. Most troubling is the fact that an under-consumption of calories has a documented effect of suppressing wound healing and immune response, and worsening the progression of infectious diseases (67-69). From this standpoint, it’s altogether unclear whether the low weights observed in these studies are induced by the diseases in question, or whether diseases are simply more prevalent in people with BMIs below 25.

Calvin’s hypothesis, though unsupported by evidence, is that no one is actually on a CR diet.
A CR diet is reduced calorie intake without malnutrition. Some of the people with BMIs below 25 may have an underlying health issue, such as HIV, which is causing their BMI to drop or mortality to rise, but I speculate that most people with a BMI below 25 are suffering from malnutrition, which is causing the increased mortality observed in persons with BMI below 24-25. Sarcopenia in the elderly is another possibility, though age-adjusted studies appear to refute this hypothesis (4).

We can attempt to look at other cultures to see if lower caloric consumption has similar effects there.

Gerontologists and anthropologists have observed that the longest-lived national and ethnic groupings of humans tend to eat the least. Japan has long had the highest life expectancy of any developed country (20). Japanese life expectancy at birth stood at 87.17 years in 2016, as compared to 81.40 years for the United States and 84.43 being the average of 18 high-income countries (20). Japanese are estimated to eat 23% less than Americans (21).

However, this finding is purely correlational in nature. Although reverse causation – that people eat less because they live longer – can be ruled out, the correlation could be coincidental, pleiotropic, or for genetic rather than dietary reasons. The FOXO3A gene, rather than CR, has been proposed as the reason for variations in longevity between ethnic populations (17). Several other genes, like APOE and CETP, have been suggested as alternative genetic causes of these ethnic longevity differences (18). Gerontologists have aggressively suggested that smaller humans tend to live longer (4) (13) (14), and that members of ethnic or national groups, such as the Japanese, who live longer tend to be physically smaller, and centenarians within this ethnic group tend to be smaller than those who live shorter lives (13). One proposed reason that smaller individuals and ethnic populations tend to live longer is lower levels of GH and IGF-1 due to genetic factors (15). As has been discussed, IGF-1 is associated with increased mortality due to various illnesses and also makes the individual physically larger. CR advocates have equally argued that social, environmental, and economic factors causing CR in these population groups cause the drop in GH and IGF-1, increasing longevity in these groups. A Washington University study of the effects of CR on a group of humans on a long-term diet of 1800 kcal per day versus an experimental group ingesting 2500 kcal per day found no decrease in serum IGF levels from baseline unless protein intake was also restricted (16). This result is at odds with rodent studies, which showed decreases in IGF-1 concentrations in CR subjects versus those on normative diets (16). Other results contradict these findings. A Tufts 30% CR trial among mildly overweight (BMI 25-29.9) young adults showed significant decreases in serum insulin concentrations, contradicting the Washington University results (25). Many, many other human trials have produced contradictory results in CR trials, with the severity of the CR, weight, and age of the patients, as well as compliance with CR, having been variously proposed as explanations (21).

There is also compelling evidence in favor of CR and dietary explanations as the cause of longevity in particular populations. For example, the ethnically distinct Okinawans were for generations the Japanese ethnic group with the greatest longevity; the island has 4-5 times the centenarians per capita of any industrialized country (21). Little racial admixture has occurred on Okinawa, but as the Okinawan diet has westernized, the Okinawans have lost their longevity advantage, with Okinawan longevity dropping below the rest of Japan in 2005 (19). Older Okinawans, who continue to eat CR and protein-restricted traditional diets, have greater longevity compared to Japanese populations of equal age. For Okinawans age 60-64, all-cause mortality was half that of Japanese persons of equal age (22). Evidence from natural “experiments” during mandatory rationing and food shortages also supports the CR hypothesis. Involuntary food rationing during the World Wars also paradoxically increased lifespan. WWI-era rationing in Denmark resulting in a 34% drop in mortality over a two year period (21)(23). Similar rationing in Oslo during WWII, thought to be equivalent to 20% CR, resulted in a 30% drop in mortality (24).

The longest lived humans tend to eat the least. Though causation – whether CR causes decreased IGF levels or decreased IGF levels cause CR – cannot be definitively established, the conclusion, supported by rodent studies and defensible from surveys of humans, that CR causes a drop in IGF levels remains compelling.

So, should you, mean American Reader with 1.5 X chromosomes, adopt a CR diet? WHAT COULD GO WRONG?

Acute Risk Factors of Caloric Restriction

A good first place to look is the Minnesota Starvation Experiment. Conducted around 1944 on 32 volunteer males, the object of the experiment was to subject humans to a 25% calorie-restricted diet that simulates 6 months of famine and observe the effects. Diet was strictly controlled by housing subjects in a special dormitory and supervising them during their time outside of it. Despite the simulated famine conditions, diets were formulated to ensure that subjects received daily minimum intakes of important vitamins and minerals

An exhaustive description of the effects can be found in The Biology of Human Starvation, by Keys, but let’s go through the highlights. (70, not available online but try to find it at a library. Equal parts fascinatingly and grim, but occasionally also very funny)

First the physical: subjects of the experiment underwent a substantial drop in bodyweight (duh) over the first few weeks, after which their weight stabilized at 75% of their original bodyweight, as was the design of the experiment. In terms of physical strength and work capacity, subjects experienced loss of motor coordination, loss of strength, and a devastating negative impact on their endurance. Counts of all blood cells were down across the board per unit volume of blood, and in absolute terms. Subjects had a lowered basal metabolic rate, and an observed drop in surface but not core body temperature. Severe caloric restriction (15%+) also leads to a sharp fall in fertility for both men and women. Women undergoing caloric restriction may stop menstruating. (not observed in the Minnesota study, which was all-male) Finally, a starvation state can lead to bradycardia, starvation edema, fainting, and looking like a cartoon skeleton (70)(77).

Psychologically, the first and most significant observed effect was a severe preoccupation with food, and a permanent feeling of being cold. The latter was both a true sensory perception (skin temperatures of subjects were lower than normal) and a subjective sensation. Additionally, subjects experienced a loss of sexual interest. The subjects were capable of achieving erections physiologically, but not psychologically. Subjects also felt a loss of motivation to engage in self-improvement or social activities. By month 6 of semi-starvation, more than half of all subjects were routinely failing to complete basic maintenance tasks such as cleaning, and most had dropped out of university classes they were initially attending. After subjects were released from the experiment, several developed eating disorders, and fasting in general can induce eating disorders where none were otherwise present, both binging and anorexia.

Advocates of intermittent fasting, which is a diet that is much easier to maintain, often say that you eventually adapt to the feeling of acute, distracting hunger that strikes you when you are on a short (eg 1 or 2 day) fast (Original research). No such adaptation was observed for the subjects of the Minnesota experiment, and if anything morale of the subjects deteriorated steadily throughout all 6 months of the experiment. In principle, we need not assume that you cannot psychologically adapt to permanent starvation conditions, however mice that undergo lifetime caloric restriction do show a permanently depressed level of motility, eg they just hate moving around.

Evidence from other sources also indicates that lowered caloric intake leads to worsened progression of infectious diseases and slowed wound healing. This point may initially appear controversial because some studies indicate faster and greater response to mitogens, but studies using live pathogens prove this point fairly conclusively. Crucially, this aspect of starvation biology is one that would not be revealed in CR Mouse studies. Lab mice are generally kept in aluminum shoeboxes in a strictly sterile environment most of their lives. They have little opportunity to suffer injuries or heal from the same, and rarely experience infections. If they do, they are quite likely to die and be excluded from analysis. Unless you happen to live in a sterile aluminum shoebox as well, consider this as you interpret CR studies (67-69).

How does this square with the smaller diets in East Asia? Okinawans reportedly ate a diet that was at a similar level of caloric restriction (20% relative to western ND) to the Minnesota experiment, however obviously the entire island wasn’t driven sterile or languid. Note however, that this difference is reported only in absolute terms, not as calories per unit of body weight. Factor 1 is probably stature. Long-term caloric shortages have been shown in both mice and humans to lead to shorter stature and smaller size. If you were reared from youth to eat a relatively smaller diet, your long-term caloric requirements could probably be lowered somewhat. This is borne out in the average heights and weights of Okinawans of this time period, often reported to be less than 5 feet tall. This also squares with studies on longevity between different mouse strains, which routinely report that smaller overall stature (or length) has a positive correlation to longevity.

Factor 2 may be local weather conditions (Okinawa is sub-tropical) Temperatures have an impact on the ability to tolerate a restricted diet long-term. One notable result observed in investigations of Okinawans is the higher thermogenesis and lower oxygen consumption in Japanese and Okinawan mitochondrial haplogroups, suggesting both lower generation of ROS, and likely an ability to tolerate lower caloric consumption while maintaining adequate body temperature (76), which is an important aspect of determining basal metabolic rate. The BMR of Japanese people and Okinawans can be considered as lower or higher depending on whether it is measured through thermogenesis or oxygen consumption, which measure subtly different things.

This discrepancy suggests to us that even in the event that you are able to maintain a traditional Okinawan diet, if you were reared in America, it’s quite possible that you would have the ol’ Minnesota Boner Downer experience attempting to do so.

The outcomes of a lesser caloric restriction would be easier to tolerate for the average westerner, but will also be less effective. Whether there exists a sweet spot in which you are calorically restricted, but don’t hate life and can lift a broom is probably a subjective judgement.

Overall Conclusions

None of the evidence in favor of CR is indisputable. CR-ROS, the hypothesis that calorie restriction reduces oxidative radicals, remains compelling, but direct evidence in humans is lacking. Numerous model animal studies have shown a link between CR, reduced mortality, and life extension. Population studies support the CR hypothesis, but the effects of CR cannot be easily disentangled from genetic, social, environmental, or non-CR dietary factors. CR experiments in humans and rhesus monkeys produced contradictory results, and in some cases the tradeoffs between early and late mortality are a judgment call. Progerias in the obese and biomolecular evidence of cellular and tissue-level anti-aging effects of CR remain the strongest evidence for CR’s potential to extend human life.

We, the authors, conclude that the evidence as it stands weakly supports the conclusion that CR modestly extends human life. We expect that an individual engaging in 20-30% CR versus a normative, non-obesogenic diet without malnutrition might enjoy a 10%-20% increase in longevity. A 10%-15% CR relative to a normative diet may increase lifespan by perhaps 5-10%.

As with all good science, this conclusion raises still more questions. 20-30% CR might result in a 10% increase in longevity, but is that worth it? Calvin, one of the authors, is a practicing intermittent faster and can testify that CR and IF are unpleasant, difficult, and sometimes painful.

Scientific investigation adds another layer to this subjective answer: starvation conditions are likely to expose you to infections of greater severity, potential sterility, negative impacts on your physical abilities, and subjective but significant impacts on your psychological state, including motivation, attention, and libido.

The field of gerontology and the general study of aging continues to lurch forward – not at the pace we want it to, necessarily, but it’s still developing anyway. New drugs and treatments, including stem cell activators like GDF11, senolytic drugs, and anti-inflammatory interventions may be able to make many of the benefits of CR redundant in the relatively near future (we hope).

While CR would probably extend your life, we, the authors, don’t advocate it. The risks and miseries aren’t trivial and you probably have to go to work in order to exchange money for goods and services.

Claim 2: You, the reader, should adopt a Normative Diet
True (and basically the same as an adCR diet)
Claim 3: You, the reader, should adopt an nd-CR diet
Debatable, but no.

If you are interested in the best current options for life extension, you should consider a long-term aspirin regimen, maintaining a healthy body weight, and building a nuclear bunker in your backyard.

All the best,
–Calvin Reese, Adrian Liberman

PS(A): PLEASE NOTE: If you are over 75 years old, do not attempt Calorie Restriction. If your grandma is over 75 years old, go to her house and pour soup into her until she is overweight. This is not a joke and is entirely serious advice. Among the very elderly, being overweight serves as a protective factor that mitigates the dangers of death due to traumatic injury. The dangers of heart attacks and diabetes associated with excess weight are less than the dangers associated with sarcopenia and cachexia. Elderly people usually experience a loss of strength in esophageal muscles and for them swallowing food becomes more difficult, leading to a vicious cycle of muscle weakness and weight loss. If you have an elderly relative, please make sure they’re eating enough.

PPS: Studies excluded from this review: CALERIE: conformity to study protocol was terrible, duration too short, and they took overweight people and got them to baseline. Total tripe on a bike. CRONies: lmfao. Be skeptical of studies claiming to observe DR in a human population. Talking a large group of people into actually following a strict DR regimen long-term is borderline impossible because it fucking sucks. Sample was also self-selected.

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Getty

• The official exit poll points to a huge majority for Boris Johnson's Conservative Party
• Johnson is on course to win the party's biggest parliamentary majority for decades with the opposition Labour party on course for its worst result in a century.
• The result, if borne out, will give Johnson the freedom to radically change Britain's future outside the EU.
• It kills off any prospect of Britain's exit from the EU being prevented.
• Visit Business Insider's homepage for more stories.

The official exit poll published on Thursday evening suggests that Boris Johnson is on course for the largest Conservative majority for decades, with the opposition Labour party set for their worst result in a century.

If borne out in the official results, it will mean the UK is on course to leave the EU by the end of January 2020 with all hopes of a second referendum on Brexit now dead and gone.See the rest of the story at Business Insider

NOW WATCH: Most maps of Louisiana aren't entirely right. Here's what the state really looks like.

See Also:

• Holiday music is bad for your mental health, according to science — here's why
• Retiring early doesn't mean you'll stop making money — here's how one retired millennial made more than $60,000 in passive income in one year
• Boris Johnson had a disastrous day on the campaign trail which supporters fear could cost him the election

A new article in Science, "Evidence, alarm, and the debate over e-cigarettes," warns that, when it comes to vaping, "prohibitionist measures threaten public health." This may not be news to those that have followed the burgeoning medical and social science literature on e-cigarettes and vaping, but it is quite notable to see this message in a journal as prestigious as Science.

Written by researchers from the schools of public health at Ohio State, Emory, New York University and Columbia, the article explains the importance adopting prudent harm reduction strategies to address the health consequences of tobacco use and the risks of adopting unnecessarily prohibitionist or restrictive policies.

The article begins:

This is a moment for legitimate alarm at the intersection of two distressing but distinct epidemiological patterns involving e-cigarettes ("vaping"): an increase in vaping among youth and a sudden outbreak of acute lung injuries and deaths in the United States, associated most strongly with vaping tetrahydrocannabinol (THC), the main psychoactive compound in cannabis. Discussions of vaping, however, often neglect distinctions between nicotine and THC; between adults and youth; and between products obtained through the retail and black markets. As we move to confront these challenges, we face the danger that justifiable alarm will turn alarmist, short-circuiting careful analysis of the full range of evidence and focusing attention on the most frightening, thus enhancing the prospect of adopting counterproductive policy. We suggest that the evidence warns against prohibitionist measures. Restricting access and appeal among less harmful vaping products out of an abundance of caution while leaving deadly combustible products on the market does not protect public health. It threatens to derail a trend that could hasten the demise of cigarettes, poised to take a billion lives this century.

Surveying the relevant literature, the article notes that there is widespread support for the proposition that "vaping nicotine is much safer than smoking" and that "Careful analysis of all the data in context indicates that the net benefits of vaped nicotine products outweigh the feared harms to youth." Among other things, the authors note, is that e-cigarettes have been shown to be "more effective than medicinal NRTs [nicotine replacement therapies] at helping smokers quite" and that the availability of flavors often play a key role in helping smokers quit.

They write:

The most conservative estimates suggest that were vaping nicotine to replace most smoking over the next 10 years, 1.6 million premature deaths would be avoided and 20.8 million quality adjusted years of life would be saved in the United States alone. The greatest gains would be among younger cohorts.

Despite the growing body of research supporting the role of e-cigarettes as part of a broader tobacco harm reduction strategy, regulatory measures threatening to squelch the e-cigarette market and curtail the usefulness of vaping as a smoking cessation tool proliferate at all levels of government. Perhaps this article will help turn the tide and lead to more effective—and more life-saving—approach to tobacco.

NASA

• The Geminids meteor shower, a trail of asteroid dust that Earth passes through each December, peaks on Friday.
• NASA's record-breaking Parker Solar Probe spotted the dust trail from space for the first time ever.
• As it circles the sun 21 more times, the probe will help scientists study the unknown structure of the Geminids trail.
• Visit Business Insider's homepage for more stories.

The Geminids meteor shower peaks on Friday night, and for the first time ever, a spacecraft has spotted the asteroid dust that makes those shooting stars.

Since NASA's Parker Solar Probe launched in August 2018, it has rocketed around the sun three times, getting closer than any spacecraft before it and traveling faster than any other human-made object in history. Scientists released findings from the probe's first batch of data this month, which revealed never-before-seen activity in the plasma and energy at the edges of the sun's atmosphere.See the rest of the story at Business Insider

NOW WATCH: Here's what you're actually seeing when you spot a meteor shower

See Also:

• Holiday music is bad for your mental health, according to science — here's why
• NASA has pinpointed an area where astronauts could land on Mars. Ice is so accessible there that they could dig it up with a shovel.
• Retiring early doesn't mean you'll stop making money — here's how one retired millennial made more than $60,000 in passive income in one year

SEE ALSO: Astronauts on the space station see vibrant desert patterns, roiling storms, and volcanic eruptions. These are the best photos ever taken from the ISS.

His time as a consultant is haunting him now.

The post How to Buy Contact Lenses in Lithuania appeared first on Marginal REVOLUTION.

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The post China fact(s) of the day appeared first on Marginal REVOLUTION.

Sen. Kamala Harris speaks during a rally launching her presidential campaign on January 27, 2019, in Oakland, California.  | Noah Berger/AFP/Getty Images

The California senator cited fundraising troubles as a central reason for her decision.

Sen. Kamala Harris, following a sharp decline in recent polls, is dropping out of the 2020 race.

Harris, once seen as one of the most promising presidential candidates in the Democratic field, struggled to identify a distinct message, and had trouble connecting with voters as a result. She announced her decision via a Medium post on Tuesday, after telling staff earlier in the day.

“I’ve taken stock and looked at this from every angle, and over the last few days have come to one of the hardest decisions of my life,” Harris wrote. “My campaign for president simply doesn’t have the financial resources we need to continue. ... In good faith, I can’t tell you, my supporters and volunteers, that I have a path forward if I don’t believe I do.”

Harris had been a rumored presidential contender ever since she was elected to the Senate in 2016, and announced her candidacy to great fanfare during an Oakland rally this past January. She had a history-making record in political office, as the first black woman and the first Asian American woman to be San Francisco district attorney and California attorney general. As part of her campaign, she sought to highlight the contributions of women of color to the Democratic Party and boost other minority candidates, an effort she says she plans to continue focusing on.

“Our campaign uniquely spoke to the experiences of Black women and people of color — and their importance to the success and future of this party,” she wrote. “Our campaign demanded no one should be taken for granted by any political party.”

Harris was strongest on the debate stage when discussing those issues; she enjoyed a surge over the summer after her stunning confrontation of Biden over his previous opposition to federally mandated busing — and her personal connection to the topic — during the June debate.

Her campaign, however, appears not have been prepared to navigate that momentary success, according to a New York Times report. This fall, she fielded criticism about its muddled strategy, abrupt firings of staffers, and unwillingness to fully confront her record as a prosecutor. On top of that, fundraising was proving to be a growing challenge for Harris, who brought in $11.6 million in the third quarter of 2019 compared to $24.6 million raised by Sen. Elizabeth Warren and $19 million raised by South Bend, Indiana, Mayor Pete Buttigieg.

In spite of the latest declines, Harris’s decision to drop out is somewhat surprising since she’s still polling ahead of most of the Democratic field and has qualified for the next debate later this month.

According to the RealClearPolitics polling average, Harris was firmly in the second tier of candidates when she decided to end her campaign. She was polling behind frontrunners including former Vice President Joe Biden but ahead of many others who are still in the race, including Sens. Cory Booker and Amy Klobuchar. Still, her recent numbers, which put her at 3.4 percent on average, pale compared to the 15 percent polling high she once hit.

These declines, it seems, mirrored the disarray within her campaign, which opted to shift an overwhelming swath of resources to Iowa, where Harris was still meeting with voters over Thanksgiving.

Harris’s lack of a specific message was seen as hurting her candidacy

Though Harris had sought to build a broad coalition of voters, something she succeeded at during her Senate run, experts have said her unclear ideological positioning has prevented her from establishing a specific lane of support. Harris, who is viewed as more moderate than multiple leading candidates, has also tried to court progressive voters — with limited success.

One example: She backed Medicare-for-all, but then released a plan that doesn’t go quite as far as that of Sanders or Warren in eliminating private insurance. Additionally, Harris’s prosecutorial record has prompted critiques from liberals who argue that her approach toward issues such as truancy and wrongful convictions aren’t as progressive as she’s tried to frame them.

“She’s in a no person’s land,” San Jose State University political science professor Larry Gerston previously told Vox. “She is to the right of Bernie Sanders and Elizabeth Warren, she’s to the left of Pete Buttigieg.”

Harris’s initial bet on bringing the party together had also yet to come to fruition, in part because of how crowded the field has been — and how her competitors have been able to hang onto their core contingencies of support. Harris had focused significant efforts on winning over more African American voters, especially in the crucial early primary state of South Carolina, but Biden has managed to keep a solid base of voters there.

Harris’s policies, too, were criticized for their lack of a clear focus, though several centered heavily on improving wages and economic mobility for the middle class. Her landmark proposal, the LIFT Act, would give middle-class households a monthly cash payment amounting to as much as $3,000 per year for single people and $6,000 per year for married couples. Other proposals aimed to increase wages for teachers and public defenders.

Harris also made gender equity a key prong of her political platform, pushing proposals that sought to curb restrictive state abortion laws, establish a federal paid family leave program and penalize companies that don’t address internal wage gaps. Harris’s plan to require states that have violated Roe v. Wade to obtain federal approval before adopting new abortion laws has garnered support from several other 2020 candidates.

Harris had a breakout moment in June but lacked consistency

The peak of Harris’s campaign came in mid-June when she took on Biden over the issue of using busing to desegregate schools. During a Democratic debate, she pressed him on his work alongside segregationists and opposition to busing.

The problem was, her subsequent debate performances and policy roll-outs weren’t quite consistent enough to sustain this enthusiasm. As a result, Harris saw her poll numbers continue to slide in the months since, coupled with media reports of internal turmoil on her campaign.

Before her run for the presidency, Harris was well-known for her role on the Senate Judiciary Committee, questioning Trump administration officials including Bill Barr and Supreme Court Justice Brett Kavanaugh. Her Senate term extends through 2022, when she’ll be up for reelection once again in California.

As a Morning Consult poll found, Sen. Elizabeth Warren has the most to gain in support from Harris’s departure. A large proportion of Harris backers have listed Warren as their second choice. Others have favored Biden and Buttigieg, as well.

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This is from the WSJ:

WSJ: Has the Fed done enough work to explain to the public why low inflation is actually a problem? Most people hear “inflation’s low” and they say, “Great. Good job.” They hear you say, “Well, we want it to be a little bit high.” Have people done enough work to explain to people why actually this is a problem?

MR. KAPLAN [Dallas Fed President]: Well, the answer is I don’t think it is well understood out there. And this is why when I talk about low inflation, I prefer to talk about in the context of nominal GDP. People understand if nominal GDP is too low, why that’s an issue. They understand higher nominal GDP is better. I think I prefer to talk about lagging inflation in the context of nominal GDP. It is what pays the debt service on the U.S. debt. And we want to grow nominal GDP even though we, the published GDP numbers are [adjusted for inflation]. Nominal GDP is ultimately where it gives you the cash flow to service your debt and to spend on other priorities of the country. And so talking about low inflation in isolation, yes, it may be a challenge for us to do more communication to explain why that’s an issue. The way I’ve tried to explain it when I talk to people in my district and throughout the country is in the context of GDP. It’s important to have higher nominal GDP.

HT: Alex Schibuola, David Beckworth

Associated Press

• The FAA plans to keep full control of certifying individual new Boeing 737 Max planes as they roll off the production line, the regulator said Tuesday.
• Normally, once the plane type is certified by the regulator, the plane maker is responsible for ensuring that individual units conform to regulatory requirements. Airlines also typically conduct inspections when taking delivery of new planes.
• Boeing's plan to begin delivering new planes to airline customers in December, before the plane was certified to fly passengers again, was cast into serious doubt.
• Sign up for Business Insider's transportation newsletter, Shifting Gears, to get more stories like this in your inbox.
• Visit Business Insider's homepage for more stories.

The FAA said on Tuesday that it planned to exercise full control over all aspects of certification of Boeing's 737 Max, even once the plane returns to commercial service.

Relatively routine activities, such as certifying individual airplanes as they roll off the production line — as opposed to certifying the overall type of plane — will be performed by FAA officials, an agency spokesperson told Business Insider.See the rest of the story at Business Insider

NOW WATCH: WeWork went from a $47 billion valuation to a failed IPO. Here's how the company makes money.

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SEE ALSO: Boeing 737 Max: Here's the complete history of the plane that's been grounded since 2 crashes killed 346 people 5 months apart.

Over at Econlog, I have a post discussing China’s recent decision to beef up the enforcement of intellectual property rights.  Check it out.

In other news, China is about to roll out a major land reform:

“This is the first time I’ve owned an industrial property,” said Mr Shi, 48, who had rented in seven locations before settling down in Dongheng. “I don’t have to worry about getting kicked out by landlords any more.”

Mr Shi’s good fortune is the result of an experiment in land reform that has been rolled out in 33 counties across China. It allows semi-autonomous collectives to sell certain types of rural land to third parties and to keep the bulk of the proceeds.

The model, which will be extended to the rest of the country at the beginning of next year, has been lauded as a means of bringing prosperity to rural businesses and communities and stimulating China’s flagging economy.

The article also points to some downsides with the plan, and I don’t know enough to comment on the specifics.  In the past, however, real estate reform has been a big deal in China.  In the late 1970s, they began giving farmers more property rights, and a couple decades later they allowed urban residents to own their own home.  Both changes had a massive (positive) impact on the Chinese economy.

China is loosening rules on foreign investment:

BASF has broken ground on a $10bn petrochemical complex in southern China, becoming the latest foreign company to increase its presence in the country as Beijing gradually relaxes restrictions on overseas investment. . . .

Beijing loosened restrictions that excluded foreign companies from investing or taking ownership stakes in industrial and financial sectors after the pace of growth of foreign direct investment into China slowed to just 3 per cent last year. 

Foreign companies have long been excluded from several high-growth sectors or forced to form joint ventures with Chinese companies. US and European chambers of commerce have called on Beijing to accelerate access for foreign investment. 

The BASF facility, in the city of Zhanjiang, is the first of its kind in China that will be fully owned by the company after Beijing allowed full foreign ownership of chemical “cracking” facilities used to produce plastics. 

Global stocks are up today, partly due to expectations of a phase one trade deal with China.  Another factor was the Hong Kong elections:

The Stoxx Europe 600 Index advanced, with all 19 industry sectors in the green. Equities climbed across Asia, led by those in Hong Kong, where local elections brought a landslide victory to pro-democracy candidates. 

It seems like the markets hope that this leads to fewer protests:

A record turnout helped pro-democracy parties win a majority in 17 of 18 district councils. [Stock market] Bulls hope the poll result will inspire disaffected Hong Kongers to focus on conventional politics rather than street protests.

In my view, Hong Kongers would be wise to continue the street protests, but in a non-violent fashion. Unfortunately, the recent escalation of violence plays right into Beijing’s hands. The Chinese government would prefer not to intervene in Hong Kong, and strangely enough the violence might actual make them less likely to do so.

Some people predicted blood in the streets, similar to Tiananmen Square in 1989. That may still happen, but Beijing may also be content for there to be blood in the streets from clashes between protesters and police. Recall that China doesn’t want to give democratic rights to Hong Kong because they fear it would cause urban Chinese on the mainland to demand similar rights. As long as there is “blood in the streets”, then mainland Chinese will not be attracted to the Hong Kong model.

A better option would be to adopt a two track strategy. Continue the street protests and have their newly elected officials (who admittedly have little power) do as much as they can to improve the economic situation in Hong Kong, especially housing. That should be combined with non-violent street protests to keep the pressure on.

I strongly recommend this Bloomberg article, which points out that violent protests can lead to a counterproductive rise in nationalism:

I, for one, do not mind the fact that my hometown Shanghai has doubled in size, or that my local dialect is no longer the only one heard on the streets. In exchange, I’m exposed to more diverse cuisines when I visit and meet more interesting people. And thanks to the wonderful, hard-working “little brothers” — almost always migrants — I can get bubble tea delivered to my doorstep within half an hour. 

In that sense, the most cosmopolitan Chinese cities now resemble New York. It doesn’t matter where you’re from; as long as you live there, you can call yourself a New Yorker. Hong Kong, on the other hand, has grown bitterly divided into tribal camps — locals, expats, mainlanders and domestic helpers. . . .

If the central government had qualms about taking a hard line against the protesters before, it surely doesn’t now that they enjoy negligible support from mainland Chinese. An even simpler strategy would be to let Hong Kong decline slowly. Neighboring Shenzhen, home to local champions such as Huawei Technologies Co Ltd. and Tencent Holdings Ltd., is already keen to steal away high-tech firms. Corporate tax rates at the Qianhai free trade zone, for instance, are lower than Hong Kong’s.

And this is not just a question of money. I am not the only liberal mainlander living in Hong Kong. We naturally root for the city’s democratic advances. After all, why did we leave China in the first place? Why shouldn’t Hong Kong, one of the world’s wealthiest and most global metropolises, be governed by its people?

Yet, our support for the protests is rapidly dwindling because we suspect that the anger on the streets has less and less to do with the city’s political system, and more to do with a nativist dislike of mainlanders and immigrants — not unlike the anger driving populist protests in the U.S. and Europe.

Of course, mainland China is to blame for Hong Kong’s divisions, but nonetheless the local Hong Kongers should avoid playing into China’s hand. Beijing wants it to look like self government in Hong Kong has failed.

Actually, it’s never been tried.

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When video game developer Valve first released Half-Life in 1998, there weren’t many games like it. First-person shooters were cheap, one-dimensional, frequently racist affairs. Half Life, with its immersive environment, dark humor, and Gordon Freeman, a mute MIT theoretical physicist as its protagonist, laid the groundwork for a more ambitious era of modern video games. A generation of fans have been waiting for a follow-up to 2004’s Half-Life 2—which has seen no updates since 2007—and Valve today (Nov. 21) finally delivered. Well, sort of. The company unveiled its first full-length virtual reality game, Half-Life: Alyx.

Half Life: Alyx is not quite a sequel or a prequel. It’s set between the events of Half-Life and 2004’s Half-Life 2. It features resistance fighter Alyx Vance as the protagonist, a character we were introduced to during Half-Life 2. As the child of a scientist, Vance grew up in the confines of the Black Mesa Research Facility (which serves as the main setting for the franchise) and grew up to become one of Freeman’s closest allies in Half-Life 2. Alyx follows Vance and her father, Eli, as they build an early resistance to The Combine, an alien species that took over Earth in the first game. It also features the return of the G-Man, the mysterious bureaucrat in a suit and tie who both helps and harms our main characters. According to the developer, the game will also feature “world exploration, puzzle solving, visceral combat, and an intricately woven story that connects it all with the characters iconic to the Half-Life universe.” Valve will release Alyx in March 2020, but it’s available for pre-order today.

Valve (which owns Steam, the world’s most popular PC gaming platform), has chosen to release the game on a variety of different VR devices instead of exclusively on its own headset. The company this spring debuted a $499 VR headset, the Valve Index, officially entering the VR space currently occupied by HTC Vive, Facebook’s Oculus Rift, and Windows Mixed Reality devices). Although VR gaming is still very much in its infancy, the hope with the Index is that the device will introduce VR to a wider audience, given the premium price of most high-end VR headsets make them out-of-reach for all but the most hardcore PC gamers.

But there’s an incentive for those who already own the company’s own VR hardware. Valve is making Half-Life Alyx free for current and future owners of the Valve Index headset. (Alyx will also be available on any VR device that can connect to Steam.) Since the video game developer is expected to release another two Half-Life games exclusively for VR, this could be a good reason for devotees of the franchise to splurge.

Sometimes you're better off just keeping your mouth shut, and especially if you're a British royal who kept hanging out with a serial pedophile and sex trafficker after his conviction. Prince Andrew tried defusing the situation that had long blown up in his face, and not only did his idea]]

South Dakota has employed a very unique advertising strategy to combat meth use in the state. The slogan for the state's new anti-drug campaign is "Meth. We're on it." 

In announcing the campaign, Gov. Kristi Noem (R) wrote that last year, 13 South Dakotans lost their lives because of methamphetamines and 3,366 were arrested on related offenses. To curb usage, Noem announced on Monday the state's "largest and most aggressive" campaign yet. 

As with many aspects of our seemingly endless drug war, South Dakota's campaign has good intentions. But it's not the intention that has people talking.

"Meth. We're on it," reads the campaign's logo in big, bold lettering that are plastered over an outline of the state. If that wasn't enough to grab attention, the campaign and its logo can be viewed at the website onmeth.com.

A company called Broadhead LLC received $448,914 to design the campaign. The state is now running ads and posters featuring a diverse group of South Dakotans saying, "I'm on meth."

Whether the state succeeds in reducing meth use and helping people who want to quit do so, they've already succeeded in "raising awareness."

South Dakota has launched a campaign to combat meth.

With this new logo.https://t.co/u5l7HF7mK9 pic.twitter.com/OvRjkCqlHl

— Mike Baker (@ByMikeBaker) November 18, 2019

South Dakota taxpayers paid $450k for a new anti-meth PSA campaign. And here's what the state came up with https://t.co/1MATJPBULv pic.twitter.com/bsZKkXCPNL

— Lachlan Markay (@lachlan) November 18, 2019

Is South Dakota trying to advertise meth? pic.twitter.com/KOTESkbaip

— Ian Miles Cheong (@stillgray) November 18, 2019

Phrasing.https://t.co/VIgjjJxVA5

— Ben Collins (@oneunderscore__) November 18, 2019

The new slogan is even trademarked to thwart any copycats.

I love that they trademarked it. Don't worry, South Dakota, no one's going to take your slogan. https://t.co/XPxUJuyIAC

— Robert Maguire (@RobertMaguire_) November 18, 2019

According to Facebook, this campaign is a refresh of the state's "Meth Changes Everything" marketing strategy. 

The new campaign directs people to a tipline where residents can report suspected drug activity to the state attorney general. It also includes classroom resources reminiscent of a certain other anti-drug campaign aimed at young people. 

But lest this seem only like a hilarious way to lock more people up, the campaign also includes funding for substance abuse treatment facilities and a confidential locator for connecting with those facilities. South Dakotans can also receive financial assistance for treatment. 

Reason has reached out to the South Dakota Department of Social Services for comment on the campaign, the treatment facilities, and literally anything about this campaign other than the insane slogan that is currently breaking the internet. The story will be updated with comment.

UPDATE: A representative from Broadhead responded to Reason's request for comment. According to the company, "The campaign was selected through a Request for Proposal process. A team of representatives from various state agencies as well as representatives from the Governor's Office participated in the selection process."