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Zephyr López Cervilla

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By attacking Assange you're backing the Spanish imperialists

Get to know your friends and foes: Julian Assange was cut off from Internet access in the Ecuadorian embassy in London because he was denouncing the political persecution against the Catalan independence movement, and the Spanish imperialist state pressured the Ecuador government to stop him.
If you're a foe of Mr. Assange you're a liberticidal asshole.

For those of you who by attacking Assange are also giving support to the Spanish imperialist regime, this is the fascist principles the Spanish statists resort to justify any violent political repression against independent movements (in Castilian, not "Spanish", that's just one more among many manipulations carried out by the Spanish imperialists):

«España es, ante todo, una unidad de destino;
El separatismo ignora u olvida la realidad de España. Desconoce que España es, sobre todo, una gran unidad de destino.
Los separatistas se fijan en si hablan lengua propia, en si tienen características raciales propias, en si su comarca presenta clima propio o especial fisonomía topográfica.
Pero –habrá que repetirlo siempre– una nación no es una lengua, ni una raza, ni un territorio. Es una unidad de destino en lo universal.
Esa unidad de destino se llamó y se llama España.
Bajo el signo de España cumplieron su destino –unidos en lo universal– los pueblos que la integran.
Nada puede justificar que esa magnífica unidad, creadora de un mundo, se rompa».

«Puntos iniciales». Falange Española (Madrid, 1933-12-07) no. 1 pp. 6-7

«2. España es una unidad de destino en lo universal. Toda conspiración contra esa unidad es repulsiva. Todo separatismo es un crimen que no perdonaremos.
La Constitución vigente, en cuanto incita a las disgregaciones, atenta contra la unidad de destino de España. Por eso exigimos su anulación fulminante.

3. Tenemos voluntad de Imperio. Afirmamos que la plenitud histórica de España es el Imperio. Reclamamos para España un puesto preeminente en Europa. No soportamos ni el aislamiento internacional ni la mediatización extranjera.
Respecto de los países de Hispanoamérica, tendemos a la unificación de cultura, de intereses económicos y de Poder. España alega su eje espiritual del mundo hispánico como título de preeminencia en las empresas universales».

— Ramiro Ledesma Ramos, José Antonio Primo de Rivera y Sáenz de Heredia. «27 puntos de La Falange Española». Falange Española de las JONS (c. octubre 1934) ; Pedro M Tavera (originales). “Los XXVI puntos del Estado español”. Gráficas Reunidas SA (junio 1940)

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Further reading:

• Stephanie Kirchgaessner (Rome), Sam Jones (Madrid), Dan Collyns (Lima). "Assange 'split' Ecuador and Spain over Catalan independence: WikiLeaks founder met separatists and tweeted on the issue, which sources say triggered a backlash from Madrid." The Guardian (2018-05-16)
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"Are Sports Drinks Safe & Effective?" [Answer: No, They're Crap]
• Michael Greger MD. (2018-05-04) [6 min]

• Hoffman MD, Bross TL 3rd, Hamilton RT. "Are we being drowned by overhydration advice on the Internet?" Phys Sportsmed (2016 Nov) vol. 44 (4) pp. 343-348 DOI: 10.1080/00913847.2016.1222853

• Rosner MH. "Preventing Deaths Due to Exercise-Associated Hyponatremia: The 2015 Consensus Guidelines." Clin J Sport Med (2015 Jul) vol. 25 (4) pp. 301-2 DOI: 10.1097/JSM.0000000000000223

A low-sodium diet does have "beneficial" effects other than lowering blood pressure. It facilitates acclimation to physical activity in hot environments, contributing to increase your sweat rate, it prevents exercise-associated hyponatraemia by minimising the sodium and other electrolytes lost in your sweat, a low-sodium diet also reduces your calciuria, thus contributing to preserve the calcium of your body:

• Cappuccio FP et al. "Unravelling the links between calcium excretion, salt intake, hypertension, kidney stones and bone metabolism." J Nephrol (2000 May-Jun) vol. 13 (3) pp. 169-77

• Frassetto L et al. "Diet, evolution and aging--the pathophysiologic effects of the post-agricultural inversion of the potassium-to-sodium and base-to-chloride ratios in the human diet." Eur J Nutr (2001 Oct) vol. 40 (5) pp. 200-13

• Chinevere TD et al. "Effect of heat acclimation on sweat minerals." Med Sci Sports Exerc (2008 May) vol. 40 (5) pp. 886-91

• Nielsen B et al. "Human circulatory and thermoregulatory adaptations with heat acclimation and exercise in a hot, dry environment." J Physiol (Lond) (1993 Jan) vol. 460 pp. 467-85

• Takamata A et al. "Relationship of osmotic inhibition in thermoregulatory responses and sweat sodium concentration in humans." Am J Physiol Regul Integr Comp Physiol (2001 Mar) vol. 280 (3) pp. R623-9

• Shibasaki M and Crandall CG. "Mechanisms and controllers of eccrine sweating in humans." Front Biosci (Schol Ed) (2010 Jan 1) vol. 2 pp. 685-96

• Armstrong LE et al. "Responses to moderate and low sodium diets during exercise-heat acclimation." Int J Sport Nutr (1993 Jun) vol. 3 (2) pp. 207-21

• Magalhães FC et al. "Thermoregulatory efficiency is increased after heat acclimation in tropical natives." J Physiol Anthropol (2010) vol. 29 (1) pp. 1-12

Population studies on sodium intake:

• Intersalt Cooperative Research Group. "Intersalt: an international study of electrolyte excretion and blood pressure. Results for 24 hour urinary sodium and potassium excretion. Intersalt Cooperative Research Group." BMJ (1988 Jul 30) vol. 297 (6644) pp. 319-28

• Elliott P et al. "Intersalt revisited: further analyses of 24 hour sodium excretion and blood pressure within and across populations. Intersalt Cooperative Research Group." BMJ (1996 May 18) vol. 312 (7041) pp. 1249-53

• MacGregor GA and Wardener HE. "Salt Diet and Health." Cambridge University Press (1998 Aug 11)
Ch. "Populations, salt and blood pressure." pp. 100-126

Further reading:

• Graudal NA, Hubeck-Graudal T, Jürgens G. "Effects of low-sodium diet vs. high-sodium diet on blood pressure, renin, aldosterone, catecholamines, cholesterol, and triglyceride (Cochrane Review)." Am J Hypertens (2012 Jan) vol. 25 (1) pp. 1-15

• O'Donnell MJ, Mente A, Smyth A, Yusuf S. "Salt intake and cardiovascular disease: why are the data inconsistent?" Eur Heart J (2013 Apr) vol. 34 (14) pp. 1034-40

• Powles J, Fahimi S, Micha R, Khatibzadeh S, Shi P, Ezzati M, Engell RE, Lim SS, Danaei G, Mozaffarian D; Global Burden of Diseases Nutrition and Chronic Diseases Expert Group (NutriCoDE). "Global, regional and national sodium intakes in 1990 and 2010: a systematic analysis of 24 h urinary sodium excretion and dietary surveys worldwide." BMJ Open (2013 Dec 23) vol. 3 (12) art. e003733

• Aaron KJ, Sanders PW. "Role of dietary salt and potassium intake in cardiovascular health and disease: a review of the evidence." Mayo Clin Proc (2013 Sep) vol. 88 (9) pp. 987-95

Comment on above article:

• DiNicolantonio JJ, O'Keefe JH, Lucan SC. "Population-wide sodium reduction: reasons to resist." Mayo Clin Proc (2014 Mar) vol. 89 (3) pp. 426-7

Authors' reply:

• Aaron KJ, Sanders PW. "Population-wide sodium reduction: reasons to resist." Mayo Clin Proc (2014 Mar) vol. 89 (3) pp. 427-8

• Mozaffarian D, Fahimi S, Singh GM, Micha R, Khatibzadeh S, Engell RE, Lim S, Danaei G, Ezzati M, Powles J; Global Burden of Diseases Nutrition and Chronic Diseases Expert Group. "Global sodium consumption and death from cardiovascular causes." N Engl J Med (2014 Aug 14) vol. 371 (7) pp. 624-34

Comments on the above article:

• Alderman MH. "Sodium and cardiovascular disease." N Engl J Med (2014 Nov 27) vol. 371 (22) p. 2137

• Graudal N. "Sodium and cardiovascular disease." N Engl J Med (2014 Nov 27) vol. 371 (22) pp. 2136-7

Authors' reply:

• Mozaffarian D, Singh GM, Powles J. "Sodium and cardiovascular disease." N Engl J Med (2014 Nov 27) vol. 371 (22) pp. 2138-9

• O'Donnell M, Mente A, Rangarajan S, PURE Investigators et al. "Urinary sodium and potassium excretion, mortality, and cardiovascular events." N Engl J Med (2014 Aug 14) vol. 371 (7) pp. 612-23

Comment on above article:

• Cook NR. "Sodium and cardiovascular disease." N Engl J Med (2014 Nov 27) vol. 371 (22) p. 2134

• Saulnier PJ, Gand E, Hadjadj S; SURDIAGENE Study Group. "Sodium and cardiovascular disease." N Engl J Med (2014 Nov 27) vol. 371 (22) pp. 2135-6

• Batuman V. "Sodium and cardiovascular disease." N Engl J Med (2014 Nov 27) vol. 371 (22) pp. 2134-5

Authors' reply:

• O'Donnell M, Mente A, Yusuf S. "Sodium and cardiovascular disease." N Engl J Med (2014 Nov 27) vol. 371 (22) pp. 2137-8

• Mente A, O'Donnell MJ, Rangarajan S, PURE Investigators et al. "Association of urinary sodium and potassium excretion with blood pressure." N Engl J Med (2014 Aug 14) vol. 371 (7) pp. 601-11

Comment on above article:

• Divisón Garrote JA, Escobar Cervantes C, Seguí Díaz M. "Relationship between urinary sodium and potassium excretion and blood pressure." Semergen (2015 Mar) vol. 41 (2) pp. 110-1

Comment on above articles:

• He FJ, Ivković V, Jelaković B, Morris J, MacGregor GA. "Estimation of sodium excretion should be made as simple as possible, but not simpler: misleading papers and editorial on spot urines." J Hypertens (2015 Apr) vol. 33 (4) pp. 884-6

Authors' reply:

• Mente A, O'Donnell MJ, Yusuf S. "Response to 'Estimation of sodium excretion should be made as simple as possible, but not simpler: misleading papers and editorial on spot urines'." J Hypertens (2015 Apr) vol. 33 (4) pp. 887-90

Comment on above articles:

• Oparil S. "Low sodium intake--cardiovascular health benefit or risk?" N Engl J Med (2014 Aug 14) vol. 371 (7) pp. 677-9

• Huynh K. "Risk factors: Sodium intake and health outcomes." Nat Rev Cardiol (2014 Oct) vol. 11 (10) p. 556

• Allison SJ. "Hypertension: urinary sodium and potassium excretion: association with blood pressure and clinical outcomes." Nat Rev Nephrol (2014 Oct) vol. 10 (10) p. 541

• Campbell NR, Lackland DT, Niebylski ML, Nilsson PM. "Is reducing dietary sodium controversial? Is it the conduct of studies with flawed research methods that is controversial? A perspective from the World Hypertension League Executive Committee." J Clin Hypertens (Greenwich) (2015 Feb) vol. 17 (2) pp. 85-6

• Mente A, O'Donnell MJ, Rangarajan S et al. "Validation and comparison of three formulae to estimate sodium and potassium excretion from a single morning fasting urine compared to 24-h measures in 11 countries." J Hypertens (2014 May) vol. 32 (5) pp. 1005-14; discussion 1015

Comments on above article:

• Ruilope LM. "Can we make an adequate estimation of urinary sodium excretion avoiding 24-h urine collection?" J Hypertens (2014 May) vol. 32 (5) p. 977

• Majoor CJ, Vogt L. "Can sodium excretion from single fasting morning urine really be used for estimation of dietary sodium intake?" J Hypertens (2014 Dec) vol. 32 (12) pp. 2500-1

• Campbell N. "Validation and comparison of three formulae to estimate sodium and potassium excretion from a single-morning fasting urine compared to 24-h measures in 11 countries." J Hypertens (2014 Dec) vol. 32 (12) pp. 2499-500

Authors reply:

• Mente A, O'Donnell MJ, Yusuf S. "Reply to both letters." J Hypertens (2014 Dec) vol. 32 (12) pp. 2501-3

• McCallum L, Lip S, Padmanabhan S. "The hidden hand of chloride in hypertension." Pflugers Arch (2015 Mar) vol. 467 (3) pp. 595-603

• Cogswell ME, Mugavero K, Bowman BA, Frieden TR. "Dietary Sodium and Cardiovascular Disease Risk--Measurement Matters." N Engl J Med (2016 Aug 11) vol. 375 (6) pp. 580-6

Comments on the above article:

• O'Donnell M, Mann JF, Schutte AE, Staessen JA, Lopez-Jaramillo P, Thomas M, Mente A, Saulnier PJ, Yusuf S. "Dietary Sodium and Cardiovascular Disease Risk." N Engl J Med (2016 Dec 15) vol. 375 (24) pp. 2404-2406

• Alderman MH. "Dietary Sodium and Cardiovascular Disease Risk." N Engl J Med (2016 Dec 15) vol. 375 (24) p. 2406

• Johns DM. "Dietary Sodium and Cardiovascular Disease Risk." N Engl J Med (2016 Dec 15) vol. ;375 (24) p. 2407

• Graudal N. "Dietary Sodium and Cardiovascular Disease Risk." N Engl J Med (2016 Dec 15) vol. 375 (24) pp. 2406-7

Authors' reply:

• Cogswell ME, Frieden TR. "*Dietary Sodium and Cardiovascular Disease Risk."* N Engl J Med (2016 Dec 15) vol. 375 (24) pp. 2407-2408

• Webster J et al. "Understanding the science that supports population-wide salt reduction programs." J Clin Hypertens (Greenwich) (2017 Mar 27) DOI: 10.1111/jch.12994

• Ronald Hoffman. "Revisiting salt intake – are you eating too much or too little?" Dr. Ronald Hoffman (February 25, 2017)

• Cappuccio FP and Campbell NR. "Population Dietary Salt Reduction and the Risk of Cardiovascular Disease: A Commentary on Recent Evidence." J Clin Hypertens (Greenwich) (2017 Jan) vol. 19 (1) pp. 4-5


Pooled analysis:

• Mente A, O'Donnell M, Rangarajan S; PURE, EPIDREAM and ONTARGET/TRANSCEND Investigators et al. "Associations of urinary sodium excretion with cardiovascular events in individuals with and without hypertension: a pooled analysis of data from four studies." Lancet (2016 Jul 30) vol. 388 (10043) pp. 465-75


• Lancet. "Evidence-based policy for salt reduction is needed." Lancet (2016 Jul 30) vol. 388 (10043) pp. 438

Comments on editorial:

• Houser S. "Dear food industry: please don't pass the salt." Lancet (2016 Oct 29) vol. 388 (10056) pp. 2109-2110

• Schofield G, Henderson G, Crofts C. "Beyond salt-where next for hypertension epidemiology?" Lancet (2016 Oct 29) vol. 388 (10056) pp. 2110-2111

Early comments on pooled analysis:

• O'Brien E. "Salt--too much or too little?" Lancet (2016 Jul 30) vol. 388 (10043) pp. 439-40

• Bayer R, Johns DM, Galea S. "A false aura of scientific controversy around salt?" Lancet (2016 Oct 29) vol. 388 (10056) p. 2109

• Alderman MH. "Dietary sodium: paradigm shifts from public health to clinical medicine." Lancet (2016 Oct 29) vol. 388 (10056) p. 2110

• Wald N and Law M. "Sodium and cardiovascular disease." Lancet (2016 Oct 29) vol. 388 (10056) pp. 2111-2112

• Strazzullo P, Giampaoli S, Iacoviello L, Rossi L, Veglio F, Zoccali C. "Sodium and cardiovascular disease." Lancet (2016 Oct 29) vol. 388 (10056) p. 2111

• Katz J. "Sodium and cardiovascular disease." Lancet (2016 Oct 29) vol. 388 (10056) pp. 2112-2113

• Cappuccio FP. "Sodium and cardiovascular disease." Lancet (2016 Oct 29) vol. 388 (10056) p. 2112

Authors' reply to early comments on pooled analysis:

• Mente A, O'Donnell MJ, Yusuf S. "Sodium and cardiovascular disease - Authors' reply." Lancet (2016 Oct 29) vol. 388 (10056) pp. 2113-2114

Press release of pooled analysis:

• McMaster University. "Low-salt diets may not be beneficial for all, study suggests: Salt reduction only important in some people with high blood pressure." ScienceDaily (May 21, 2016)

Excerpt from early review of pooled analysis:

«In a pooled analysis of four partially manufacturer-supported studies involving 133,118 individuals from 49 countries (roughly half hypertensive and half normotensive), investigators sought to define the relationship between sodium intake and cardiovascular events. The study group comprised participants in four prospective studies for whom measures of 24-hour urinary sodium excretion were available. These measures were used to infer intake. The median follow-up was 4.2 years.»

— Harlan M Krumholz, MD, SM. "The Benefits and Detriments of Salt: It's Complicated - Harlan M. Krumholz, MD, SM reviewing Mente A et al. Lancet 2016 May 20. O'Brien E. Lancet 2016 May 20." NEJM Journal Watch (June 15, 2016)

Further reading:

• Kong YW et al. "Sodium and Its Role in Cardiovascular Disease – The Debate Continues." Front Endocrinol (Lausanne) (2016 Dec 23) vol. 7 art. 164

• Brown MJ. "Renin: friend or foe?" Heart (2007 Sep) vol. 93 (9) pp. 1026–1033

Why would you want to block renin, aldosterone or adrenalin? How much sodium did hunter-gatherer populations use to take? Were all dying of cardiovascular events because of their higher levels of renin, aldosterone and adrenalin?

High-sodium diets induce greater caloric intake:

• Rakova N et al. "Increased salt consumption induces body water conservation and decreases fluid intake." J Clin Invest (2017 May 1) vol. 127 (5) pp. 1932-1943

• Kitada K et al. "High salt intake reprioritizes osmolyte and energy metabolism for body fluid conservation." J Clin Invest (2017 May 1) vol. 127 (5) pp. 1944-1959

• Gina Kolata. "Why Everything We Know About Salt May Be Wrong." The New York Times (May 8, 2017)

Recent meta-analyses:

• Adler AJ, Taylor F, Martin N, Gottlieb S, Taylor RS, Ebrahim S. "Reduced dietary salt for the prevention of cardiovascular disease." Cochrane Database Syst Rev (2014 Dec 18) (12) art. CD009217

• Taylor RS, Ashton KE, Moxham T, Hooper L, Ebrahim S. "WITHDRAWN: Reduced dietary salt for the prevention of cardiovascular disease." Cochrane Database Syst Rev (2013 Sep 12) (9) art. CD009217

• Taylor RS, Ashton KE, Moxham T, Hooper L, Ebrahim S. "Reduced dietary salt for the prevention of cardiovascular disease: a meta-analysis of randomized controlled trials (Cochrane review)." Am J Hypertens (2011 Aug) vol. 24 (8) pp. 843-53

• Taylor RS, Ashton KE, Moxham T, Hooper L, Ebrahim S. "Reduced dietary salt for the prevention of cardiovascular disease." Cochrane Database Syst Rev (2011 Jul 6) (7) art. CD009217

Related article commenting on above meta-analysis:

• He FJ and MacGregor GA. "Salt reduction lowers cardiovascular risk: meta-analysis of outcome trials." Lancet (2011 Jul 30) vol. 378 (9789) pp. 380-2

Meta-analysis' authors' comment on related article:

• Taylor R, Hooper L, Ebrahim S. "*Dietary salt and cardiovascular disease."* Lancet (2011 Dec 10) vol. 378 (9808) p. 1993

Comments on related article:

• Satin M. "Dietary salt and cardiovascular disease." Lancet (2011 Dec 10) vol. 378 (9808) pp. 1993

• Alderman MH, Cohen H. "Dietary salt and cardiovascular disease." Lancet (2011 Dec 10) vol. 378 (9808) pp. 1993-4

Authors' reply to comments on related article:

• He FJ and MacGregor GA. "Dietary salt and cardiovascular disease – Authors' reply." Lancet (2011 Dec 10) vol. 378 (9808) p. 1994

2006 meta-analysis:

2004 meta-analysis:

2003 meta-analyses:

2002 meta-analysis:

2001 related article:

Related lecture:

• Jason Fung. "Dietary Villains - Part 2: Salt Scare." Jason Fung's YouTube channel (Sep 17, 2013) [30 min]

Related video:

• Olivia Gordon (host), Cynthia McKelvey (writer), Jenova Payton (script supervisor), Alyssa Lerner (script editor), Hank Green (executive producer). "Why Is Salt So Bad for You, Anyway?" SciShow (May 27, 2017) [2 min]
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Hayek was an anarcho-liberal, my ass!

«My thesis is essentially the same one also advanced by my friend Ralph Raico: Hayek is not a classical liberal at all, or a "Radikalliberaler" as the NZZ, as usual clueless, has just recently referred to him. Hayek is actually a moderate social democrat, and since we live in the age of social democracy, this makes him a "respectable" and "responsible" scholar. Hayek, as you may recall, dedicated his Road to Serfdom to "the socialists in all parties." And the socialists in all parties now pay him back in using Hayek to present themselves as "liberals."

Now to the proof, and I rely for this mostly on the Constitution of Liberty, and his three volume Law, Legislation, and Liberty which are generally regarded as Hayek's most important contributions to the field of political theory.

According to Hayek, government is "necessary" to fulfill the following tasks: not merely for "law enforcement" and "defense against external enemies" but "in an advanced society government ought to use its power of raising funds by taxation to provide a number of services which for various reasons cannot be provided, or cannot be provided adequately, by the market." (Because at all times an infinite number of goods and services exist that the market does not provide, Hayek hands government a blank check.)

Among these goods and services are

"protection against violence, epidemics, or such natural forces as floods and avalanches, but also many of the amenities which make life in modern cities tolerable, most roads … the provision of standards of measure, and of many kinds of information ranging from land registers, maps and statistics to the certification of the quality of some goods or services offered in the market."

Additional government functions include "the assurance of a certain minimum income for everyone"; government should "distribute its expenditure over time in such a manner that it will step in when private investment flags"; it should finance schools and research as well as enforce "building regulations, pure food laws, the certification of certain professions, the restrictions on the sale of certain dangerous goods (such as arms, explosives, poisons and drugs), as well as some safety and health regulations for the processes of production; and the provision of such public institutions as theaters, sports grounds, etc."; and it should make use of the power of "eminent domain" to enhance the "public good."

Moreover, it generally holds that "there is some reason to believe that with the increase in general wealth and of the density of population, the share of all needs that can be satisfied only by collective action will continue to grow."

Further, government should implement an extensive system of compulsory insurance ("coercion intended to forestall greater coercion"), public, subsidized housing is a possible government task, and likewise "city planning" and "zoning" are considered appropriate government functions — provided that "the sum of the gains exceed the sum of the losses." And lastly, "the provision of amenities of or opportunities for recreation, or the preservation of natural beauty or of historical sites or scientific interest … Natural parks, nature-reservations, etc." are legitimate government tasks.

In addition, Hayek insists we recognize that it is irrelevant how big government is or if and how fast it grows. What alone is important is that government actions fulfill certain formal requirements. "It is the character rather than the volume of government activity that is important." Taxes as such and the absolute height of taxation are not a problem for Hayek. Taxes — and likewise compulsory military service — lose their character as coercive measures,

"if they are at least predictable and are enforced irrespective of how the individual would otherwise employ his energies; this deprives them largely of the evil nature of coercion. If the known necessity of paying a certain amount of taxes becomes the basis of all my plans, if a period of military service is a foreseeable part of my career, then I can follow a general plan of life of my own making and am as independent of the will of another person as men have learned to be in society."

But please, it must be a proportional tax and general military service!

I could go on and on, citing Hayek's muddled and contradictory definitions of freedom and coercion, but that shall suffice to make my point. I am simply asking: what socialist and what green could have any difficulties with all this? Following Hayek, they can all proudly call themselves liberals.

In distinct contrast, how refreshingly clear — and very different — is Mises! For him, the definition of liberalism can be condensed into a single term: private property. The state, for Mises, is legalized force, and its only function is to defend life and property by beating antisocial elements into submission. As for the rest, government is "the employment of armed men, of policemen, gendarmes, soldiers, prison guards, and hangmen. The essential feature of government is the enforcement of its decrees by beating, killing, and imprisonment. Those who are asking for more government interference are asking ultimately for more compulsion and less freedom."

Moreover (and this is for those who have not read much of Mises but invariably pipe up, "but even Mises is not an anarchist"), certainly the younger Mises allows for unlimited secession, down to the level of the individual, if one comes to the conclusion that government is not doing what it is supposed to do: to protect life and property. And the older Mises never repudiated this position. Mises, then, as my own intellectual master, Murray Rothbard, noted, is a laissez-faire radical: an extremist.»

— Hans-Hermann Hoppe. "Why Mises (and not Hayek)?" Mises Daily Articles (2011-10-04)


• Hans-Hermann Hoppe (lecturer). "The Hayek Myth." 2012 Annual Meeting, Property & Freedom Society (Nov 2012) [37 min]
Cast (script):

• Hans-Hermann Hoppe (lecturer), Douglas E French (introducer). "Why Mises (and not Hayek)? · On Politics, Money, and Banking." Supporters Summit 2011 in Vienna, Mises Institute (Vienna, 2011 Sep 19-23) [44 min]·-politics-money-and-banking

Further reading:

• Odd J Stalebrink. "The Hayek and Mises Controversy: Bridging Differences." ["La polémica de Hayek y Mises: Salvando las diferencias"] The Quarterly Journal of Austrian Economics (Spring 2004) vol. 7 no. 1 pp. 27-38

• Joseph T Salerno. "Mises and Hayek Dehomogenized." ["Mises y Hayek diferenciados"] Review of Austrian Economics (1993) vol. 6 no. 2 pp. 113-146
Supplementary material:

• Ludwig von Mises. "Review: 'The Constitution of Liberty,' by FA Hayek." ["There Is Freedom or There Is Not: Mises Critiques Hayek - Mises praises every aspect of Hayek's Constitution of Liberty but one."] Christian Economics (1960 Aug 1)

• hayekian. "Hayek vs. Mises, Rand, Rothbard and Hoppe, and the growth of the ‘Alt-Right’." Medium (2017-02-24)
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"Your Questions and E-mails: Acidic vs Alkaline diet" The Skeptics' Guide to the Universe (2018-04-14) ep. 666

Question #1: Acidic vs Alkaline Diet
In the past few years I've heard a lot about avoiding acidic foods in favor of a more alkaline focused diet. Everything I google seems to point towards avoiding acidic foods like coffee. It seems to me that most evidence is anecdotal and/or contradictory. Have you guys discussed this on the show or written about this in the past? I'd love to hear your take on the movement. Love the show and have really changed my thought processes since I started listening. I am a young engineer and have always thought of myself as skeptical of what I read; however, I have been able to increase my vigilance against absurd headlines and find myself catching and disproving my own cognitive biases that I have accumulated over my life. Thank you for helping me to think more clearly and see the (what seems like purposeful) deception included in many of the science based news articles today. Best, Trace Maurer

It should be distinguished the acidity or alkalinity of the food you consume with the acidifying or alkalinising effect that the metabolisation of that food may cause in your body. The argument wielded by some of the panelists that since the pH of your blood (and other extracellular fluid) is kept within "narrow" range then such effects must be negligible doesn't hold water.

First, in "healthy" humans that pH range lies between 7.35 and 7.45 for arterial blood. It has to be considered, though, that the pH scale is logarithmic. A pH of 7.35 actually means a (hydrated) hydron molar concentration of 10^ - 7.35 mol/L. An acidification from pH 7.45 to 7.35 actually means a 26% increase of hydron molar concentration:
((10^ - 7.35) - (10^ - 7.45))/10^ - 7.45 ≈ 0.26

Second, relatively "modest" concentration changes may already elicit deleterious effects. That may well explain why the blood pH must be kept within that sort of narrow range (between 7.45 and 7.35 in arterial blood pH in humans). Furhermore, changes in the pH outside 6.8 to 7.8 range result in irreversible cell damage and are incompatible with life, at least in mammals.
Just raw numbers don't tell much (if anything at all) about its physiological effects.

Third, the extracellular fluid pH homeostasis comes with a cost. "There is no such thing as a free lunch." That "narrow" range is kept in large part at the expense of much wider pH changes in urine pH. Those frequent urine pH excursions outside the well-trodden path may by themselves contribute to a variety of health issues.

Fourth, it must be treated differently short-term effects and long-term effects. For instance, in humans acclimation/acclimatisation to high-altitude has short-term beneficial effects but some long-term effects may be deleterious:

Some references on the different effects of acidifying and alkalinising diets:

• Kanbara A et al. "Urine alkalization facilitates uric acid excretion." Nutr J (2010) 9:45

For instance, by consuming more fruits and vegetables rich in organic salts such as citrate, malate and gluconate:

«Sulfur-containing amino acids in protein-containing foods are metabolized to sulfuric acid. Animal foods provide predominantly acid precursors; dietary animal protein intake is highly correlated with renal net acid excretion (r = 0.84, P < 0.0005) (9). In contrast, vegetables and fruit contain not only amino acids but also substantial amounts of base precursors; the metabolism of organic potassium salts (citrate, malate, and gluconate) in fruit and vegetables yields potassium bicarbonate (10).»

— Sellmeyer DE et al. "A high ratio of dietary animal to vegetable protein increases the rate of bone loss and the risk of fracture in postmenopausal women. Study of Osteoporotic Fractures Research Group." Am J Clin Nutr (2001) vol. 73 (1) pp. 118-22

«The intake of 'acid' is a way of everyday life, and it is known that animal proteins and cereals are rich sources of H3PO4 and H2SO4 and are recognised as 'acid-ash' foods (Barzel & Massey, 1998; Heaney, 1998). The net production of acid is related to nutrition, and there is a gross quantitative relationship between the amount of acid produced (as reflected by urine pH) and the amount of acid-ash consumed in the diet. […] Thus, consideration of a diet consisting of large quantities of fruit and vegetables (hence favouring 'alkaline-ash') may be important for bone health maintenance (Barzel, 1995).»

— New SA. "Nutrition Society Medal lecture. The role of the skeleton in acid-base homeostasis." Proc Nutr Soc (2002) vol. 61 (2) pp. 151-64

«Phosphate is considered to be the major dietary source of acid [2]. Many foods in the modern diet are considered detrimental to bone health, under the acid-ash hypothesis, due partially to their phosphate contents. These foods include meats, fish, dairy products [2,5-10], and grains [3,4,10], as well as many processed foods [3,4,10]. In contrast, this hypothesis posits that sodium is protective of bone health, which is not in agreement with concerns that sodium may compete with calcium for resorption in the kidney, and thus may compromise calcium metabolism and bone health [11,12]. The foods that are considered to protect skeletal mineral under this hypothesis are fruit and vegetables since these foods supply organic molecules that are metabolized to bicarbonate and therefore are considered "alkaline" [2-4,10,13,14].
The acid-ash hypothesis posits that meats, grains and dairy products are detrimental to bone health due to their phosphate contents [16,3,4,10], however, this meta-analysis revealed that higher dietary intakes of phosphate do not increase either urinary calcium excretion or whole body calcium loss. Further to question the acid ash hypothesis, the evidence regarding higher net acid excretion from changes in dietary protein type or amount does not support the hypothesis [20]. No studies have evaluated the effect of grain foods on bone health. Dairy products, an important source of dietary phosphate, are also an important dietary calcium source [80] and an inexpensive source of high quality protein. Protein has been found to be supportive of bone health in a prospective cohort study and a randomized controlled trial [77,78]. Considering that this study has not upheld the concept that higher intakes of phosphate are detrimental to bone mineral maintenance, the consideration of meats, grains and dairy products as detrimental to bone health on the basis of their phosphate content must be questioned. Additionally, these foods that produce acid on metabolism are important sources of nutrients that are important for bone health, including calcium [81] (dairy products), protein [82,83] (dairy products and meats), and vitamin D [84] (some dairy products).»

— Fenton TR et al. "Phosphate decreases urine calcium and increases calcium balance: a meta-analysis of the osteoporosis acid-ash diet hypothesis." Nut J (2009 Sep 15) 8:412009 Sep 15;8:41 DOI: 10.1186/1475-2891-8-41

«Urine pH has been thought to be an important factor that can modulate kidney stone formation. Nevertheless, there was no systematic evaluation of such pH effect. Our present study thus addressed effects of differential urine pH (4.0–8.0) on calcium oxalate (CaOx) crystallization, crystal-cell adhesion, crystal internalization into renal tubular cells, and binding of apical membrane proteins to the crystals. Microscopic examination revealed that CaOx monohydrate (COM), the pathogenic form, was crystallized with greatest size, number and total mass at pH 4.0 and least crystallized at pH 8.0, whereas COD was crystallized with the vice versa order. […] We concluded that the acidic urine pH may promote CaOx kidney stone formation, whereas the basic urine pH (i.e. by alkalinization) may help to prevent CaOx kidney stone disease.»

— Manissorn J et al. "Systematic evaluation for effects of urine pH on calcium oxalate crystallization, crystal-cell adhesion and internalization into renal tubular cells." Sci Rep (2017 May 11) vol. 7 (1) art. 1798 DOI: 10.1038/s41598-017-01953-4

«We evaluated the crystallization of calcium oxalate (CaOx) in undiluted urine, collected 3 hours after intake of a test meal by healthy males. In two experiments in vitro, either the total citrate concentration was increased (urine A) or the pH was elevated (urine B). In addition, in three clinical trials, the bioequivalence of orally taken potassium citrate (PC) and potassium-sodium citrate (PSC) (n = 9), and the dose-response effects of oral PC (n = 8) and oral calcium-sodium citrate (CSC; n = 8) were studied. Elevation of urinary citrate (urine A) decreased CaOx crystallization (nucleation, growth, agglomeration time), and increased the calcium and citrate content of the crystallized mass; elevation of urinary pH (urine B) also suppressed CaOx crystallization, the calculated molar ratio ionized citrate/ionized calcium at pH 7 was about twice the value observed at pH 5.5, and the ratio complexed citrate/complexed calcium was low. PC and PSC inhibited CaOx crystallization to a similar extent. CSC increased crystal growth but left agglomeration time unchanged. The urinary molar ratio (total calcium/total citrate) appeared to be directly related to the CaOx crystal growth rate.

We concluded that: (1) changes in urine pH, citrate, and calcium are reflected by CaOx crystallization; (2) free citrate and a calcium citrate complex (stoichiometry ≤ 1:1) inhibit CaOx crystallization; (3) in individuals taking PC, PSC or CSC, the renal stone risk may be characterized using the presented CaOx crystallization test and the urinary calcium/citrate ratio.»

— Fan J et al. "Calcium Oxalate Crystallization in Undiluted Urine of Healthy Males: In Vitro and in Vivo Effects of Various Citrate Compounds." Scanning Microsc (1999) vol. 13 (2-3) pp. 307-20

«The risk of calcium oxalate (CaOx) crystallization at different pH levels was determined in urine from recurrent CaOx-stone formers and normal subjects. The highest crystallization risk was observed between pH 4.5 and 5.5. In the pH range 6.5-7.5, there was a marked increase in crystallization of calcium phosphate (CaP). The results suggest the beneficial effect of moderate alkalinization in terms of a reduced CaOx crystallization. Reduced CaOx crystallization occurs at the expense of an increased formation of CaP crystals. Whether this increases the risk of CaP-stone formation is not known, but the CaP crystals were usually small, at least below pH 7.5.»

— Berg C, Tiselius HG. "The effect of pH on the risk of calcium oxalate crystallization in urine." Eur Urol (1986) vol. 12 (1) pp. 59-61

As for the alleged deleterious effects of vitamin C supplementation (a warning recurrently parroted by some of the panelists):

• Juraschek SP et al. "Effect of oral vitamin C supplementation on serum uric acid: a meta-analysis of randomized controlled trials." Arthritis Care Res (Hoboken) (2011) vol. 63 (9) pp. 1295-306

Vitamin C supplementation has been linked to higher predisposition to kidney stones (although not everybody agrees, see below), particularly in diets which are already abundant in oxalate and in people who are prone to form kidney stones:

• Thomas LD, Elinder CG, Tiselius HG et al. "Ascorbic acid supplements and kidney stone incidence among men: a prospective study." JAMA Intern Med (2013 Mar 11) vol. 173 (5) pp. 386-8 DOI: 10.1001/jamainternmed.2013.2296
Press release:

• Assimos DG. "Vitamin C Supplementation and Urinary Oxalate Excretion." Rev Urol (2004 Summer) vol. 6 (3) p. 167

"What Really Causes Kidney Stones (And Why Vitamin C Does Not)." Orthomolecular Medicine News Service (2013 Feb 11)

• Robert S. "Cardiologist Says Vitamin C Will Damage Kidney." Vitamin C Foundation Discussion Forum (2006 Jan 15)

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Vitamin supplementation, myths and facts (introduction)

Swayze Foster [15:54]: "And it's not even a vegan issue at that point. Again, a lot of people should be taking B-12, a lot of people should be taking vitamin D, and the thought that they're not because they're worried that it's going to hurt their liver,…"

— Swayze Foster. "Blaire White: Quitting vegan is your choice, but please stop spreading lies". Unnatural Vegan's YouTube channel (2008-04-02)

— Now you could make a further video correcting your "skeptic" friends at The Skeptics' Guide to the Universe (I'm dead serious, that's a widespread belief among self-proclaimed "skeptics"):

Steve Novella [15:20]: «Yeah, that's evidence-based targeted supplementation based on lab values, yeah, for known conditions, like pregnant women or trying to get pregnant taking folic acid, yeah. But vitamin supplementation, there's no evidence for it.»

— Steven Novella et al. News Item: "Vitamin C Myth." The Skeptics' Guide to the Universe (2018-03-31) ep. 664

[b]Swayze Foster[/b] [15:54]: [i]«And it's not even a vegan issue at that point. Again, a lot of people should be taking B-12, a lot of people should be taking vitamin D, and the thought that they're not because they're worried that it's going to hurt their liver,…»[/i]

— Swayze Foster. [b]"Blaire White: Quitting vegan is your choice, but please stop spreading lies".[/b] [i]Unnatural Vegan's YouTube channel (2008-04-02)[/i]

— Now you could make a further video correcting your "skeptic" friends at The Skeptics' Guide to the Universe (I'm dead serious, that's a widespread belief among self-proclaimed "skeptics"):

[b]Steve Novella[/b] [15:20]: [i]«Yeah, that's evidence-based targeted supplementation based on lab values, yeah, for known conditions, like pregnant women or trying to get pregnant taking folic acid, yeah. But vitamin supplementation, there's no evidence for it.»[/i]

— Steven Novella [i]et al.[/i] News Item: [b]"Vitamin C Myth."[/b] [i]The Skeptics' Guide to the Universe (2018-03-31) ep. 664[/i]

— Skeptics Guide to the Universe Forums» The Skeptics' Guide to the Universe» Podcast Episodes» Topic: Episode #664
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It Is Not "Dinosaur Juice"

Petroleum (crude oil) derives from marine and lacustrine organic sediments, mostly phytoplankton and zooplankton and some land vegetation:

• Jack Horner, Chris Pratt (guests), Michael Stevens (host). "Jurassic World Science feat. Chris Pratt and Jack Horner." Vsauce (June 17, 2015) [at 3:26]

«It is now well documented that practically all petroleum originates from the decomposition of organic matter in marine and lacustrine sediments of the earth's crust.»

— Hunt JM. "Generation and migration of light hydrocarbons." Science (1984) vol. 226 (4680) pp. 1265-70

«Current models suggest that the dominant form of organic matter responsible for the formation of petroleum and synthesis of crude oil is derived from microscopic, photosynthetic organisms known as phytoplankton that live at or near the surface of lakes and oceans. Associated with the phytoplankton are their microscopic predators known as zooplankton. These, together with land vegetation washed into lake or near shore marine sediments, accumulate over a period of millions of years.»

«Oil is formed when microorganisms accumulate at the bottom of the sea where oxygen is limited. There it is chemically transformed anaerobically into oil and gas by a process called maturation.
Petroleum (crude oil) is a fossil fuel produced by the decomposition of deeply buried dead organic matter from plants and animals under high temperatures and pressures over millions of years.
103. Petroleum forms from: microscopic aquatic organisms in sediments converted by heat & pressure into a mixture of hydrocarbons
Petroleum (Crude Oil) Formation: microscopic aquatic organisms in sediments converted by heat & pressure into a mixture of hydrocarbons.»

«Chapter 15

How do we think that oil and natural gas are formed? How can these substances be extracted from the seabed? Why are the physical characteristics of the surrounding rock important?

Petroleum is almost always associated with marine sediments, suggesting that the organic substances from which it was formed were once marine. Planktonic organisms, and masses of bacteria are the most likely candidates. Their bodies apparently accumulated in quiet basins where the oxygen supply was low and there were few bottom scavengers. The action of anaerobic bacteria converted the original tissues into simpler, relatively insoluble organic compounds that were probably buried—possibly first by turbidity currents, then later by the continuous fall of sediments from the ocean above. Further conversion of the hydrocarbons by high temperatures and pressures must have taken place at considerable depth, probably 2 kilometers (1.2 miles) or more beneath the surface of the ocean floor. Slow cooking under this thick sedimentary blanket for millions of years completed the chemical changes that produce oil.

Oil is less dense than its surrounding sediments, so it can migrate toward the surface from its source rock through porous overlying formations. It collects in the pore spaces of reservoir rocks when an impermeable overlying layer prevents further upward migration of the oil. When searching for oil, geologists use sound reflected off subsurface structures to look for the signature combination of layered sediments, depth, and reservoir structure before they drill.»

« Question #14: Were there any swimming dinosaurs?
Answer: No dinosaurs were adapted to an entirely aquatic life, although some may have gone into the water to get prey. Baryonyx, for example, was found with fossilized fish scales in its stomach.»
enchantedlearning. com/subjects/dinosaurs/questions/faq/Swimming.shtml

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The Kantian Universalisability Principle Fallacy

Steven Novella [1:08:56]: "[A]nd if you want to favor farming that uses no pesticides then, frankly, you are a privileged elitist who doesn't care if half the world starves because there's absolutely no way we can feed the world without using pesticides, period."

"Your Questions and E-mails: GMOs and Glyphosate." The Skeptics' Guide to the Universe (2018-02-10) ep. 657 [96 min]

— The Kantian universalisability principle fallacy: If everyone became an MD like Steve, the world would starve to death. If everyone were consuming as much meat as Steve, there wouldn't be enough farming land to feed the world. If everyone lived in a single-family detached home with a large garden like Steve, the world would run out of arable land. If everyone installed solar panels on the roof of their home like Steve, the world would generate a lot of excess power when sunny and not enough during the night and the darker hours of the day or when cloudy. If everyone went on vacation to Hawaii like Steve, the world would ruin Hawaii.

«I fully reject the Kantian universalizability principle that underlies so much of contemporary moral discussion. What if everyone acted the way you did? is not a useful means-test for one’s actions.»

— Michael Malice. "Why I won't vote this year – or any year." The Guardian (2014-10-14)

"The big criticism of Mike Pence's rule about being alone with women stems from a quintessential left-wing idea that one's behavior must be universalizable."
— Michael Malice (2017-11-17)

• Michael Malice (guest), Steve Patterson (host). "Egoism, Religion, Ayn Rand | Michael Malice." Patterson in Pursuit (2016-05-22) ep. 7 [57 min]

• Michael Malice (guest), Thomas E Woods Jr (host). "Voting: Yes or No?" The Tom Woods Show (2016-06-10) ep. 679 [42 min]

• Michael Malice (guest), Thomas E Woods Jr (host). "Rothbard v. Rand? Michael Malice and Tom Discuss." The Tom Woods Show (2017-01-05) ep. 818 [37 min]

• Michael Malice (guest), Thomas E Woods Jr (host). "The Real Reason Libertarians Don’t Matter in Politics?" The Tom Woods Show (2016-10-18) ep. 761 [29 min]

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"'Sinking' Pacific nation is getting bigger: study." (2018-02-09)

Three and four years ago I suggested a similar process:

Zephyr López Cervilla Jan 27, 2015
A question that I've never seen to have been addressed is the effect of sea level rise on the settlement of coastal and river sediments. I would expect a shift of the process upstream as a result of a precocious slowing of the velocity of the river flow. The slower the flow, the greater the amount of sediments that will settle.

Likewise, every flooding event would tend to pile more sediment deposits in the flooded areas as a result of a slower drainage, or alternatively, the flooded areas would extend upstream and more sediments would settle there.

This effect would be expected to be particularly relevant in deltas, such as the case of the Ganges Delta and upstream basin:

This process would explain how the present delta formed during or after the sea level rise that occurred at the end of the last glacial period and subsequent post-glacial period:

<< The lower "figure shows sea level rise since the end of the last glacial episode based on data from Fleming et al. 1998, Fleming 2000, & Milne et al. 2005."[7]

"[A]t least one episode of rapid deglaciation, known as meltwater pulse 1A, is agreed upon and indicated on the plot. A variety of other accelerated periods of deglaciation have been proposed (i.e. MWP-1B, 2, 3, 4), but it is unclear if these actually occurred or merely reflect misinterpretation of difficult measurements. No other events are evident in the data presented above."[7]

"The lowest point of sea level during the last glaciation is not well constrained by observations (shown here as a dashed curve), but is generally argued to be approximately 130 +/- 10 m below present sea level and to have occurred at approximately 22 +/- 3 thousand years ago. The time of lowest sea level is more or less equivalent to the last glacial maximum. Prior to this time, ice sheets were still increasing in size so that sea level was decreasing almost continuously over a period of approximately 100,000 years."[7] >>

Presumably, 22 thousand years ago the coastal deltas would be found at about 130 metres below present sea level. As sea level began to rise, the coastal deltas moved upstream, filling up with sediments the lower stretches of river basins.

According to the lower graphic, between 8 thousand and 7 years ago, the sea level rise would have been of about 10 m, that's about one-meter rise per century. Did the coastal deltas regenerate at that pace? And the lower stretch of the river basins, were they filled with sediments at similar pace? This question could be answered by determining the age of the sediments at different depths and comparing it with the estimated sea level over that period.

I expect that if the sea level continues to rise, such process will occur in some extent over the next decades and centuries, whose intensity will be dependent (among other factors) on the amount of sediments carried by the flow of each river.

If so, the land of coastal river deltas and nearby basins that is presently occupied by millions of people would progressively be covered by a layer of river sediments, thus countering at least partially the sinking of that land with respect to sea level.

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sophie helfrich Oct 23, 2013
+Zephyr López Cervilla I feel so much better now! Tons of sediments driven by the Rhin will save the netherlanders from the sea. Or maybe our friends the sediments will stay for a while in these charming towns they have in Switzerland and Germany? If you have some other link showing how frequent collapse of industrial building in Dacca will save Bangladesh from permanent flood, please, let me know.
So, don't think I feel boried by this conversation, but I have a shovel to buy, in the very unlikely hypothesis of lost sediments invading my basement instead of going to Rotterdam.

Zephyr López Cervilla Oct 24, 2013
+sophie helfrich: "Tons of sediments driven by the Rhin will save the netherlanders from the sea."

— The reason why sealevel along the coast of Netherlands isn't expected to rise significantly isn't related to river sediments. It's caused by local factors and the effect is spread along all North Sea (as well as other areas).

As for the river sediments, in my opinion, those sediments would limit the loss of land area in those areas where the sea level would rise, such as in countries like Bangladesh (thanks to the sediments coming from the Ganges river).

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Zephyr López Cervilla Sep 23, 2013
Clearly, that extrapolation on the population affected by the sea level rose hasn't taken into account the effect of sedimentation on the coastline, estuaries and deltas. In many of those areas people won't have to move anywhere else because the land will be progressively covered with a layer of lime/mud/sand, thus effectively rising the height of the land surface above sea level.

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Lactase Persistence & Amylase Gene Copy Number

"Lactose tolerance" (lactase persistence) isn't a recessive trait. Yet, there're several variants which are regional population-specific:

«The ability of adult humans to digest the milk sugar lactose - lactase persistence - is a dominant Mendelian trait that has been a subject of extensive genetic, medical and evolutionary research. Lactase persistence is common in people of European ancestry as well as some African, Middle Eastern and Southern Asian groups, but is rare or absent elsewhere in the world. The recent identification of independent nucleotide changes that are strongly associated with lactase persistence in different populations worldwide has led to the possibility of genetic tests for the trait.»

— Itan Y et al. "A worldwide correlation of lactase persistence phenotype and genotypes." BMC Evol Biol (2010 Feb 9) vol. 10 art. 36
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«Lactase persistence is one of the clearest examples of niche construction in humans. Lactase is the enzyme responsible for the digestion of the milk sugar lactose and its production decreases after the weaning phase in most mammals, including most humans. Some humans, however, continue to produce lactase throughout adulthood, a trait known as lactase persistence. In European populations, a single mutation (-13910*T) explains the distribution of the phenotype, whereas several mutations are associated with it in Africa and the Middle East. Current estimates for the age of lactase persistence-associated alleles bracket those for the origins of animal domestication and the culturally transmitted practice of dairying.»

— Gerbault P et al. "Evolution of lactase persistence: an example of human niche construction." Philos Trans R Soc Lond B Biol Sci ( 2011 Mar 27) vol. 366 (1566) pp. 863-77

«The expression of the lactase enzyme (MIM 603202) in intestinal cells dramatically declines after weaning in mammals, when lactose is no longer an essential part of their diet.[1] In humans, this normal mammalian condition known as “lactase nonpersistence” (LNP, also known as “adult-type hypolactasia” or “lactose intolerance” [MIM 223100]) affects most of mankind and restricts the consumption of fresh milk among adults. However, among northern Europeans and a few other ethnic populations, intestinal lactase activity persists throughout life in a substantial proportion (up to 80%–90%) of adults, a condition known as lactase persistence (LP, or lactose tolerance [MIM 223100]). The LP/LNP phenotype is genetically determined, with LP being dominant over LNP.[2]»

— Enattah NS et al. "Evidence of still-ongoing convergence evolution of the lactase persistence T-13910 alleles in humans." Am J Hum Genet (2007 Sep) vol. 81(3) pp. 615-25

«Large differences in this genetic trait exist between populations in Africa and the Middle-East on the one hand, and European populations on the other; this is thought to be due to evolutionary pressures exerted by consumption of dairy products in Neolithic populations in Europe. In this study, we have investigated lactase persistence of 26 out of 46 individuals from Late Neolithic through analysis of ancient South-West European DNA samples, obtained from two burials in the Basque Country originating from 5000 to 4500 YBP. This investigation revealed that these populations had an average frequency of lactase persistence of 27%, much lower than in the modern Basque population, which is compatible with the concept that Neolithic and post-Neolithic evolutionary pressures by cattle domestication and consumption of dairy products led to high lactase persistence in Southern European populations.»

— Plantinga TS et al. "Low prevalence of lactase persistence in Neolithic South-West Europe." Eur J Hum Genet (2012 Jul) vol. 20 (7) pp. 778-82
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A further example is the gene copy number of the gene o genes that encode for the amylase enzyme. Humans whose ancestors had been agriculturalists for millennia have more copies of those genes in their genome than humans of some populations of traditional pastoralists and hunters and gatherers of non-arid environments (who usually consume much smaller amounts of starches than the individuals from hunter-gatherer populations living in arid environments). And so it happens with dogs. The specimens of some dog breeds have more copies of amylase genes than those of other dog breeds and dogs more than wolves. Isn't perhaps that kind of gene duplication an example of an evolutionary adaptation by the effect of environmental pressures?

«Starch consumption is a prominent characteristic of agricultural societies and hunter-gatherers in arid environments. In contrast, rainforest and circum-arctic hunter-gatherers and some pastoralists consume much less starch. This behavioral variation raises the possibility that different selective pressures have acted on amylase, the enzyme responsible for starch hydrolysis. We found that copy number of the salivary amylase gene (AMY1) is correlated positively with salivary amylase protein level and that individuals from populations with high-starch diets have, on average, more AMY1 copies than those with traditionally low-starch diets. Comparisons with other loci in a subset of these populations suggest that the extent of AMY1 copy number differentiation is highly unusual. This example of positive selection on a copy number-variable gene is, to our knowledge, one of the first discovered in the human genome. Higher AMY1 copy numbers and protein levels probably improve the digestion of starchy foods and may buffer against the fitness-reducing effects of intestinal disease.»

— Perry GH et al. "Diet and the evolution of human amylase gene copy number variation." Nat Genet (2007 Oct) vol. 39 (10) pp. 1256-60

«Prior to the advent of modern dog-feeding practices, there was likely substantial variation in dietary landscapes among disparate dog breeds. As such, we investigated one type of genetic variant, copy number variation, in three metabolic genes: glucokinase regulatory protein (GCKR), phytanol-CoA 2-hydroxylase (PHYH), and pancreatic α-amylase 2B (AMY2B). These genes code for proteins that are responsible for metabolizing dietary products that originate from distinctly different food types: sugar, meat, and starch, respectively. After surveying copy number variation among dogs with diverse dietary histories, we found no correlation between diet and positive selection in either GCKR or PHYH. Although it has been previously demonstrated that dogs experienced a copy number increase in AMY2B relative to wolves during or after the dog domestication process, we demonstrate that positive selection continued to act on amylase copy number in dog breeds that consumed starch-rich diets in time periods after domestication. Furthermore, we found that introgression with wolves is not responsible for deterioration of positive selection on AMY2B among diverse dog breeds. Together, this supports the hypothesis that the amylase copy number expansion is found universally in dogs.»

— Reiter T et al. "Dietary Variation and Evolution of Gene Copy Number among Dog Breeds." PLoS One (2016 Feb 10) vol. 11 (2) art. e0148899

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