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Zephyr López Cervilla
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Unregistered with Thaddeus Russell
I listened to the first episode of Thaddeus Russell's podcast ("Unregistered with Thaddeus Russell") this morning. Very edifying and enlightening. He's been guest of "The Tom Woods Show" twice (ep. 895 and 321), and guest of "The Joe Rogan Experience" thrice (ep. 952, 740 and 553).

"Unregistered with Thaddeus Russell" Podcast homepage:

Guest appearances:

The Tom Woods Show
Ep. 896
Ep. 321

The Joe Rogan Experience
Ep. 952 [Live]
Ep. 952
Ep. 740
Ep. 553

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• Jeff John Roberts. "Democrats Are 3 Times More Likely to Unfriend You on Social Media, Survey Says." Fortune (December 19, 2016)

On Google+, liberals, predominantly women, will block you instead if you make a political comment with which they don't agree, even if you aren't a conservative.

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Brain Energy Metabolism: Focus on Astrocyte-Neuron Metabolic Cooperation

« Introduction

Glucose is the obligatory energy substrate of the adult brain. Nevertheless, under particular circumstances the brain has the capacity to use other blood-derived energy substrates, such as ketone bodies during development and starvation (Nehlig, 2004, Magistretti, 2008) or lactate during periods of intense physical activity (van Hall et al., 2009). Glucose enters cells trough specific glucose transporters (GLUTs) and is phosphorylated by hexokinase (HK) to produce glucose-6-phosphate. As in other organs, glucose 6-phosphate can be processed via different metabolic pathways (Figure 1A ), the main ones being (1) glycolysis (leading to lactate production or mitochondrial metabolism), (2) the pentose phosphate pathway (PPP), and (3) glycogenesis (in astrocytes only, see below). Overall, glucose is almost entirely oxidized to CO2 and water in the brain (Clarke and Sokoloff, 1999). Nevertheless, as evidenced by the different metabolic routes that glucose can follow, each individual brain cell does not necessarily metabolize glucose to CO2 and water. Indeed, a wide range of metabolic intermediates formed from glucose in the brain can subsequently be oxidized for energy production (e.g., lactate, pyruvate, glutamate, or acetate) (Zielke et al., 2009).
Since neurons account for most of the energy consumption during brain activation, it was first rationally assumed that CMRglc measurements from 18F-fluoro-2-deoxyglucose (FDG)–PET signals directly reflected the neuronal use of glucose (Sokoloff et al., 1977). In addition, neurometabolism was postulated to be a strictly oxidative (i.e., oxygen-depending) process—an assumption based on the higher efficiency to produce ATP from glucose oxidation in the mitochondria (oxidative process) compared to glycolysis (nonoxidative process; i.e., lactate producing) (Figure 1A).

In the mid-1980s, an important series of PET studies conducted by Fox and Raichle challenged this assumption, and led to a major breakthrough in our understanding of the mechanisms underlying task-induced increases in glucose metabolism. In awake adult humans, they observed that the activity-dependent (visual or somatosensory) increases in blood flow and glucose utilization were only marginally matched by parallel increases in oxygen consumption (Fox and Raichle, 1986, Fox et al., 1988) (Figure 1B). Such uncoupling between CBF and CMRO2 created the rationale for developing blood oxygenation level-dependent (BOLD) fMRI contrast (Ogawa et al., 1992, Magistretti and Pellerin, 1996, Raichle and Mintun, 2006). These fundamental observations also brought support to the notion that the metabolic needs of active neural tissue are met, at least partially, by nonoxidative glucose metabolism (i.e., glycolysis). This hypothesis was then further supported by various 1H nuclear magnetic resonance studies showing activity-dependent increases in lactate levels in different brain areas (Figley and Stroman, 2011, and references therein), giving empirical demonstration that glycolytic metabolism increases with corresponding elevations in brain activity. It is now generally accepted that following transient changes in neural activity, (1) blood delivery increases with metabolic demand, (2) CBF and CMRglc increase more than oxygen utilization, and (3) both oxidative and nonoxidative processes are involved to meet the increased metabolic requirements (Figley and Stroman, 2011).

These observations raised fundamental questions as to the molecular and cellular mechanisms that could reconcile the coexistence of increases in oxidative and nonoxidative glucose metabolism during synaptic activity. Specifically, the open questions were as follows: are the changes of glucose metabolism (oxidative versus glycolytic) taking place in different cell compartments; and to which precise cellular processes are they linked? The evidence pointing at a major contribution of astrocytes to neuroenergetics (Magistretti et al., 1981, Pellerin and Magistretti, 1994) has provided a key to the understanding of these questions.
Metabolic Specialization of Neurons and Glia

While the brain is a high energy-consuming organ, it contains little energy reserves and is therefore highly dependent upon the uninterrupted supply of energy substrates from the circulation. Impairment in this process results in perturbation of neurological functions, loss of consciousness, and coma within minutes. As already mentioned, brain cells can efficiently utilize various energy substrates in addition to glucose, including lactate, pyruvate, glutamate, and glutamine (Zielke et al., 2009). Most of these metabolites are formed endogenously using glucose as the source of carbon, and—because cerebral metabolism is a compartmentalized process—complex intercellular trafficking of these metabolites occurs within the brain.

Among these substrates, lactate has been the center of much attention in recent years. Lactate is present in the extracellular space in concentrations similar to those of glucose (between 0.5 and 1.5 mM), and while it has long been considered a metabolic dead end, this view has drastically changed in light of the growing evidence indicating that it represents an important energy source for the brain (Schurr et al., 1999, Gallagher et al., 2009, Smith et al., 2003, Boumezbeur et al., 2010b). Interestingly, emerging evidence suggests that the end product of glycolysis is lactate (rather than pyruvate) (Schurr and Payne, 2007). In line with this, the existence of a putative mitochondrial lactate oxidation complex has been reported in neurons which would allow lactate entry and oxidation in the mitochondria (Hashimoto et al., 2008).

Importantly, both astrocytes and neurons have the capacity to fully oxidize glucose and/or lactate (Zielke et al., 2009), which is in accordance with the observation that both cell type processes contain equivalent numbers of mitochondria (Lovatt et al., 2007). However, as will be described in the following sections, neurons and astrocytes preferentially use different metabolic pathways in physiological conditions, which is in part due to cell type-specific expression patterns of key genes regulating energy metabolism (Lovatt et al., 2007, Herrero-Mendez et al., 2009, Vilchez et al., 2007). As a result, neurons and astrocytes present different (but complementary) metabolic profiles, paving the way for extensive metabolic cooperativity.

Metabolic Profile of Neurons

Neurons Rely on Oxidative Metabolism to Meet Their High Energy Needs
Consistent with their higher energy requirements, neurons sustain a high rate of oxidative metabolism compared to glial cells (Lebon et al., 2002, Itoh et al., 2003, Bouzier-Sore et al., 2006, Boumezbeur et al., 2010a). Interestingly, a large body of evidence shows that neurons can efficiently use lactate as an energy substrate (Schurr et al., 1997, Bouzier et al., 2000, Qu et al., 2000, Serres et al., 2005, Boumezbeur et al., 2010b) and even show a preference for lactate over glucose when both substrates are present (Itoh et al., 2003, Bouzier-Sore et al., 2006).

Recent evidence provides insights into the mechanisms underlying these neuronal features. Indeed, it has been reported that the enzyme 6-phosphofructose-2-kinase/fructose-2,6-bisphosphatase-3 (Pfkfb3) is virtually absent in neurons, due to its constant proteasomal degradation, which is in stark contrast with the high expression levels observed in astrocytes (Almeida et al., 2004, Herrero-Mendez et al., 2009). This enzyme is responsible for the generation of fructose-2,6-bisphosphate (fructose-2,6-P2), a potent activator of the glycolytic enzyme phosphofructokinase-1 (PFK). As a result of a low production of fructose-2,6-P2, neurons display a slower glycolytic rate and, unlike astrocytes, are unable to upregulate this pathway in response to NO-induced cellular stress (Almeida et al., 2004, Herrero-Mendez et al., 2009). Remarkably, the activation of neuronal glycolysis via Pfkfb3 overexpression leads to oxidative stress and apoptosis (Herrero-Mendez et al., 2009), suggesting that neurons cannot afford to sustain a high glycolytic rate. The authors showed that the increase in glucose flux via the glycolytic pathway occurs at the expense of metabolism through the PPP—which is essential for the production of NADPH and therefore for the maintenance of the cellular antioxidant potential (see below). While the exact contribution of the pentose phosphate and glycolytic pathways to neuronal glucose consumption remains to be directly established in normal conditions both in vitro and in vivo, it appears that a fine balance between the glycolytic pathway and the PPP has to be maintained in neurons in order to meet their energy needs while maintaining their antioxidant potential—both aspects being essential for their survival. Consistent with this, the use of lactate as an oxidative substrate may provide a convenient means for neurons to produce high amounts of ATP while circumventing the glycolytic pathway, thereby sparing glucose for the PPP (Bolanos et al., 2010).

Metabolic Profile of Astrocytes

Astrocytes Are Highly Glycolytic
Although astrocytes display lower rates of oxidative metabolism compared to neurons, they avidly take up glucose and characteristically present a high glycolytic rate (Itoh et al., 2003, Herrero-Mendez et al., 2009, Bittner et al., 2010). A large portion of the glucose entering the glycolytic pathway in astrocytes is released as lactate in the extracellular space (Itoh et al., 2003, Bouzier-Sore et al., 2006, Lovatt et al., 2007, Pellerin and Magistretti, 1994, Serres et al., 2005). The glycolytic nature of astrocytes and their preference for the production and release of lactate over the entry of pyruvate in the tricarboxylic acid (TCA) cycle are the result of a specific gene expression profile which involves several enzymes and transporters acting in concert to produce this phenotype.
The Astrocyte-Neuron Lactate Shuttle

Astrocytes are generally considered to account for only 5%–15% of the brain's energy expenditure (Attwell and Laughlin, 2001, Magistretti, 2008). Recent evidence suggesting that the energetic cost of action potentials is lower that previously proposed (Alle et al., 2009) leaves open the possibility that the contribution of astrocytes to the overall brain energetic costs may have been underestimated. Nevertheless, experimental evidence demonstrates that the amount of glucose that astrocytes actually take up is disproportionally high in comparison to their energy requirements. For example, in acute cerebellar slices, the uptake of fluorescent glucose analogs is several-fold higher in Bergmann glia than in Purkinje cells (Barros et al., 2009). In the resting rat brain, other studies have shown that astrocytes are responsible for approximately half of glucose uptake (Nehlig et al., 2004, Chuquet et al., 2010), and that this proportion increases even further upon functional activation (Chuquet et al., 2010).

How can these data be reconciled with the fact that neurons—not astrocytes—have the highest energy needs? The transfer of energy substrates from astrocytes to neurons could provide a simple explanation for this apparent paradox. This is a central point of the astrocyte-neuron lactate shuttle (ANLS) model proposed over a decade ago by Pellerin and Magistretti (Figure 3A) (Pellerin and Magistretti, 1994). The essence of this model is that (1) neuronal activity increases extracellular glutamate (via glutamatergic neurotransmission), which is avidly taken up via a Na+–dependent mechanism by specific glial glutamate transporters; (2) the resulting increase in [Na+]i activates the Na+/K+ ATPase (in particular by mobilizing its alpha2 subunit), thereby increasing ATP consumption (Magistretti and Chatton, 2005), glucose uptake, and glycolysis in astrocytes; (3) this in turn leads to a large increase in the production of lactate which is released in the extracellular space; and (4) lactate can be used as an energy substrate for neurons for oxidative-derived ATP production (for review, see Pellerin et al., 2007, Magistretti, 2009).
Astrocytic Glycogen Metabolism

Despite its relatively low level in the CNS compared to peripheral tissues, glycogen is the largest energy reserve of the brain. It represents an advantageous form of glucose storage, as it can be rapidly metabolized without requirements for ATP, and unlike fatty acids it can yield ATP under anaerobic conditions. Interestingly, at the cellular level, glycogen has been found to be almost exclusively localized in astrocytes in the adult brain (Magistretti et al., 1993, Brown, 2004). […] The restricted cellular localization of glycogen raises an obvious question: why is the main energy reserve of the brain found in astrocytes instead of neurons, which are the most energy-requiring neural cell type? This suggests that glycogen metabolism may involve metabolic interactions between astrocytes and neurons. […] Furthermore, studies showing that increasing astrocytic glycogen stores preserves neuronal function and viability in conditions of limited energy availability, such as hypoglycemia, provided additional evidence for neuron-glia metabolic coupling involving glycogen (Brown and Ransom, 2007, Brown, 2004; and references therein). While glycogen mobilization may also fulfill the astrocytes' own metabolic needs (Sickmann et al., 2009, Walls et al., 2009), glycogen breakdown typically results in lactate production and release in the extracellular space (Walls et al., 2009, Dringen et al., 1993). Considering the role of astrocytic glucose-derived lactate in fuelling neuronal energy needs (described above in the ANLS section), this positions lactate as a likely candidate to account for the protective effects of glycogen. In support of this, axonal function was demonstrated to be preserved during aglycemia through the transfer of glycogen-derived lactate from astrocytes to axons in an optic nerve preparation (Tekkok et al., 2005, Brown et al., 2005).

In addition to its role as an emergency energy reserve, there is compelling evidence indicating other important roles for glycogen in normal brain functions.
As a whole, these observations demonstrate that astrocytic glycogen is more than a simple emergency reserve, and plays an important and active role in complex brain physiological functions, in particular through an astrocyte-to-neuron transfer of energy metabolites in the form of lactate. It thus appears that both glucose- and glycogen-derived lactate are important to sustain neuronal function, as postulated by the ANLS.
Metabolic Plasticity in Astrocytes as a Protective Mechanism

A large body of experimental evidence suggests that astrocytes have a greater metabolic plasticity than neurons, i.e., they can better adapt their energy metabolism to face various cellular challenges. A striking example is the differential response of astrocytes and neurons following the inhibition of mitochondrial respiration induced by NO. Astrocytes respond to NO with an increase in glucose metabolism through the glycolytic pathway, thereby limiting the fall in ATP levels and preventing apoptosis. In neurons, however, this response does not seem to be present, and a similar NO challenge causes a massive ATP depletion, leading to apoptosis (Almeida et al., 2001). Another strong indication of the limited metabolic plasticity of neurons is provided by recent studies which have shown that driving a higher glycolytic rate (Herrero-Mendez et al., 2009) or glycogen synthesis (Vilchez et al., 2007) in neurons causes apoptotic cell death, even though these pathways are generally innocuous (or even beneficial) in astrocytes.»

« Figure 3
Astrocyte-Neuron Metabolic Interactions

(A) Schematic representation of the astrocyte-neuron lactate shuttle (ANLS). Glutamate (Glu) released at the synapse activates glutamatergic receptors (GluR) and is associated with important energy expenditures in neuronal compartments. A large proportion of the glutamate released at the synapse is taken up by astrocytes via excitatory amino acid transporters (EAATs, more specifically GLT-1 and GLAST) together with 3 Na+ ions. This Na+ is extruded by the action of the Na+/K+ ATPase, consuming ATP. This triggers nonoxidative glucose utilization in astrocytes and glucose uptake from the circulation through the glucose transporter GLUT1 expressed by both capillary endothelial cells and astrocytes. Glycolytically derived pyruvate is converted to lactate by lactate dehydrogenase 5 (LDH5; mainly expressed in astrocytes) and shuttled to neurons through monocarboxylate transporters (mainly MCT1 and MCT4 in astrocytes and MCT2 in neurons). In neurons, this lactate can be used as an energy substrate following its conversion to pyruvate (Pyr) by LDH1 (mainly expressed in neurons). Neurons can also take up glucose via the neuronal glucose transporter 3 (GLUT3). Concomitantly, astrocytes participate in the recycling of synaptic glutamate via the glutamate-glutamine cycle. Following its uptake by astrocytes, glutamate is converted to glutamine (gln) by the action of glutamine synthetase (GS) and shuttled to neurons, where it is converted back to glutamate by glutaminases (GLS).

(B) Glial glutamate transporters play a central role in neurometabolic coupling. Glucose utilization (as assessed by the 2-deoxyglucose [2-DG] uptake technique) was measured in the somatosensory cortex of P10 GLAST mutant mice following unilateral whisker stimulation. Representative pseudocolored digitized autoradiograms of anteroposterior coronal sections at the level of the somatosensory barrel field are shown. Whisker stimulation in GLAST+/+ mice produced a local increase in glucose utilization in the activated somatosensory cortex (i, white square). Such an increase in glucose utilization was not observed in coronal sections from GLAST−/− mice (ii, white square). Similar results were obtained in GLT-1 mutant mice. Reproduced with permission from Voutsinos-Porche et al. (2003)).

(C) Astrocytes play an important role in glutathione metabolism in the brain. The tripeptide glutathione (GSH) is synthetized by the successive actions of glutamate cysteine ligase (GCL) and GSH synthetase. Astrocytes can efficiently use oxidized cysteine (cystine) for GSH synthesis. Astrocytes release a large amount of GSH in the extracellular space, where it is cleaved by the astrocytic ectoenzyme γ-glutamyl transpeptidase (γGT). The resulting dipeptide CysGly is cleaved by the neuronal ectopeptidase aminopeptidase N (ApN), forming cysteine (Cys) and glycine (Gly), which serve as precursors for neuronal GSH synthesis. GSH is an electron donor in many reactions in both neurons and astrocytes, including the detoxification of ROS (e.g., the reduction of peroxides [ROOH] by glutathione peroxidase [GPx]). The oxidized glutathione (GSSG) formed as a result is recycled back to glutathione by the action of glutathione reductase (GR) using NADPH as an electron donor. X represents an acceptor for the γ-glutamyl moiety (γGlu) in the reaction catalyzed by γGT.»

— Bélanger M, Allaman I, Magistretti PJ. "Brain Energy Metabolism: Focus on Astrocyte-Neuron Metabolic Cooperation." Cell Metab (2011 Dec 7) vol. 14 (6) pp. 724-38 DOI:

Further reading:

• Falkowska A et al. "Energy Metabolism of the Brain, Including the Cooperation between Astrocytes and Neurons, Especially in the Context of Glycogen Metabolism." Int J Mol Sci (2015 Oct 29) vol. 16 (11) pp. 25959-81 DOI:

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"Pearl Harbour not actually an act of war
just a limited air strike with no boots on the ground."

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"Show me on this map where Syria hurt you"

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• Reuters. "U.N. has testimony that Syrian rebels used sarin gas: investigator." Chicago Tribune (May 5, 2013)

• Matthew Schofield. "New analysis of rocket used in Syria chemical attack undercuts U.S. claims." McClatchy DC Bureau (January 15, 2014)

«In perhaps the toughest comments to date, Israeli Defense Minister Ehud Barak said last week that Assad’s ouster would be “very positive” for Israel. “The toppling down of Assad will be a major blow to the radical axis,” he said in a CNN interview. “It will weaken dramatically Iran.”
Although Israeli officials now believe Assad’s days are numbered, they say they are keeping their distance from the key players in Syria. They do not want to be seen as intervening in Syrian affairs.»

— Karin Laub. "Open calls for Assad’s ouster becoming more common in Jerusalem." The Times of Israel (April 27, 2012)

«The best way to help Israel deal with Iran's growing nuclear capability is to help the people of Syria overthrow the regime of Bashar Assad.
Iran's nuclear program and Syria's civil war may seem unconnected, but they are. For Israeli leaders, the real threat from a nuclear-armed Iran is not the prospect of an insane Iranian leader launching an unprovoked Iranian nuclear attack on Israel that would lead to the annihilation of both countries. What Israeli military leaders really worry about -- but cannot talk about -- is losing their nuclear monopoly. An Iranian nuclear weapons capability would not only end that nuclear monopoly but could also prompt other adversaries, like Saudi Arabia and Egypt, to go nuclear as well. The result would be a precarious nuclear balance in which Israel could not respond to provocations with conventional military strikes on Syria and Lebanon, as it can today. If Iran were to reach the threshold of a nuclear weapons state, Tehran would find it much easier to call on its allies in Syria and Hezbollah to strike Israel, knowing that its nuclear weapons would serve as a deterrent to Israel responding against Iran itself.
Bringing down Assad would not only be a massive boon to Israel's security, it would also ease Israel's understandable fear of losing its nuclear monopoly. Then, Israel and the United States might be able to develop a common view of when the Iranian program is so dangerous that military action could be warranted. Right now, it is the combination of Iran's strategic alliance with Syria and the steady progress in Iran's nuclear enrichment program that has led Israeli leaders to contemplate a surprise attack — if necessary over the objections of Washington. With Assad gone, and Iran no longer able to threaten Israel through its, proxies, it is possible that the United States and Israel can agree on red lines for when Iran's program has crossed an unacceptable threshold. In short, the White House can ease the tension that has developed with Israel over Iran by doing the right thing in Syria.»

"NEW IRAN AND SYRIA 2.DOC." UNCLASSIFIED U.S. Department of State Case No. F-2014-20439 Doc No. C05794498 Date: 11/30/2015

«The reason the Assad government would bomb its own people with a nerve agent right now is obvious. Syrian President Assad – who has been fighting for his life for several years, and is only lately feeling safer – suddenly decided to commit suicide-by-Trump. Because the best way to make that happen is to commit a war crime against your own people in exactly the way that would force President Trump to respond or else suffer humiliation at the hands of the mainstream media.

And how about those pictures coming in about the tragedy. Lots of visual imagery. Dead babies. It is almost as if someone designed this “tragedy” to be camera-ready for President Trump’s consumption. It pushed every one of his buttons. Hard. And right when things in Syria were heading in a positive direction.

Interesting timing.
Super-powerful visual persuasion designed for Trump in particular.
Suspiciously well-documented event for a place with no real press.
No motive for Assad to use gas to kill a few dozen people at the cost of his entire regime. It wouldn’t be a popular move with Putin either.
The type of attack no U.S. president can ignore and come away intact.
A setup that looks suspiciously similar to the false WMD[1] stories that sparked the Iraq war.

I’m going to call bullshit on the gas attack. It’s too “on-the-nose,” as Hollywood script-writers sometimes say, meaning a little too perfect to be natural. This has the look of a manufactured event.»

— Scott Adams. "The Syrian Gas Attack Persuasion." Scott Adams' Blog (April 6, 2017)

• Ed Stetzer. "NEW RESEARCH: Should Christians Support Israel? Most Pastors Think So." The Exchange, (July 14, 2015)

• Bob Smietana. "American evangelicals stand behind Israel." LifeWay Newsroom, LifeWay Christian Resources (July 14, 2015)

• David Heilbroner. "Evangelicals, Israel, and the End of the World." The Huffington Post (March 18, 2010; updated May 25, 2011)

• Pat Robertson. "Why Evangelical Christians Support Israel."

"Christian Zionism." Wikipedia

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"77 Cents for Every Dollar"

"Wait a minute, I'm only getting 77% as many carrots as you're getting?"

«Women make only 77 cents per each dollar made by males. Outrageous! Sex discrimination!
So say advocates of government-enforced "equality."»

— John Stossel. "Battle of the Sexes: Women today are rarely victims of salary discrimination." (August 14, 2013)

• Glenn Kessler. "Fact Checker: Here are the facts behind that ’79 cent’ pay gap factoid." The Washington Post (April 14, 2016)

• Glenn Kessler. "Fact Checker: President Obama’s persistent ’77-cent’ claim on the wage gap gets a new Pinocchio rating." The Washington Post (April 9, 2014)

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Right to Roam and Pee

«On the first day of her action against TIGCS, Beyts told sheriff Donald Corke she was being treated for incontinence on the day she and Edwards had decided to walk through the course under Scotland’s right-to-roam legislation.

Beyts insisted she had taken every possible precaution to avoid being seen as she ducked down behind a dune to urinate “rather urgently”. She told the court it was late afternoon, raining and misty, and no one could be seen from where she was.»

— Severin Carrell . "Activist 'upset' that Trump staff secretly photographed her urinating: Rohan Beyts suing Trump’s Aberdeenshire golf resort after it claimed she breached decency laws on the course." The Guardian (3 April 2017)

What better place to pee than in a golf course? With electrolytes, it's got what plants crave. Unfortunately, there's no comments section in that page.

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Daylight Saving Time (DST) Revisited

• Nacho Catalán y Rodrigo Silva. "Así afecta el sol a nuestro horario: España desplaza entre una y dos horas el horario para acomodarse a la luz solar." El País (25 marzo 2017)

• Dr Eric Barchas. "Ask a Vet: Will Daylight Saving Time Make My Cat Bonkers?" Ask a Vet, Catster (March 13, 2017)

• Kelly Phillips Erb. "You Spring Forward For Daylight Saving Time Because Of Energy Policy, Not Farmers." Forbes (March 12, 2017)

• Rachel Wilkerson Miller. "9 Things You Probably Don't Know About Daylight Saving Time - Surprise: farmers have always been daylight saving time’s biggest opponent - Daylight saving time makes people feel A Way." BuzzFeed (March 12, 2017)

• Ashley Strickland. "Why daylight saving time can be bad for your health." CNN International Edition (March 11, 2016; Updated March 10, 2017)

• Doyle Rice (USA Today). "Love it or hate it, Daylight Saving Time is here." USA Today Network (March 9, 2017; Updated March 13, 2017)

• Sean Rossman (USA Today). "Here comes the sun: Daylight Saving Time starts Sunday." USA Today Network (March 9, 2017; Updated March 10, 2017)

• Scott Craven (The Arizona Republic). "Why Arizona doesn't observe daylight-saving time." USA Today Network (March 9, 2017; Updated March 10, 2017)

• John Siciliano. "Daylight saving time may be killing you." Washington Examiner (March 10, 2017)

• Locke Hughes. "How Does Daylight Saving Time Affect Your Health?" WebMD (March 8, 2017)

• Amanda MacMillan. "7 ways daylight saving time can affect your health: An hour of lost sleep and an out-of-whack circadian rhythm could affect your fertility, heart health, mood, and more." (March 7, 2017); (March 13, 2017)

• Montaño, Alexandra. "Executive Summary: Health Impact Review of SB 5329 Exempting the State of Washington from Daylight Saving Time and Implementing Year-Round Pacific Standard Time (2017-2018 Legislative Session)." Washington State Board of Health (February 16, 2017)

• Boston University Medical Center. "Daylight savings time impacts miscarriage rates among select IVF patients, study finds." Boston Medical Center; ScienceDaily; Medical Xpress (February 8, 2017)

• Liu et al. "Impact of daylight savings time on spontaneous pregnancy loss in in vitro fertilization patients." Chronobiol Int (2017 Feb 3) pp. 1-7 doi: 10.1080/07420528.2017.1279173

• Brinke Guthrie. "Daylight Saving time is tonight … is it really necessary?" Digital Trends (November 5, 2016)

• Brian Handwerk. "The Case for and Against Daylight Saving Time." National Geographic News (November 3, 2016)

• Editorial. "Time out: Artificial fixes to make the most of summer time may do more harm than good." Nature News (30 March 2016)

• James Alexander Webb. "Daylight Saving Time: A Government Annoyance." Mises Wire (March 11, 2016); The Daily Liberator (March 15, 2016)

• Daniel Victor. "Daylight Saving Time: Why Does It Exist? (It’s Not for Farming)." The New York Times (March 11, 2016)

• Ashley Welch. "Could daylight saving time increase your risk of stroke?" CBS News (February 29, 2016)

• Michele Debczak. "Here's How Daylight Saving Time Affects Your Part of the Country." (November 22, 2015)

• Shari Rudavsky (The Indianapolis Star). "10 things we STILL hate about Daylight Saving Time." USA Today Network (March 9, 2015)

• Cox Media Group National Content Desk. "Hearing Held on Eliminating Daylight Saving Time." WSB Radio, Cox Media Group (March 9, 2015)

• Josh Guckert. "Daylight Saving Time is Just More Big Government, Let’s End It." The Libertarian Republic (March 8, 2015)

• John Oliver. "Daylight Saving Time - How Is This Still A Thing?" Last Week Tonight with John Oliver, HBO (March 8, 2015) [3 min]

• Laurence M Vance. "Republicans and Daylight Saving Time." (March 8, 2015)

• Donna Boynton. "Deadly car crashes spike after changing clocks for Daylight Saving Time." (March 6, 2015; Updated March 7, 2015)

"Russian clocks go back for last time." BBC News (25 October 2014)

• Smith AC. "Spring Forward at Your Own Risk: Daylight Saving Time and Fatal Vehicle Crashes." University of Colorado Boulder (October 2014) Working Paper 14-05

• American College of Cardiology. "Daylight saving impacts timing of heart attacks." ScienceDaily (March 29, 2014)

• Julie Campbell. "The impact of one hour of sleep on health care costs." Live Insurance News (March 10, 2014)

• Chris Kline ( "Why Arizona doesn't follow Daylight Saving." East Valley Tribune (March 9, 2014)

• Denise Chow. "Daylight Saving Time: Why Do We Adjust Clocks in March?" LiveScience (March 7, 2014)

• Brian Handwerk. «Daylight Saving Time 2014: When Does It Begin? And Why? Why we "spring forward," and arguments for and against daylight saving time.» National Geographic News (March 6, 2014)

• EDW Lynch. "Proposal: U.S. Should Abolish Daylight Saving Time and Replace It with 19 Time Zones." Laughing Squid (November 6, 2013)

• EDW Lynch. "An Economist’s Proposal for Abolishing Daylight Saving Time and Reducing the Number of U.S. Time Zones." Laughing Squid (November 4, 2013)

• Laura Poppick. "5 Weird Effects of Daylight Saving Time." LiveScience (November 2, 2013)

• Allison Schrager. "Five more reasons to kill daylight saving time." Quartz (November 2, 2013)

• Allison Schrager. "The US needs to retire daylight savings and just have two time zones—one hour apart." Quartz (November 1, 2013)

• Allison Schrager. "Daylight Saving Time Is Terrible: Here's a Simple Plan to Fix It - Losing another hour of evening daylight isn't just annoying. It's an economically harmful policy with minimal energy savings." The Atlantic (November 1, 2013)

• Alexander Abad-Santos. "Daylight Saving Time Is America's Greatest Shame: Daylight Saving Time is the greatest continuing fraud ever perpetrated on the American people. And this weekend, the effect of this cruel monster will rear its ugly head again." The Atlantic (November 1, 2013)

"US lost almost half a billion dollars due to Daylight Saving Time." (12 March 2013)

• Karen Kaplan. "Change to daylight saving time takes biggest health toll today," Los Angeles Times (March 11, 2013)

• Daniel Lemire. "Current Daylight saving time policies are insane." Daniel Lemire's blog (March 11, 2013)

• Mark J Perry. "Daylight saving time costs about $2 billion each year." AEIdeas, American Enterprise Institute (March 9, 2013)

• Anthony Carboni. "Why We Have Daylight Saving Time." D News; Seeker (March 9, 2013) [3 min]

• Pete Donohue and Nancy Dillon. "Watch out! Experts says car crashes spike on the Monday after daylight savings time goes into effect." New York Daily News (March 8, 2013)

• Bora Zivkovic. "Let's Not Spring Forward." A Blog Around The Clock, Scientific American (March 7, 2013)

"Lost sleep and cyberloafing." PAMPLIN (College of Business Magazine, Virginia Tech) (Spring 2012)

• Wagner DT et al. "Lost sleep and cyberloafing: Evidence from the laboratory and a daylight saving time quasi-experiment." J Appl Psychol (2012 Sep) vol. 97 (5) pp. 1068-76 (Epub 2012 Feb 27)

• Laurence M Vance. "Daylight Saving Time and Republicans." (March 12, 2012)

• Joe Satran. "Daylight Savings Time Invented By George Vernon Hudson, 19th-Century Entomologist (PHOTOS)." The Huffington Post (March 9, 2012)

• Claire Penhorwood. "How to survive the daylight saving time switch: The health effects of daylight saving time and how to mitigate them." CBC News (March 8, 2012; Last Updated: March 9, 2012)

• University of Alabama at Birmingham. "Heart Attacks Rise Following Daylight Saving Time." ScienceDaily (March 7, 2012)

• Jennifer Lollar. "Heart attacks rise following daylight saving time." UAB News (March 6, 2012)

• Janszky I et al. "Daylight saving time shifts and incidence of acute myocardial infarction--Swedish Register of Information and Knowledge About Swedish Heart Intensive Care Admissions (RIKS-HIA)." Sleep Med (2012 Mar) vol. 13 (3) pp. 237-42

• Brian Handwerk. "Daylight Saving Time 2011: Why and When Does It End? Why fall back? Should daylight savings be stopped? Get the facts." National Geographic News (November 5, 2011)

• CGP Grey ("Colin Gregory Palmer Grey"). "Daylight Saving Time Explained." CGPGrey Channel (October 24, 2011) [7 min]
CGP Grey's blog:

• Benyamin Cohen. "Do we still need daylight saving time?: Everyone from the candy lobby to TV networks is weighing in on the debate." (October 19, 2011)

• Rasmussen Reports Staff. "47% Don’t Think Daylight Saving Time Worth the Hassle." Rasmussen Reports (March 13, 2010)

• Lahti T et al. "Daylight Saving Time Transitions and Road Traffic Accidents." _Journal of Environmental and Public Health (2010) vol. 2010 art. ID 657167 3 pages doi: 10.1155/2010/657167

• Schneider AM and Randler C. "Daytime sleepiness during transition into daylight saving time in adolescents: Are owls higher at risk?" Sleep Med (2009 Oct) vol. 10 (9) pp. 1047-50

• American Psychological Association. "Daylight-saving Time Leads To Less Sleep, More Injuries On The Job, Study Finds." ScienceDaily (September 1, 2009)

• Barnes CM and Wagner DT. "Changing to daylight saving time cuts into sleep and increases workplace injuries." Journal of Applied Psychology (2009) vol. 94 (5) pp. 1305-1317

• Tony Wright. "Daylight Savings Time costs the United States $480,000,000." RescueTime (March 11, 2009)

• Berk M et al. "Small shifts in diurnal rhythms are associated with an increase in suicide: The effect of daylight saving." Sleep and Biological Rhythms (2008) vol. 6 (1) pp. 22–25

• Janszky I and Ljung R. "Shifts to and from daylight saving time and incidence of myocardial infarction." N Engl J Med (2008 Oct 30) vol. 359 (18) pp. 1966-8

• Matthew J. Kotchen MJ and Grant LE. "Does Daylight Saving Time Save Energy? Evidence from a Natural Experiment in Indiana." NBER (October 2008) Working Paper 14429

• Coate D and Markowitz S. "The effects of daylight and daylight saving time on US pedestrian fatalities and motor vehicle occupant fatalities." Accid Anal Prev (2004 May) vol. 36 (3) pp. 351-7

• Varughese J and Allen RP. "Fatal accidents following changes in daylight savings time: the American experience." Sleep Med (2001 Jan) vol. 2 (1) pp. 31-36

• Coren S. "Accidental Death and the Shift to Daylight Savings Time." Percept Mot Skills (1996 Dec) vol. 83 (3 Pt 1) pp. 921-2

• Coren S. "Daylight Savings Time and Traffic Accidents." N Engl J Med (1996 Apr 4) vol. 334 (14) pp. 924

• George Gibbs. "Hudson, George Vernon." Dictionary of New Zealand Biography (1996) vol. 3; Te Ara - the Encyclopedia of New Zealand

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"George Hudson (entomologist)." Wikipedia

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• Bryan Caplan (guest) and Dave Rubin (host). "Debating Immigration, Open Borders, and Pacifism." (Bryan Caplan Pt. 3) The Rubin Report (March 23, 2017) [30 min]

Libertarianism is as alien to most Americans as it is to South Americans. On the other hand, there are also libertarians in South America, even a university in Guatemala, Universidad Francisco Marroquín.
Also, most people change their way of thinking over time, quite often influenced by their environment.
How many immigrants living in the US who came from the former socialist republics of Europe or East Asia are presently communists?
Ayn Rand immigrated to the US from the Soviet Union in 1926, when she was 21. Did she perhaps oppose libertarian ideas more than the average American of her time?

• Onkar Ghate. "The Myth about Ayn Rand and Social Security." Ayn Rand Institute (June 19, 2014)

• Ayn Rand. "The Question of Scholarships." The Objectivist (June 1966) no. 11

«Rand felt the same way about any number of government programs, including government scholarships, and such. In reality, Rand got a free education at the University of Petrograd in the Soviet Union, a newly-minted communist state; next to that, collecting Social Security is "a mere bag of shells," as Ralph Kramden would put it. But, you see, that's the whole issue, isn't it? Rand was born in the Soviet Union, and even that state wasn't "pure communism," as Marx envisioned it;…»

— Chris Matthew Sciabarra. "Ayn Rand, David Cross, and Hypocrisy." Dialectics & Liberty (Notablog), New York University (August 17, 2016)

The welfare state is much less developed in most South American countries than it is in the US, since those countries lack the resources to afford a fully developed welfare state like the American (so they haven't even yet been spoiled). Contrary to popular mythology, most immigrants don't move to the US planning to live of welfare programs, rather it's the liberals, most of them American-born, those who actively seek to enrol as many people as possible in such programs.

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«At least that's how things were for me when I was a teen-age atheist.
If you wander the streets of NYC and look like me, some ultra-Orthodox Jewish teens will eventually approach you and ask: "Are you Jewish?" If you say no, they wave good-bye.
Me: Because my father is Jewish.
(If you are completely baffled by this anecdote, remember that Jewish religious identity is matrilineal).»

— Bryan Caplan. "What Life Experience Taught Me About Religion." Library of Economics and Liberty (June 2008)

The reason Judaism doesn't fit into the definitions of race, ethnicity, or culture cleanly is because it's a lie. Judaism is just a religion trying to make itself out of more than it is, just like other religions do.
I am NOT suggesting to leave your congregation. But recognize that you are not Jews, you are atheist, descendants of Jews from a specific area, who share a culture from that area, which includes Hebrew school and other indoctrinations.
I AM stating that it is wrong to call yourself Jewish. This is just Judaism taking credit for things it doesn't deserve, and using guilt to perpetuate the myth.
Israel is not "our country" - that's just marketing. There is no need to support it blindly, just because their state religion is Judaism.
You are not hurting your family, disgracing your heritage, or helping the Nazis by telling the truth. You are NOT enabling another Holocaust. These are lies meant to manipulate you into lying.
Honesty, to oneself and others, is a mitzvah.»
[At 1:36:25]

«Judaism is Supposedly Also:
A Culture? Nope.
Definition "The totality of socially transmitted behavior patterns, arts, beliefs, institutions, and all other products of human work and thought, considered as the expression of a particular period, class, community, or population."
All the above can be abandoned. You can leave a culture but Jewish law doesn't allow this
There are no cultural characteristics that Jews have in common (though subsets do, and they expand them to all "Jews")
Bagels and mazoh brei are not more Jewish than chow is Buddhist and falafel is Muslim
Is Islam a culture? Mormonism? Amish? Branch Davidians?»
[From 20:50 to 24:00]

— Dave Silverman. "I'm an Atheist (And So Are You); Why I've Changed My Mind on Jewish Atheism". FreeThought Arizona (Tucson, October 2013) [102 min]
"David Silverman, President of American Atheists, gave this talk to the Secular Humanist Jewish Circle and FreeThought Arizona in October 2013 in Tucson."

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