23.1.18

L'eccellenza in arancione. Ecco i 227 superborghi d'Italia - Repubblica.it

http://www.repubblica.it/viaggi/2018/01/22/news/vent_anni_di_bandiere_arancioni_ecco_i_nuovi_borghi_scelti_dal_touring-187021111/

Viaggi
L'eccellenza in arancione. Ecco i 227 superborghi d'Italia

Da Gressoney a Opi, sono 19 le new entry nell'edizione 2018 dell'iniziativa firmata Touring Club. La Toscana guida la graduatoria per regioni delle piccole realtà premiate per il loro impegno nel preservare bellezza e tradizioni. E grazie al riconoscimento i villaggi si ripopolano
di GIACOMO TALIGNANI
22 Gennaio 2018

Nelle "Terre della resilienza" sono tornati i giovani. Lì, nel piccolo borgo di Morigerati, 70 anime immerse nel Parco Nazionale del Cilento e Vallo di Diano, i ragazzi dopo gli studi universitari sono tornati a casa e con agricoltura sociale, produzione di cibo locale, offerta di escursioni sul dorso di asini e trekking in mezzo alla natura hanno fermato lo spopolamento e rilanciato il turismo. Dal 2011, da quando Morigerati è una bandiera arancione, gli arrivi turistici sono aumentati del 68%, dando speranza e futuro.

Quello che è accaduto in questo piccolo centro è solo uno dei tanti esempi di "buone pratiche" premiate ogni tre anni dal Touring Club Italia che dal 1998, da un'idea nata in Liguria, insignisce con le sue bandiere arancioni i borghi più virtuosi, belli e culturalmente impegnati a preservare i loro territori in tutta Italia.

Quest'anno, a 20 anni dalla nascita dell'iniziativa, il Touring ha scelto 19 nuove bandiere (annunciate oggi) tra centinaia di candidature arrivate da tutte le regioni: siamo così a 227 borghi "arancioni" nell'intero Stivale. Il programma, va ricordato, è dedicato ai comuni con meno di 15mila abitanti e l'obiettivo delle "bandiere" è quello di aiutare la valorizzazione dell'entroterra, del suo paesaggio, storia e delle tipicità apportando un miglioramento nell'economia e nel turismo del luogo.

Ogni tre anni il Touring, con un "costante monitoraggio della qualità dell'offerta turistica", aggiorna la sua lista ampliandola e verificando se i comuni mantengono gli standard richiesti: negli ultimi 20 anni, su oltre 2.800 candidature, solo l'8% ha ottenuto il riconoscimento ma quelli premiati hanno avuto benefici importanti come il + 45% degli arrivi turistici e il + 83% di strutture ricettive (in media dall'anno di assegnazione).
San Vito al Tagliamento (Friuli Venezia Giulia)

I PIÙ PREMIATI - Ad oggi, a guidare la classifica dei più arancioni d'Italia c'è la Toscana (con 38 riconoscimenti), seguita da Piemonte (28) e dalle Marche (21). Gli esempi dei borghi che hanno saputo rilanciarsi sono tanti e tutti carichi di idee e iniziative, come quello medievale di Monteriggioni, certificato dal 2004, che con il suo Slow Travel Fest racconta il viaggiare lento; o come Civita, 900 abitanti, che in sette anni dal riconoscimento ha visto un incremento dell'80% dell'offerta turistica nonostante la Calabria sia nelle basse posizioni della classifica Touring (15esima). E poi c'è ad esempio Airole, 400 cittadini, borgo ligure dove vivono tanti stranieri come olandesi, tedeschi e francesi che hanno fatto della multiculturalità un sistema per rilanciare turismo e occupazione.

I NUOVI BORGHI - Sono 19 i nuovi borghi arancioni annunciati nel 2018 e fra le regioni spiccano Piemonte (quattro comuni), Lombardia e Abruzzo (tre ciascuno). Ci sono luoghi come Gressoney Saint Jean (AO) capace di proporre il suo Castel Savoia, dimora estiva della regina Margherita, passeggiate meravigliose lungo valli dove si degusta la Toma di Gressoney o il violino di capra, salume tipico della zona.

Oppure realtà come San Vito al Tagliamento e la sua Piazza del Popolo carica di storia, o Bellano, sulle sponde del Lago di Como, che con la sua gola naturale "Orrido" attira i visitatori per un viaggio fra marmitte e suggestive spelonche. E ancora la Chiusa di Pesio e le sue colline ricoperte di castagni secolari oppure Ozzano Monferrato e le sue tradizioni gastronomiche e artigianali locali, come i biciulant d'ausan, dolce del periodo pasquale, e il ricamo a chiacchierino; e infine l'Aliano descritta in "Cristo si è fermato a Eboli" da Carlo Levi.

TUTTI I BORGHI - Gressoney Saint Jean (AO), Agliè (TO), Chiusa di Pesio (CN), Gavi (AL), Ozzano Monferrato (AL), Almenno San Bartolomeo (BG), Bellano (LC), Pizzighettone (CR), Maniago (PN), San Vito al Tagliamento (PN), Santa Fiora (GR), Frontino (PU), Serra San Quirico (AN), Fara San Martino (CH), Lama dei Peligni (CH), Opi (AQ), Aliano (MT), Oriolo (CS), Taverna (CZ).

    

21.1.18

Il devastante impatto dello smartphone su un’intera generazione di bambini – Business Insider Italia

Il devastante impatto dello smartphone su un'intera generazione di bambini – Business Insider Italia

Il devastante impatto dello smartphone su un'intera generazione di bambini

In quanto ricercatore nel campo delle differenze tra generazioni, noto come la domanda più frequente che mi viene posta è: "Di quale generazione sono?"

Se foste nati prima del 1980, sarebbe una risposta relativamente facile: la Silent Generation era quella dei nati tra il 1925 e il 1945; i Baby Boomers dal 1946 al 1964; seguite dalla Generazione X (nati tra il 1965 e il 1979).

Dopodiché sono arrivati i Millennials, cioè i nati dopo il 1980. Dove finiscono i Millennial, e dove inizia una nuova generazione? Fino a poco tempo fa pensavo (e con me molti altri) che la data più tarda per i Millennial potesse essere il 1999 – ovvero i diciottenni di oggi.

Questa convinzione è però cambiata pochi anni fa, quando ho iniziato a notare grandi cambiamenti nel comportamento e nelle attitudini degli adolescenti, durante le ricerche annuali che conduco su 11 milioni di giovani. Intorno al 2010, i ragazzini hanno iniziato a passare il loro tempo in modo molto diverso dalle generazioni precedenti. Dopodiché, dal 2012 sono improvvisamente comparsi dei cambiamenti nel loro benessere mentale.

Leggi anche: 'Lo smartphone? È come l'automobile: non si può usare a qualsiasi età': parola di psicologa

Questi cambiamenti indicavano un passaggio generazionale avvenuto intorno al 1995, il che significava che alcuni ragazzini di questa generazione nuova, post Millennial, erano già all'università.

Tutti questi ragazzini o giovani adulti hanno una cosa in comune: la loro infanzia e adolescenza sono state corrispondenti alla comparsa dello smartphone.

Cosa rende diversa la iGen

Qualcuno li chiama Generazione Z, ma senza la Y, che dovrebbero essere i Millennial, la Z non ci sta. Neil Howe, che ha coniato il termine Millennial con il suo collaboratore William Strauss, ha proposto che questa ultima generazione sia chiamata Homeland Generation, anche se dubito che qualcuno voglia sentirsi chiamare come un'agenzia governativa (la Homeland Security ndr).

Un'indagine del 2015 ha rivelato che due adolescenti americani su tre posseggono un iPhone. È per questa ragione che li ho chiamati iGen. Come ho spiegato nel mio libro "iGen: Why Today's Super-Connected Kids are Growing up Less Rebellious, More Tolerant, Less Happy – and Completely Unprepared for Adulthood," questa è la prima generazione a passare la propria adolescenza su uno smartphone.

Cosa rende diversa la iGen? Ogni aspetto della loro vita è stato influenzato dall'essere cresciuti con uno smartphone. Nelle vaste indagini analizzate per il mio libro ho potuto vedere come abbiano passato molto tempo su internet, 'messaggiando' con gli amici o sui social, per una media di sei ore al giorno, così da avere poco tempo libero per qualsiasi altra cosa.

Leggi anche: La tecnologia ci rende più stupidi individualmente e più intelligenti collettivamente

Come, ad esempio, andare in giro con gli amici, un tempo attività tra le preferite dai ragazzi. Che si tratti di andare a una festa, o in un centro commerciale, guardare un film, o girare senza meta, i ragazzi iGen partecipano alle attività sociali in misura molto minore dei loro predecessori Millennial.

Gli iGen mostrano altre notevoli differenze con i Millennial: dal 2012, la depressione, l'ansia e la solitudine sono schizzate verso l'alto, mentre la felicità diminuiva.

Il tasso di suicidi è aumentato di oltre il 50%, così come il numero di adolescenti con depressione a livelli patologici.

Una relazione che non può essere ignorata

Mi sono chiesta se queste tendenze – i cambiamenti di come i giovani passano il loro tempo libero, e la loro salute mentale in decadimento – fossero in relazione.

I giovani che passano più tempo sugli schermi sono meno felici e più depressi, e quelli che passano il loro tempo con gli amici sono più felici e meno depressi, ho riscontrato con una certa sicurezza.

Naturalmente, la relazione non dimostra la causa: forse sono gli infelici a usare di più tablet e smartphone.

L'uso dei social media è stato messo in relazione all'infelicità. AGF

Comunque, come ho descritto nel mio libro, ho saputo di tre studi che hanno eliminato questa possibilità, almeno per ciò che riguarda i social media. In due di questi, si esaminava come l'uso dei social media porti a un minor benessere, mentre un minor benessere non porta all'uso dei social media.

Leggi anche: Clash Royale & Co., allarme del Garante per l'infanzia: 'Un Far West senza regole'. Ecco chi guadagna sulla pelle dei bambini

Nel frattempo, nel corso di un'altra ricerca del 2016, era stato chiesto a degli adulti di non usare Facebook per una settimana, mentre altri avrebbero continuato. Chi si era tenuto lontano dal social network aveva finito la settimana più sereno, meno solo e meno depresso.

Cos'altro si è perso?

Molti genitori potrebbero preoccuparsi che i ragazzi passino così tanto tempo sul telefono, perché ciò rappresenta una rottura radicale con la loro adolescenza di un tempo. Stare tutto questo tempo sugli schermi non è però solo diverso: è davvero peggiore, e in molti modi.

Stare meno tempo con gli amici significa sviluppare meno attitudine alla socialità. Uno studio del 2014 ha verificato come ragazzini tra gli 11 e i 12 anni che avevano frequentato un campeggio senza usare gli schermi mostravano una maggiore capacità di leggere le emozioni sui volti altrui, indicando come le vite sature di tablet e smartphone degli iGen potrebbero atrofizzare la loro socialità.

Inoltre, gli iGen leggono libri, riviste e giornali in misura molto minore di quanto le generazioni precedenti facessero in gioventù: nell'indagine annuale Monitoring the Future, la percentuale di liceali degli ultimi anni che avessero letto autonomamente un libro o una rivista quasi ogni giorno era crollata dal 60% del 1980 al 16% del 2015. Come risultato probabile di questo calo, dal 2005 la media SAT del punteggio relativo alla lettura è calata di 14 punti. Ho saputo da ambienti universitari come gli studenti hanno difficoltà a leggere periodi lunghi, e raramente affrontano il libro di testo previsto.

Non voglio certo dire che ci sia poco da fare, per i giovani iGen. Sono fisicamente più sicuri e protetti, e più tolleranti delle generazioni precedenti. Sembrano inoltre avere una più forte etica del lavoro, e attese più realistiche di quanto i Millennials mostrassero alla loro età. Lo smartphone minaccia però di farli deragliare ancora prima della partenza.

Per essere chiari, un uso moderato dello smartphone e dei social media – fino a un'ora al giorno – non causa problemi di salute mentale. Tuttavia molti ragazzi (e adulti) passano molto più tempo sul loro telefono di quanto dovrebbero.

Con una mia certa sorpresa, i giovani iGen che ho intervistato mi hanno detto che  piuttosto che comunicare via telefono vorrebbero vedere i loro amici di persona.

I genitori tendono a preoccuparsi se i loro figli passano troppo tempo con gli amici – come fosse una distrazione, o un'esposizione al rischio di cattive compagnie o una perdita di tempo. Potrebbe invece essere ciò di cui gli iGen hanno bisogno.

* Professore di psicologia, San Diego State University.

Questo articolo è tradotto da The ConversationPer leggerlo in lingua originale vai qui

20.1.18

The most ignored causes when your results are lacking – Part 1: Stress – Borge Fagerli

The most ignored causes when your results are lacking – Part 1: Stress – Borge Fagerli

The most ignored causes when your results are lacking – Part 1: Stress

Today, it's becoming increasingly trendy to throw around the term "living a balanced lifestyle" without actually defining it properly. It shouldn't imply an incessant glorification of "YOLO" where you one moment are rushing through a Crossfit-WOD so intense that you're bleeding out of your ears, and in the next you're throwing up brownies and tequila after being smashed out of your mind all weekend.

Facetous, I know, but it isn't too far from what I see these days in the fitness sphere.

This a major improvement from eating broccoli, rice and dry chicken six times a day and otherwise trying to find The Optimal Program, but the pendulum tends to swing a little too far in the other direction sometimes.

I'm probably one of the (if not the biggest) defenders of a lifestyle-based approach, but when something doesn't work as expected, we also tend to blame single factors.

The wrong exercise or execution of it, low carb or sugar, saturated fat or vegetable oils, heavy metals in food, parabens in plastic and cosmetics, stress during the week, stress during the weekend, stress during Christmas or Eastern holidays….

How can I handle all that family time and its mandatory feasting, without ending up as an audience favorite of The Biggest Loser contest?

The answer: There is no single solution or prescription that is going to make your life perfect.

In the middle of all of this, you should ask yourself: What is perfect? And who gets to decide the definition of perfect? And why do you change the definition the closer you get to it?

It all ends up with you spending your life chasing something you'll never achieve because you don't know what it means or because you always change the definition of it.

There's a reason why people who focus on the process itself have higher self-confidence and achieve better results than people who are goal-oriented. 

Unfortunately, I'm not going to give you to the recipe on how to be happy in this article, but watch this TED-talk for some pointers – and I will tell you something about how your lifestyle and how your APPROACH to this lifestyle can affect you.

Stress – Negative, but Not for Everyone, All the Time

The effect of stress on recovery is more comprehensive than you think. When you live a very stressful life, you'll die sooner – let's start there. Intuitively, you know this, but you're most likely underestimating this effect.

Cortisol is one of the primary stress hormones, which influences the effect of many other hormones. This is especially apparent through symptoms like chronic fatigue syndrome/ME, exhaustion and post-traumatic stress syndrome (PTSD). We think of these as psychological phenomena, but chronically increased cortisol can disturb the central regulation of other types of hormones, that will affect your whole body.

Somewhat of a chicken-or-egg paradox going on here, but cortisol can be said to be the primary link between your psychology and your physiology.

Stress and Training Results

Hollander et al. (2013) did a study on the effect of academic stress among students. The students who were extremely stressed increased their leg press less than the ones who weren't experiencing as much stress.

The extremely stressed group also put on more bodyfat and reduced the cross-sectional area (CSA) of their legs (which indicates muscle loss), while the low-stressed group lost bodyfat and increased their leg CSA.

This study included both men and women, and the researchers couldn't find any differences between sexes.

Other research confirms that psychological stress reduces strength gains, meaning that the speed of recovery after a specific strength workout can double from 24-48 hours to 72-96 hours (which would make high-frequency training impossible). Other studies show that wounds require 40% more time to heal under extreme stress. Another study found that the risk for injuries doubled in periods of high academic stress in football players, and that this stress could play a more significant role than the physical stress from training.

Stress in the right dosage can increase your performance, so even if you feel nervous, it could often mean that you're going to do better when you face a challenge.

Stressed people need to have a lower training frequency and/or training load to recover, and in many cases, to get any results at all.

Stress and Food

There is something called "healthy stress"—positive stress or eustress. This is an increase in cortisol that is functional and something positive. When you work out, cortisol mobilizes energy from energy substrates (fat and glycogen), so that you can continue to work out and recover afterwards. This mechanism also suppresses inflammation and keeps the body functional during and after training. This illustration sums up how cortisol and eustress are linked.

Like almost every physiological process, and like the tale of Goldilocks and the Three Bears, too much or too little is usually destructive, whereas "just enough" is positive.

Sympathetic dominance, or "fight-or-flight" refers to acute stress, and this will suppress your appetite. You don't care about food when you're busy or engaged in something stressful, so hunger during a workout is an obvious sign that you're not in the "zone" or "flow state" as Mihály Csíkszentmihályi has named it.

Chronic stress, however, is going to increase the appetite. More specifically, it makes you self-medicate on food—appropriately called "comfort food." People vary in how prone they are to "comfort eating," depending on how much cortisol they secrete. Food stimulates the production of dopamine, serotonin, and opioids—substances that naturally gives you a rush and a feeling of happiness. Food generally stimulates parasympathetic dominance in the nervous system, the "rest and digest" mode.

Carbohydrates can under certain circumstances fight stress by increasing the production of insulin. Insulin inhibits cortisol directly and increases branched chain amino acids (BCAA) in our brains, so that the amino acid tryptophan can easily cross the blood-brain-barrier and then convert into the neuro-transmitter of happiness—serotonin. The preference for high-carb food has also been documented to be associated with a lack of sleep.

The fact that so many resort to chocolate and candy under stress is actually a cultural thing. Before we knew what this was, we ate the sweetest foods that nature could offer at that time: fruit, berries, and honey.

Unfortunately, comfort eating doesn't work.

One of the most basic concepts of human psychology is that we continuously seek to feel better by using different reward strategies, and this has a tendency to get priority over health and body composition. Still,the relationship between emotions and obesity is too complex for us to say that it's all about rewarding ourselves. And as Tremblay et al. (2015) talks about in this excellent article, the feeling of satiety and satisfaction that we get when we eat is regulated by these factors:

  • Sensory and cognitively: taste, smell, consistency, and expectations about the reward, based on earlier experiences.
  • Amount: How much the amount of food stretches the stomach, the macronutrient distribution, how much calories there is in a meal, the micronutrient content, and how food affect the microbiome (bacteria in the intestines) and the other way around – how healthy the microbiota is will affect your food intake and how you digest it.
  • Energy status and energy balance: calories in and out, insulin, metabolism, amino acids, glucose, nutrient partitioning, fat, and muscle mass.

The food industry knows how to manipulate this by increasing palatability (combinations of sweet, salty, fatty, sour and different additives that stimulate our appetite) and by making ads for their products more visually pleasing. There is, however, no doubt that humans as a species are unique when it comes to our appetite not being regulated by physiological needs only, but also by psychological factors.

There is obviously nothing to be gained from comfort eating. It's a short-term fix for happiness, but it rarely (never) solves the underlying problem. It's better to resolve the external stress with better planning, and the internal stress by using various stress management strategies.

A good way to separate emotional hunger and cravings from actual physical hunger is to consider if you would like to eat a full meal consisting of meat/chicken, potatoes, rice, vegetables etc. or if the only thing that's going to help is ice cream and chocolate.

Perhaps a little silly, but this is actually a simple method that's going to tell you about the underlying issue. It's up to you how you're going to solve it when you know the answer. (YOLO?) But don't fool yourself, if you don't want anything but ice cream you are seeking external stimuli to calm down internal turmoil, there is no physical need for those calories.

Planning

There are hundreds of books and guides on how to plan your day better, but Kevin Kruse has recently interviewed over 200 people who are successful in what they're doing, including seven billionaires, 13 Olympic athletes, and many skilled entrepreneurs. A simple question provided many interesting and educational responses.

What is the Secret to Being Productive?

  1. Only focus on one thing. Ultra-productive people know what their "most important task" is, and work on that for 1-2 hours every morning, without any distractions. What task is going to have the largest effect on how to reach your goals? This is how you should start your day.
  2. They don't do to-do lists. Instead, plan according to your calendar. Only 41% of the things on a to-do list is going to be done. All of these undone tasks lead to stress and sleep deprivation because of what's called the Zeigarnik effect, which mainly means that tasks that are written down are going to stay in your head until you've finished them. Extremely productive people put everything on their calendars, and do them when it's time to do them. And no, this doesn't mean that you're going to fill your calendar with so many tasks that you, in reality, are going to need 100 hours a day to get everything done.
  3. They're always home for dinner. Kevin first learned this from Intel's Andy Grove, who said: "There's always more that has to be done, that should be done, and that could be done." Extremely successful people know what they value the most in life. Work—yes, of course—but also everything else that really matters. There's no right answer here, but these other values are for most people: family time, exercise, and the ability to give something in return. They have consciously and strategically divided their 1,440 available minutes per day on every area that they value the most, and then they stick to it—instead of filling their calendars with every possible thing they can think of, just because they can't handle being alone with their thoughts.
  4. They use a notebook. Richard Branson has many times said that he wouldn't be able to build Virgin without a notebook, which he brings along wherever he goes. In one interview the Greek shipping mogul Aristoteles Onassis said: "Always bring a notebook. Write down everything. It's a million-dollar trick they don't teach you in school!" Ultra-productive people relieve their minds by writing down every important thought they have. There's something special about writing something down physically that makes it easier to manifest and to make room for other thoughts in your head.
  5. They check their e-mail only a couple of times per day. Ultra-productive people don't check their e-mail or social media constantly throughout the day. They don't check every vibration or sound to see who has requested their attention in their inbox. In the same way, it would be disrespectful if someone followed you around all day asking for your attention every fifth minute, right? Instead, like everything else, they plan a time to check their e-mail fast and efficiently. For some, it's only once a day, and for others who normally get many e-mails, it is every morning, afternoon and evening. (I, personally, don't think the evening is advisable, then you're only going to be thinking about it once you go to bed).
  6. They avoid meetings as much as possible. When Kevin asked Mark Cuban to give his best productivity tips, he replied: "Never accept meetings unless somebody is writing a check." Meetings are notorious time thieves. They start late, have the wrong people in them, they go on endlessly without a real topic, and they go far beyond the originally scheduled times. You should avoid meetings whenever you can, and you should set up fewer meetings yourself. And keep it short and concise if you need to have one. I'm obviously not talking about social meetings with friends or going on dates. You'll have more time for this when you free up time from unnecessary meetings. In Norway, we have a certain "meeting illness" where it's almost a mandatory company policy to have a meeting about every minor detail that could've easily been solved through e-mail communication (we have started using Slack in MyRevolution.no where I work part-time as the Product/R&D Manager).
  7. They often say No. "The difference between successful people and extremely successful people is that the extremely successful say No to almost everything," the billionaire Warren Buffet once stated. And if something isn't "Fuck yes" then it's "Fuck No". Remember, you only have 1440 minutes available in one day. Don't give them away recklessly. You may have created an illusion of everyone having high expectations for you all the time, but you should stop and consider how true this really is. If you disappeared for the next 6-12 months, do you think the world would go on, and would all these people solve their problems and tasks on their own? It can be both scary and relieving to realize that you're not as important as you think. Another perspective is that you should demand the same respect for your time of the people you're going to be around, as they expect you to give them. This means that not anyone should be able to waltz into your life and expect you to drop everything you're doing just to stimulate their needs, whenever it suits them. If you feel that you have to do this to be validated or liked, then my advice is to carefully assess the people around you and whether they should really be in your inner circle.
  8. They follow the 80/20 rule, also known as the Pareto Principle. In most cases, 80% of the results come from only 20% of the activities you're doing. Ultra-productive people know what activities are going to give the best results. Focus on these and ignore the rest. This is also closely linked to number 7 on this list.
  9. They delegate tasks to others. Ultra-productive people don't ask the question: "How can I do this task?" Instead, they ask: "How can this task be done as efficiently as possible?" You have to let go of the need for control so that you can prioritize what you like the most and what you know best.
  10. They start the process instantly, they delegate tasks, or they place a task where it belongs in their calendar for future execution. How often do you read an e-mail and then save it for later? Extremely successful people strive to attend to tasks immediately. If it takes less than five or ten minutes, do it now. This reduces stress since it won't be in the back of your head all day long, and it's more effective because you don't have to read or evaluate over and over again. If it's something you can't do or don't want to do yourself, read number 9 again. If it's something you need to do, but can't do right now, read number 2.
  11. They practice a consistent morning routine. Kevin's biggest surprise, while he was interviewing 200 extremely successful people, was how many of them wanted to share their morning ritual. They nourished their body with water, a healthy breakfast, easy workout/activity, and nourished their mind with meditation or prayer, inspiring reading or journal writing.
  12. Energy is everything. You can't create more minutes, but you can increase your energy by creating more attention, focus, and productivity. Extremely successful people don't skip meals, sleep, or breaks in the hunt for perfectionism or more of everything. Instead, they look at food as fuel, sleep as recovery, and breaks as possibilities to recharge so they can have an even bigger benefit of the time they have available. As some of you might be aware of, I worked with Ari Whitten when he developed The Energy Blueprint (click for free video training), which goes deeper into the scientific evidence of maximizing your energy levels.

Stress Management

Stress managing strategies are classified as either passive/evasive or active and proactive.

Many spend their lives being passive and avoid dealing with situations or emotions. Instead, they ask others to help or validate them (social distraction), or they seek out various things for short-term relief or distraction like comfort eating, alcohol, drugs – or imagining they are living someone else's life through movies or reality shows.

You won't get rid of the problem if you ignore or postpone it.

Active stress-management is – not surprisingly – the most effective strategy, and this means that you deal with or eliminate situations or feelings or the resulting emotions that occur. By constantly practicing coming up with solutions, your brain will become a problem-solving machine vs. a problem-oriented robot.

You often hear psychologists emphasize emotionally focused stress management: accept responsibility, focus on the positive sides, seek social support and so on. This could be sufficient for some, but it's still just a Band-Aid compared to dealing with the root cause of the issue.

  • Fight with your partner? Talk about it, without being confronting or accusing. Recognize and listen so that you understand how the other one is feeling, find an amicable solution that both can accept, and be prepared to give to get something back – rather than expecting something up front before you're willing to give something back.
  • Trouble at work? Talk to your colleague or boss. Present the situation concisely and based on as much information as possible, without getting too emotionally involved.
  • An unexpected bill? Talk to the creditor and ask for a deferred payment or an installment plan. The bill isn't going to disappear just because you haven't opened it. It'll grow, and in a worst-case scenario, a lack of payment will result in you losing your credit rating. Deal with it, it's just a bill after all, and as a member of society, you have to expect many more of these in your adult life.

When you handle the problem immediately, you take advantage of the acute stress reaction. This makes you think clearly and with a better chance to figure out the necessary tools or resources, motivate you to follow through on the plan, and mobilize energy to get you through to the other side in one piece.

And sometimes, the stress you experience today may seem important, but that's only because you are so focused on the moment.

The philosopher Massimo Pigliucci, author of the book How To Be A Stoic, describes how he used Google Street View and Google Earth to handle anxiety, and I urge you to try it:

Search up your home address or your current location. Zoom until you get down to Street View.

This is you and your current problems.

Now start zooming out. First the satellite view of where you are now (kinda scary how detailed a picture taken from space can be, right?). Then the block or neighborhood. Zoom further out and you are at city level. Then the county you live in, the part of the country, the country. Zoom further out and you are now at the part of the world you reside with your problems. Zooming out and out, until you see the whole planet and solar system (if you use Google Earth).

Notice how this feels—what does it do to you and your seemingly-important problems?

If this simple exercise doesn't help, it may help you to simply reflect on your past. Just with an important twist: Realise that every single problem you've ever had, is currently solved. You managed to handle every heart-wrenching crisis, in your own way – for good or for bad.

The point being that every single disaster, problem or concern eventually and inevitably had to give up, and that thing you are worrying about now is probably not that big of a deal when you consider it from that perspective.

Many of us tend to live in a constant state of anxious anticipation of the next thing that can go wrong, and some of us are better at it than most. Always expecting the worst possible outcome may lead to maladaptation and waste of precious resources.

If you consider the worst possible scenario and the best possible scenario – what really ends up happening is usually closer to the latter than the former.

The usual Zen-Buddhism perspective of just being "present in the moment" can sometimes be hard to put into practice. I find it easier to use the above-mentioned strategy of reflecting on your past and already-handled problems to realize that your anxiety is most likely unjustified.

Stress is bound to happen, but you should train yourself to control it and focus it.

An effective stress management strategy is to organize your day into high-stress and low-stress periods. Stress should follow your biorhythm. Most people think of their periods of stress spread over the work week, where they are chronically stressed or depressed Monday through Friday, while weekends and holidays are the time to relax or go into total hibernation because the stress has been accumulating for too long.

This is wrong.

What You Can Learn from the Fastest and Strongest on the Planet

Research on both animals and elite athletes shows that they experience less stress than the average person. They are more calm and balanced (parasympathetic dominance), but they become more excited during periods of stress (sympathetic dominance) – like hunting, competition or training.

They have the ability to hide in a bush (animals, not athletes), or to go up to a barbell loaded with hundreds of kilos in an almost hypnotic state (athletes, not animals), and then maximally activate the stress response so that their bodies can mobilize energy in a few seconds or even milliseconds of optimal performance, and then unwind.

Stress is intermittent, not chronic.

Two lionesses ready for action. The top one can be tempting to cuddle with, but could kill you without warning. The bottom one can, incidentally, also be tempting to cuddle with, and could kill you with no warning—during PMS.

If you have a regular nine-to-five job, this usually means that the first part of the day is high-stress, and workouts should happen sometime during this part of the day.

When you get home, relax.

Turn off your phone and/or Wi-Fi-connection.

Those of you who are self-employed or freelancers need to be more conscious of your biorhythm because your office is often your home.

I recommend having your own room in the house where you work, and even though I'm not always the best at this myself, I strongly advise that you follow the 12 point list in the previous chapter on planning.

Implement consistent routines, and restrict the times you are checking your inbox—and if you do, respond immediately or have workflow strategies that allow you to archive it for later attention.

I prefer to work out between 12-2 p.m., but this is just a personal compromise—I have better workouts, but it disturbs my workflow.

If I work out after 4-5pm, I'll be able to go home and spend rest of the evening eating, relaxing and nourish my malnourished social network—but then I'll also be more exhausted, and I won't get as much out of my workout at that time.

So I have split my day up into two work phases where I'm also the most productive: 8-11am and 3-6pm.

I am better at analytic work (so looking at client's progress reports, answering e-mails etc) whereas I find myself more creative in the afternoon (which is when I'm writing articles such as this one).

You should track your own ups and downs for a few days, being aware of when you are the most focused, energetic, creative and so on. Tailor your daily routine around your peaks as much as practically possible. I obviously realize that this isn't always possible for a lot of people, so just do the best you can.

Although it has been shown that chronotypes can be reset with proper management of light-dark cycles and even meal timing (as I will cover in part 2), this is also the premise of Michael Breus' book The Power of When: Discover Your Chronotype–and the Best Time to Eat Lunch, Ask for a Raise, Have Sex, Write a Novel, Take Your Meds, and More

Meditation

I've been through everything from TM/Transcendental (mantra-based) to Reiki and Mindfulness meditation, and I can whole-heartedly say that meditation is one of the best things you can do for stress management.

On the other hand, I have to admit that I still don't have consistent routines, and I go through periods where I "forget" it. Just by writing this article, I am reminded that this is something I need to pick up again.

Many studies on mindfulness are unfortunately not very good, but there are still some convincing studies. Meditation is a "reset button" for your brain. The reduction in anxiety and depression has a convincing scientific background. It doesn't work as well for everyone, but the only way to find out is to try it out—and like everything else you have to take into account that you won't experience all the benefits the first time you try it. You need training to become good at meditation, just like lifting weights.

Mindfulness meditation is focusing on something that doesn't cause an emotional reaction, like an object, your breath, or a so-called "body scanning" where you're consciously aware of tension and relaxation in your head, neck, chest, back, hips – and further down your body all the way down to your fingers and toes.

It's easier to do the training/meditation in a quiet environment or with earplugs, with your eyes closed, in a relaxed position sitting up straight in a chair or on the floor. Bonus point if you can do it in a Lotus-position.

It can be tempting to lie down, and this is fine as long as you can stay awake. Apps like Headspace and Calm give you a guided meditation for free, and you have to pay to get the longer and more comprehensive meditations.

Even though you can argue that meditation could be seen as a passive stress-management strategy, it's still proactive considering you will be in a better shape to handle stress and solve problems more rationally with a clear vs. cluttered mind.

Nature Calls

It may sound odd, but it's scientifically documented: Exposure to nature – to the mountains, the sea, the forest and the beach reduces stress in different contexts (2, 3, 4). Exercising outside is considered as requiring less effort and is subjectively less challenging. Even rates of cancer are lower in greener areas.

It's obviously not always practical, even though it's desirable. Fortunately, something as simple as indoor plants and flowers reduces your stress levels, and if you have a small garden nearby, it is incredibly de-stressing to plant some seeds. Just be careful where you get the seeds from.

Siggy found a lot of pleasure in his new garden. The parts of it he can remember, that is… (Hint: This plant goes by the name Mary Jane).

Invest in some plants. See if you can get a few fresh breaths of nature to/from work or the gym, even though it's a detour.

Even using a bedside clock or app on your phone with birdsong or other nature sounds is a better way to start the day than bells and screaming alarms.

Here in Norway, we are lucky to have nature all around us, and the impact it has on overall life quality can't be understated. Even with our ridiculous taxes and rules enforced upon us, we have our mountains, fjords, and forests that keep us just sane enough to tolerate the government sticking their hands in our pockets at every opportunity they have.

You'll be surprised at how problems and stress that used to be so unbearable and insurmountable in your mind, appears unimportant and irrational when you get outside. Or you'll find a workable solution spontaneously and almost magically once you get some sunlight and fresh air.

Another bonus is that the sunlight and daylight are essential for us to keep up a good biorhythm, and this, activity and sleep quality are some things we'll take a closer look at in the next part.

In part 2, we'll take a look at Biorhythm and Lifestyle, and you'll get an understanding of things you never could imagine had such a dramatic influence on your health, mood, and performance.

Did you enjoy the article? Please share it on Facebook by clicking this link.

9.1.18

Criptovalute: Telegram prepara la più grande Ico di sempre - Repubblica.it

Criptovalute: Telegram prepara la più grande Ico di sempre - Repubblica.it

Criptovalute: Telegram prepara la più grande Ico di sempre


ROMA - Potrebbe essere la più grande Initial coin offering di sempre. E a lanciarla non sarebbe una giovanissima startup ma un'app di messaggistica da 180 milioni di utenti: Telegram. A svelare il progetto, che potrebbe realizzarsi a marxo, è TechCrunch: la chat considerata ''di ferro'' dal punto di vista della sicurezza punta a raccogliere 500 milioni di dollari vendendo Gram, ovvero la criptovaluta proprietaria in cambio di euro e dollari. Una novità, visto che la maggior parte delle Ico preferisce raccogliere bitcoin o ethereum. In più, Telegram non deve costruire da zero una base utenti. E questo potrebbe giocare a favore di una propria criptovaluta, che di fatto avrebbe già, al momento del battesimo, la possibilità di circolare su vasta scala.

Le nuove risorse dovrebbero servire per creare nuovi servizi, che potrebbero trasformare in modo radicale l'app. O, meglio, creerebbero un ecosistema su blockchain. Il fondatore, Pavel Durov, non vuole solo una propria moneta ma anche una rete decentralizzata (denominata Telegram Open Network, Ton), su cui far viaggiare messaggi, file ma anche monete e "contratti intelligenti".

Telegram si trasformerebbe così in una piattaforma multiservizi, sul modello di WeChat, ma che utilizza la blockchain per trasferire denaro (soprattutto in piccole somme) in modo istantaneo e con costi di transazione ridotti al minimo. Ton potrebbe essere utilizzato anche da terze parti (cioè da altri siti e piattaforme).

Viste le fiammate delle criptovalute, il team di Telegram starebbe pensando a un sistema per limitare le spinte speculative: Durov e i suoi collaboratori dovrebbero mantenere la proprietà del 52% dei Gram (le criptovalute emesse, da scambiare con altri utenti o da usare per usufruire dei servizi di Telegram). Il progetto procederà per gradi, con la blockchain di Telegram operativa dal primo trimestre 2019. L'operazione ha, dalla sua, la simpatia della comunità blockchain. Ma il progetto potrebbe essere condizionato dagli interventi regolatori sulle Ico.

4.1.18

Quei rischi comuni che Berlino non sopporta - Corriere.it

Quei rischi comuni che Berlino non sopporta - Corriere.it

Quei rischi comuni che Berlino non sopporta

Marzo 2012: mentre la Grecia fa default, il presidente della Bundesbank, Jens Weidmann, scrive a Draghi chiedendo l'introduzione di un meccanismo di garanzia in Target 2, il sistema di pagamenti interbancari transfrontalieri Ue. Allora sul sitema la Germania aveva un surplus di 600 miliardi, Italia e Spagna avevano un deficit di 250 ciascuna, la Grecia di 150.Per Weidmann gli squilibri di Target 2 sono «salvataggi sostitutivi» della periferia da parte dei Paesi core. E si appella alla clausola di non-salvataggio dei trattati per chiedere che i saldi negativi siano coperti da valide garanzie, preferibilmente l'oro delle loro banche centrali nazionali. Nel 2012 Draghi lasciò cadere. Ma oggi che gli squilibri di Target 2 hanno toccato nuovi record, i tedeschi ci fanno i conti in tasca: date le sue riserve auree (85 miliardi) l'Italia potrebbe garantire appena il 20% del suo disavanzo Target 2; la Spagna meno del 3%! Se i deficit Target 2 dovessero essere collateralizzati, allora una volta esaurite le garanzie ammissibili, (analogamente al Gold Standard) un paese non potrebbe più aumentare il disavanzo Target 2 e la moneta dei suoi cittadini varrebbe meno di quella degli altri residenti nell'Eurozona. Inevitabilmente i cittadini di quel paese reagirebbero alla minaccia accelerando la fuga di capitali in atto da metà 2014. Per l'Italia i dati della bilancia dei pagamenti mostrano che da allora il settore privato non bancario ha investito massicciamente in azioni e fondi comuni esteri. Finora l'emorragia è di 300 miliardi. Se la proposta di Weidmann venisse accolta avremmo controlli dei capitali e corse agli sportelli. Perciò bisogna rispondere «nein». I razionamenti di liquidità su Grecia e Cipro hanno alimentato i timori e la fuga di capitali dalla periferia; segregare ulteriormente i rischi come vuoleBerlino potrebbe essere fatale per l'euro. Target 2 riflette proprio le logiche segregazioniste sottese alle misure straordinarie della Bce sotto la spinta tedesca. I prestiti straordinari (Ltro) tra il 2011 e il 2012 sono stati usati dalle banche periferiche per saldare crediti commerciali verso le banche franco-tedesche e assorbire le loro esposizioni in titoli di Stato del Sud Europa. Se fossero andati direttamente a imprese e famiglie, i saldi Target 2 non si sarebbero mossi. Parimenti se col Qe la Bce avesse comprato direttamente i titoli di Stato senza coinvolgere le banche centrali nazionali. La condivisione dei rischi è vitale per l'Eurozona. Di recente ho proposto una riforma del Meccanismo europeo di Stabilità nel senso di un risk sharing sui debiti pubblici da attuare secondo logiche di mercato. La via giusta per ripristinare quel clima di fiducia che manca da troppo tempo.

Mcgill S. Designing Back Exercise - From Rehabilitation to Enhancing.pdf

3.1.18

Body weight homeostat that regulates fat mass independently of leptin in rats and mice

Body weight homeostat that regulates fat mass independently of leptin in rats and mice

Body weight homeostat that regulates fat mass independently of leptin in rats and mice

  1. Claes Ohlssonb,1
  1. Contributed by Jan-Åke Gustafsson, November 8, 2017 (sent for review September 7, 2017; reviewed by Wolfgang Langhans and Subburaman Mohan)

Significance

The only known homeostatic regulator of fat mass is the leptin system. We hypothesized that there is a second homeostat regulating body weight with an impact on fat mass. In this study we have added and removed weight loads from experimental animals and measured the effects on the biological body weight. The results demonstrate that there is a body weight homeostat that regulates fat mass independently of leptin. As the body weight-reducing effect of increased loading was dependent on osteocytes, we propose that there is a sensor for body weight in the long bones of the lower extremities acting as "body scales." This is part of a body weight homeostat, "gravitostat," that keeps body weight and body fat mass constant.

Abstract

Subjects spending much time sitting have increased risk of obesity but the mechanism for the antiobesity effect of standing is unknown. We hypothesized that there is a homeostatic regulation of body weight. We demonstrate that increased loading of rodents, achieved using capsules with different weights implanted in the abdomen or s.c. on the back, reversibly decreases the biological body weight via reduced food intake. Importantly, loading relieves diet-induced obesity and improves glucose tolerance. The identified homeostat for body weight regulates body fat mass independently of fat-derived leptin, revealing two independent negative feedback systems for fat mass regulation. It is known that osteocytes can sense changes in bone strain. In this study, the body weight-reducing effect of increased loading was lost in mice depleted of osteocytes. We propose that increased body weight activates a sensor dependent on osteocytes of the weight-bearing bones. This induces an afferent signal, which reduces body weight. These findings demonstrate a leptin-independent body weight homeostat ("gravitostat") that regulates fat mass.

Epidemiologic studies demonstrate that subjects spending much time sitting have increased risk of obesity, diabetes, and cardiovascular diseases. There is even epidemiologic evidence for an association between sitting time and overall mortality (1, 2). The mechanism for the antiobesity effect of standing is essentially unknown. It is probable that part of the effect of high sitting time on cardiometabolic phenotypes is caused by the associated low degree of exercise. However, the results of some articles demonstrate that the association of a sedentary behavior, as reflected by much sitting time, with the metabolic syndrome, is independent of physical activity (3, 4). We hypothesized that there is a homeostat (5) in the lower extremities regulating body weight with an impact on fat mass. Such a homeostat would (together with leptin) ensure sufficient whole body energy depots but still protect land-living animals from becoming too heavy. A prerequisite for such homeostatic regulation of body weight is that the integration center, which may be in the brain, receives afferent information from a body weight sensor. Thereafter, the integration center may adjust the body weight by acting on an effector (6).

Results

Body Weight Sensing for Fat Mass Homeostasis in Mice with Diet-Induced Obesity.

To investigate our hypothesis that there is a homeostatic regulation of body weight and fat mass based on loading, we implanted capsules that weighed 15% of the body weight into the abdomen of adult Sprague-Dawley rats and C57BL6 mice with diet-induced obesity (load). Control animals were implanted with an empty capsule of equal size (3% of the body weight). We found that increased loading suppressed the biological body weight both in rats and mice (Fig. 1 A and B). The difference in biological body weight between rodents with load and control rodents was first seen on day 2 after implantation and was larger on day 14 when the experiment was terminated (Fig. 1 A and B). At the end of the experiment the total body weight (= biological body weight + capsule weight) was rather similar in the load and control mice (Fig. S1A). Calculations of the efficiency of the homeostatic regulation of total body weight at 2 wk after initiation of the loading revealed that ∼80% of the increased loading was counteracted by reduced biological weight (Fig. S1B). The increased loading also reduced the amount of white adipose tissue (WAT), as illustrated by representative MRI slices (Fig. 1C) and quantified by WAT dissection (Fig. 1D) and serum leptin levels (Fig. 1E). These findings demonstrate that there is an efficient body weight sensing mechanism for the homeostatic regulation of body weight.

Fig. 1.
Fig. 1.

Body weight sensing for fat mass homeostasis in rats and mice with diet-induced obesity. (A) Effect of loading on change in biological body weight (= total body weight − capsule weight) in rats (n = 8) and (B) mice (n = 10) implanted with capsules weighing 15% of the body weight (load) or empty capsules (control; ∼1.5% and ∼3% of the body weight for rats and mice, respectively). (C) Coronal (Top) and corresponding transversal (Bottom) MR images of a control (Left) and a load (Right) animal (day 14), acquired without fat suppression. Hyperintense regions represent body fat. Yellow dotted line and white bar indicate the position of the corresponding transversal images Below and 10 mm, respectively. (D) The fat mass (day 14), (E) the serum leptin levels (day 14), and (F) the food intake as percent of body weight (days 4–6) were measured in load and control rats (n = 8) and (G) mice (n = 10). (H) The effect of pair feeding on body weight change in control mice compared with ad libitum fed control and load mice (n = 9). (I) Change in biological body weight, (J) the fat mass (day 17), and (K) the skeletal muscle mass (day 17) after removal of load (heavy capsule followed by empty capsule) or sustained load (heavy capsule followed by heavy capsule) 14 d after the first implantation (n = 10). (L) HOMA-IR in fasted control and load mice (n = 10). (M) Blood glucose, (N) blood glucose area under the curve (AUC), (O) serum insulin, and (P) insulin AUC during an oral glucose tolerance test in load and control mice (n = 10). (Q) Effect of loading on long-term change in biological body weight in load and control mice (n = 10) followed during 7 wk after capsule implantation. Data are expressed as mean ± SEM *P < 0.05, **P < 0.01, ***P < 0.001.

The possible mechanism behind the suppression of body weight by increased loading was investigated on day 6 after implantation of capsules, a time point when the difference in body weight was still robustly increasing between load and control rodents (Fig. 1 A and B). There was no significant difference between mice with load and control mice in UCP1 mRNA levels in brown adipose tissue (BAT) (Fig. S1C), in oxygen consumption as a measure of energy expenditure (Fig. S1D), in respiratory quotient (RQ) (Fig. S1E), or in motor activity (Fig. S1F). Importantly, load decreased food intake, both calculated as percent of body weight (Fig. 1 F and G) and calculated as food intake per animal in both rats and mice (Fig. S1 G and H).

Control mice pair fed with the same amount of food as the load mice decreased their body weight to the same extent as the load group (Fig. 1H). Therefore, the decreased biological body weight in the animals with increased loading did not seem to be caused primarily by increased energy expenditure, but rather by decreased food intake. An alternative loading procedure using capsules implanted s.c. on the back of the mice was also used. Increased loading suppressed the biological body weight in adult mice with diet-induced obesity also in this model (Fig. S1I). These experiments revealed that increased loading reduces the biological body weight. We next evaluated whether reduced loading also influences the biological body weight by comparing mice with sustained loading (heavy capsule followed by heavy capsule) and mice with removal of loading (heavy capsule followed by empty capsule; Fig. 1I). Removal of the loading increased the biological body weight and the fat mass (Fig. 1J) but not the skeletal muscle mass (Fig. 1K), demonstrating that the body weight sensor is functional in both directions.

Loading improved insulin sensitivity as indicated by substantially reduced fasting homeostatic model assessment of insulin resistance (HOMA-IR) index (Fig. 1L) and reduced serum insulin before, during, and after oral glucose administration compared with control mice (Fig. 1 O and P). In addition, loading increased glucose tolerance as indicated by decreased levels of circulating glucose after oral glucose administration (Fig. 1 M and N and Fig. S1 K and L). Although loading reduced the absolute serum insulin levels throughout the glucose tolerance test (GTT) (Fig. 1 O and P), the induction of serum insulin from baseline was normal during the test (Fig. S1 M and N).

We also performed a long-term study, demonstrating that the effect of loading on biological body weight remained until the experiment was terminated at day 49 (Fig. 1Q).

Leptin-Independent Body Weight Sensing for Fat Mass Homeostasis.

A prerequisite for homeostatic feedback regulation of energy depots in body fat tissue (energy balance) is that energy regulating parts of the brain receive information from fat tissue about its size. The fat-derived hormone leptin, discovered by Friedman and coworkers over 20 y ago, is so far the only known such afferent homeostatic factor (79). In the present study, we next investigated the interactions between increased loading, a stimuli normally reflecting increased body fat mass, and leptin. The loading-induced decrease in body weight was seen in leptin-deficient obese (Ob/Ob) mice (Fig. 2A), in the same way as in wild-type mice (Fig. 1B). In addition, the combined effect of increased loading and leptin treatment was studied in wild-type mice. Leptin was given to loaded and control mice on days 11–15 after implantation of capsules. It was found that leptin treatment suppressed body weight (Fig. 2B) and body fat (Fig. 2C) to a similar extent in loaded and control mice, while none of the treatments affected muscle mass (Fig. 2D). Thus, the loading-induced homeostatic regulation of body weight was independent of the well-established fat mass reducing effect of leptin, revealing two independent negative feedback systems for fat mass homeostasis.

Fig. 2.
Fig. 2.

Leptin-independent body weight sensing for fat mass homeostasis. (A) The effect of increased loading on the change in body weight in leptin deficient Ob/Ob mice (control n = 7 and load n = 10). The effect of combined loading and leptin treatment (1.5 µg/g BW twice daily) on (B) changes in biological body weight, (C) fat mass, and (D) muscle mass in mice (n = 10). Data are expressed as mean ± SEM *P < 0.05.

Since the body weight reducing effect of increased loading was caused by reduced food intake, we analyzed the expression of appetite regulating genes in the hypothalamus. Increased loading augmented the expression of the obesity promoting neuropeptides AgRP and NPY (Fig. S1J). These two peptides are expressed by essentially the same neurons in the arcuate nucleus of the hypothalamus and their expression is suppressed by leptin. Therefore, the increase in AgRP and NPY expression is likely to be a failed compensatory mechanism induced by low fat mass and low serum leptin in the mice exposed to increased loading (Fig. 1 D and E and Fig. S1J), consistent with a leptin-independent mechanism for increased loading to reduce body weight.

The Suppression of Body Weight and Fat Mass by Loading Is Dependent on Osteocytes.

It is known that osteocytes can sense dynamic short-term high-impact bone loading for local bone adaptation (1012). We therefore postulated that chronic static moderately increased bone loading, induced by increased body weight, also activates osteocytes, and thereby reduces fat mass via a systemic signal. To determine the role of osteocytes for the suppression of body weight by increased loading, we established an osteocyte depleted transgenic mouse model using diphtheria toxin-driven cell depletion specifically of DMP1 positive osteocytes (Fig. S2). The normal suppression of body weight by increased loading observed in mice with intact osteocytes (Fig. 3A) was lost in osteocyte-depleted mice (Fig. 3B). Increased loading decreased the weight of WAT (Fig. 3C) and serum leptin levels (Fig. 3D) in mice with intact osteocytes but not in osteocyte-depleted mice, while there was no significant differences in the skeletal muscle weight between the groups (Fig. 3E). These findings demonstrate that the suppression of body weight by loading is dependent on osteocytes. We propose that increased body weight activates a sensor dependent on the osteocytes of the weight-bearing bones. This induces an afferent signal to reduce food intake (Fig. 3F).

Fig. 3.
Fig. 3.

The suppression of body weight and fat mass by loading is dependent on osteocytes. Effect of increased loading on change in biological body weight in (A) control female mice with intact osteocytes (control n = 11 and load n = 12) and in (B) osteocyte-depleted (OCyD) female mice (n = 9). The effect of loading of control mice with intact osteocytes and OCyD mice on (C) fat mass, (D) serum leptin levels, and (E) muscle mass, as measured 21 d after initiation of loading. Data are expressed as mean ± SEM *P < 0.05. (F) Hypothesis for homeostatic regulation of body fat mass by two different signal systems. The first previously known pathway is fat-derived leptin in circulation acting on the brain to decrease food intake and fat mass. The second mechanism is that increased fat mass is counteracted by the body weight homeostat (gravitostat). Increased body weight activates a sensor dependent on the osteocytes of the weight-bearing bones. This induces an afferent signal to reduce food intake.

A growing body of data indicates that the skeleton is an endocrine organ that regulates energy and glucose metabolism through, at least in part, the release of the bone-derived hormone osteocalcin (13, 14). We therefore hypothesized that the homeostatic regulation of body weight and fat mass by osteocytes in response to changes in body weight may be mediated by osteocalcin, or another known bone-derived circulating factor. To investigate this hypothesis, we determined the effect of increased loading for 6 d on the bone expression and circulating levels of four bone-derived candidate factors (sclerostin, osteocalcin, FGF23, and lipocalin 2) that might mediate this effect (Fig. S3). As previously shown for dynamic short-term high-impact loading, static moderately increased loading for 6 d reduced the bone expression of Sost (the gene coding for the bone mass suppressing factor sclerostin) (Fig. S3A). However, serum levels of sclerostin were not affected by increased loading (Fig. S3B). Although osteocalcin is a crucial regulator of energy metabolism in rodents, no effect of increased loading on the expression of osteocalcin in bone (Fig. S3C) or on circulating levels of total (Fig. S3D), carboxylated (Fig. S3E), or undercarboxylated (Fig. S3F) osteocalcin was observed. Furthermore, serum testosterone levels, known to be regulated by bone-derived osteocalcin and to regulate fat mass, were not affected by loading (15) (Fig. S3G). FGF23 is an osteocyte-derived endocrine acting factor. Increased loading did not significantly alter FGF23 expression in bone (Fig. S3H) or serum FGF23 levels (Fig. S3I). It was recently demonstrated that bone-derived lipocalin 2 suppresses appetite via a MC4R-dependent pathway (16). Increased loading did not significantly alter lipocalin 2 mRNA levels in bone (Fig. S3J) or serum lipocalin 2 levels in mice (Fig. S3K). These findings do not support that any of the four main bone-derived circulating candidate factors mediate the effect of the osteocyte-dependent body weight sensing mechanism.

Effect of Loading on Biological Body Weight in Relation to Other Known Body Fat Regulators.

As described above (Fig. 2 AB), the decrease in body weight by loading was independent of leptin. We next investigated the suppression of body weight by increased loading in relation to other known fat mass regulating signals (Fig. S4). To regulate fat mass, the hypothalamus needs afferent signals from the gastrointestinal tract, e.g., by the hunger and adiposity-inducing hormone ghrelin (17). We found that loading suppressed body weight in mice lacking the ghrelin receptor (Fig. S4A). Moreover, body weight was decreased by loading in mice lacking the receptor for glucagon-like peptide 1 (GLP-1) (Fig. S4B), an insulin-releasing hormone, described to regulate body weight (18). Thus, we found no evidence that loading is dependent on fat mass-regulating signals from the gastrointestinal tract. A major regulator of body fat in the hypothalamus is the circuit involving the neuropeptide α-MSH acting on the melanocortin receptor-4 (MC4R) (19, 20). The body weight decreasing effect of loading was also found in MC4R gene knockout mice (Fig. S4C). Therefore, the suppression of body weight by loading is independent of the α-MSH MC4R system, a major mediator of effects by leptin and GLP-1. Estrogen receptor-α (ER-α) signaling is involved in the regulation of both fat mass and bone mass. It has been shown that local bone formation induced by short-term high-impact loading is dependent on ER-α (10). However, our results from ER-α knockout mice indicate that ER-α is dispensable for the systemic regulation of body weight induced by chronical static moderately increased loading (Fig. S4D). We next determined whether neuronal signaling might mediate the loading-induced decrease in body weight. However, neither the sympathetic marker noradrenaline in urine (Fig. S5A) nor the parasympathetic marker serum choline levels (Fig. S5B) were regulated by loading. These findings demonstrate that increased body weight activates a sensor dependent on the osteocytes of the weight-bearing bones. This induces an afferent food intake reducing signal that needs further study (Fig. 3F).

Discussion

The present findings reveal a body weight homeostat that regulates fat mass independently of leptin in rodents with diet-induced obesity. Increased body weight activates a sensor dependent on the osteocytes of the weight-bearing bones. This induces an afferent signal to reduce body weight.

We observed that increased loading decreased body weight, while decreased loading increases body weight, demonstrating that the body weight sensor is functional in both directions. Importantly, several authors have found that removal of fat by lipectomy causes a compensatory increase in fat mass and body weight in mice and rats lacking leptin activity (2123). These data support our conclusion that a leptin-independent regulation of fat mass does exist, but they do not provide information about the possible mechanism. The present data, indicating that loading can regulate fat mass, raise the possibility that the increase in fat mass observed after lipectomy in leptin-deficient mice is due to decreased loading. Increased loading reduced the biological body weight via reduced food intake. The normal motor activity and the notion that the mice appeared healthy indicate that the effects of increased loading on food intake and body weight were specific.

It is well established that leptin signaling is necessary to prevent severe obesity (7, 24). However, most patients with obesity have high endogenous serum leptin levels and do not respond to exogenous leptin treatment. This indicates that, during these circumstances, leptin is not sufficient to suppress fat mass. This has been referred to as leptin resistance (7, 25).

We propose that both leptin signaling and body weight sensing are necessary for an optimal fat mass homeostasis. Pharmacologically, combined targeting of both the body weight sensing mechanism and leptin signaling may be useful for obesity treatment (Fig. 3F). In line with this, weight loading and leptin treatment suppressed body weight in an additive manner in the present study.

As described above, there is an established epidemiologic link between numbers of hours per day spent in the sitting position and several metabolic diseases, including obesity, diabetes, and cardiovascular diseases. However, the reason for this has been unknown (1, 2). We propose that much sitting time results in decreased loading of osteocytes in the weight-bearing long bones and, thereby, the homeostatic regulation of body weight does not activate its afferent signal to the brain, resulting in obesity (Fig. 3F). In addition, it is possible that secular trends of increased sitting time, via reduced activation of the body weight sensing mechanism, might have contributed to the obesity epidemic. The fact that loading was effective in decreasing fat mass in both Sprague-Dawley rats and C57BL mice with diet-induced obesity, well established models of clinical obesity (26, 27), suggests that increased standing time and, thereby, increased loading will be effective in decreasing human obesity. In addition, our findings demonstrate that loading increases insulin sensitivity. Further studies are needed to investigate whether this effect is completely or only partly due to decreased body fat mass.

The present findings reveal a body weight homeostat that regulates fat mass independently of leptin. We suggest that this body weight homeostat is called "gravitostat" (Latin gravis, meaning heavy; Latin status, meaning stable). The gravitostat, like other homeostats is based on communication between a sensor, an integration center, and an effector. Its sensor is most likely located in the weight-bearing lower extremities. Our data indicate that at least part of this sensor is in osteocytes. Increased fat mass is counteracted both by the gravitostat and by increased fat-derived leptin (7, 24) (Fig. 3F). The gravitostat activates an afferent signal for body weight homoeostasis to reduce food intake (Fig. 3F). Leptin has the capacity to decrease body weight, to some extent mediated by reduced food intake (7, 9). Therefore, both the gravitostat and leptin are eventually acting on the brain and seem to have their integrative centers there (Fig. 3F). Although both leptin and the gravitostat have the capacity to regulate fat mass, it has been proposed that the role of leptin primarily is in the lower end of fat mass homeostasis (25, 28), while the present data demonstrate that the gravitostat is efficient in diet-induced obesity. Future studies are warranted to determine whether activation of the gravitostat explains the beneficial effects of standing. Furthermore, when evaluated in a relevant disease model, it was observed that loading relieved diet-induced obesity and improved insulin sensitivity, suggesting the gravitostat is an interesting drug target for metabolic diseases (Fig. 3F).

Materials and Methods

Animals.

All animal procedures were approved by the Ethics Committee on Animal Care and Use of Gothenburg University. C57BL/6 mice were purchased from Taconic, leptin-deficient Ob/Ob mice were purchased from The Jackson Laboratory and Ghrelin receptor knockout (GHSR KO) mice were obtained from Deltagen. MC4R KO mice, GLP-1R KO mice, and ERα KO mice were developed as previously described (19, 20, 29, 30). All knockout mice and their controls were on a C57BL/6 background. Sprague-Dawley rats were purchased from Charles River Laboratories.

To generate the osteocyte-depleted mice, DMP-1 promoter-Cre mice (31) were crossed with ROSA26 promoter-Flox-STOP-Flox-DTR mice (32) (Fig. S2). Diphtheria toxin receptor (DTR) mRNA was compared between cortical bone, kidney, and liver with RT-PCR (Fig. S2C). Sost mRNA was measured in cortical bone as a marker of osteocyte depletion (OCyD) in mice expressing DTR and given diphtheria toxin (Fig. S2D).

Immunohistochemistry.

The number of osteocytes and empty osteocyte lacunae in femur was evaluated blinded using a bright field microscope. Briefly, femur was fixed, paraffin embedded, sectioned, and stained with hematoxylin and eosin. Three evenly spread out sections of femur were used for counting. Osteocytes and empty lacunae were counted from cortical bone covering on average 0.16 mm2 per section and located 5 mm from the tip of the epiphyseal plate. The number of apoptotic osteocytes was measured as cells with TUNEL positive staining. Briefly, three femur sections neighboring the sections used for counting empty lacunae were stained using TUNEL assay (ApopTag Fluorescein In Situ Apoptosis Detection Kit, S7110; Millipore) in accordance with instructions provided and counterstained with DAPI. Using a wide field fluorescent microscope (Leica DMRB; Leica Microsystems), images were taken covering on average 0.16 mm2 of cortical bone per section and located 5 mm from the tip of the epiphyseal plate. Background autofluorescence was reduced by applying a digital channel subtraction method to the images. TUNEL positive cells and DAPI positive cells were counted within the images.

In a separate experiment, blue β-gal staining of femoral bone sections was used as a marker of cells with active DMP-1 promoter. DMP-1 promoter-Cre mice or wild-type mice were crossed with ROSA26 promoter-Flox-STOP-Flox-β-gal mice. The staining with β-gal in cortical bone was compared between ROSA26 promoter-Flox-STOP-Flox-β-gal mice with and without DMP-1 promoter-Cre.

Loading.

Two- to 3-mo-old mice and rats were fed a high-fat diet (60% fat, D12492; Research Diets) during 4 wk and then a capsule that weighed 15% of the body weight (load) or 3% of the body weight (control) was implanted intraperitoneally or s.c. into the adult animals under isoflurane anesthesia. After the implantation, the body weight was measured daily or several times per week until the end of each experiment.

Removal of load was done in one experiment in which the capsules were exchanged 2 wk after the first surgery and half of the mice with load capsules got control capsules (removal of load) and half of them got new load capsules (sustained load) with a follow-up period of 3 wk after removal of load.

Indirect Calorimetry, Food Intake, and Activity Measurement.

Oxygen consumption and carbon dioxide production was measured by indirect calorimetry in an INCA Metabolic System (Somedic) as previously described (33). The RQ was calculated by the formula RQ = VCO2/VO2. The measurement was done on days 4–6 after implantation of capsules in C57BL/6 mice and the food intake was monitored during the same period for both mice and rats. We also performed a pair feeding study, in which we fed control mice the same amount of food as ad libitum fed load mice. The motor activity was measured in automated activity chambers, so-called Locoboxes, consisting of a plastic cage (55 × 55 × 22 cm) inside a ventilated cabinet (Kungsbacka Mat-och Reglerteknik AB).

Glucose Tolerance Test.

Oral GTT was performed on C57BL/6 mice 3 wk after capsule implantation. The mice received oral glucose [2 g/kg body weight (BW); Fresenius Kabi] by gavage after 5 h of fasting. Blood samples were collected from the tail vein at 0, 15, 30, 60, and 120 min after the glucose gavage. Blood glucose concentrations were determined at the above-mentioned time points using an Accu-Check Compact Plus glucometer (Roche Diagnostics). Serum insulin concentrations were measured at time points 0, 15, 60, and 120 min after the glucose administration using the Ultrasensitive Mouse Insulin ELISA kit (90080; Chrystal Chem, Inc.) according to the protocol provided by the manufacturer.

Leptin Treatment.

Control and loaded C57BL/6 mice were given murine leptin (1.5 µg/g BW; Pepro-Tech) or saline twice daily in s.c. injections on days 11–15 after the capsule implantation.

Gene Expression.

Cortical bone from femur and tibia, hypothalamus, and interscapular BAT were dissected, snap frozen in liquid nitrogen, and kept in −80 °C until analysis. The cortical bones were homogenized with TriZol reagent (Invitrogen) before extraction. mRNA from all tissues was extracted using RNeasy Lipid Tissue Mini Kit (Qiagen) and the mRNA concentration of the samples was measured by NanoDrop spectrophotometry. cDNA was synthesized from 1 µg mRNA with iScript cDNA Synthesis Kit (Bio-Rad).

Real-time PCR was performed using Step-One-Plus or the ABI Prism 7900 Sequence Detection System (Applied Biosystems). The hypothalamus samples were analyzed with Universal Taqman Master Mix (Applied Biosystems) in a 48-gene custom-made TaqMan low-density array card and normalized to glyceraldehyde-3-phosphate dehydrogenase (GAPDH, Mm99999915_g1). The cortical bone samples were analyzed by assays for osteocalcin (Mm01741771_g1), sclerostin (Mm00470479_m1), FGF23 (Mm00445621_m1), and lipocalin 2 (Mm 01324470_m1) and normalized to 18S (4310893E). The BAT samples were analyzed with an assay for Ucp1 (Mm0124486_m1) and normalized to 18S (4310893E). The relative mRNA levels were obtained by using the comparative threshold cycle (Ct) method and calculated with the ΔΔCt equation.

Serum and Urine Analyses.

Blood samples were collected at the end of each experiment and the serum was separated and kept in −80 °C until analysis. Serum was analyzed in duplicates by ELISAs for leptin (Chrystal Chem, Inc), sclerostin (ALPCO immunoassays), osteocalcin (Immutopics), Gla-osteocalcin and Glu-osteocalcin (Takara Clontech), FGF23 (Kainos Laboratories, Inc), lipocalin 2 (R&D Systems), and choline (Abcam). Serum testosterone was analyzed by a gas chromatography-tandem mass spectrometry method as previously described (34). Urine samples were analyzed by ELISA for noradrenaline (Labor Diagnostika Nord) and the urine was also analyzed for creatinine (Crystal Chem, Inc) to normalize the noradrenaline levels.

MRI.

A 7T MR system (software: ParaVision 5.1; Bruker BioSpin MRI GmbH) and a 50-mm quadrature transmit/receive volume coil (RAPID Biomedical GmbH) were used to produce coronal images of each animal separately and transversal images of pairs of animals from the load and control groups. The pairing ensured identical MRI signal enhancement characteristics for both groups, to facilitate subsequent comparison of body fat content.

The coronal images were acquired using a 2D multi slice multi echo (MSME) sequence with repetition time (TR) = 1,000 ms, echo time (TE) = 12.3 ms, number of signal averages (NSA) = 2, slice thickness = 1 mm, field of view (FOV) (read × phase) = 64 × 28 mm2, in-plane resolution = 160 × 160 mm2, and receiver bandwidth (BW) = 120 kHz. The transversal images were acquired with slightly adjusted acquisition parameters (MSME sequence: TR = 1,000 ms, TE = 9.5 ms, NSA = 45, slice thickness = 0.7 mm, FOV = 46 × 35 mm2, in-plane resolution = 177 × 177 mm2 and BW = 120 kHz). Both coronal and transversal image series were acquired twice, with and without fat suppression, and coronal images were resampled to 177 × 177 mm2 for visualization purposes. Regions of hyperintense MR signal (relative to muscle and organs) in a nonfat suppressed image were assumed to represent fat if the corresponding region in the fat-suppressed image was hypointense.

Statistics.

Data were analyzed using two-tailed Student's t test assuming equal variance between control and load groups or between "sustained load" and "removal of load" groups. When more than two groups were compared, ANOVA followed by Tukey's post hoc test was used. P < 0.05 was considered statistically significant. All data are presented as mean ± SEM.

Data Availability Statement.

The authors declare that all data supporting the findings of this study are available within the paper and its Supporting Information files.

Acknowledgments

We thank Dr. Mikael Johansson (Department of Languages and Literatures, Gothenburg University) for advice regarding linguistics and senior research engineer Staffan Berg (Department of Neuroscience and Physiology, Gothenburg University) for development of loading capsules. This work was supported by the NovoNordisk Foundation, the Swedish Research Council, the Swedish Government [under the Avtal om Läkarutbildning och Medicinsk Forskning (Agreement for Medical Education and Research)], the Knut and Alice Wallenberg Foundation, EC Framework 7, and the Torsten Söderbergs Foundation.

Footnotes

  • Author contributions: J.-O.J., V.P., S.L.D., M.E.J., J.-Å.G., S.H.W., and C.O. designed research; V.P., D.A.H., E.S., F.A., T.B., M.M., J.B., J.W., B.A., A.E.T., K.S., and S.H.W. performed research; R.D.C. and D.J.D. contributed new reagents/analytic tools; J.-O.J., V.P., D.A.H., E.S., T.B., J.B., J.-Å.G., S.H.W., and C.O. analyzed data; and J.-O.J., V.P., J.-Å.G., S.H.W., and C.O. wrote the paper.

  • Reviewers: W.L., ETH Zurich; and S.M., Jerry L. Pettis Memorial VA Medical Center and Loma Linda University.

  • The authors declare no conflict of interest.

  • This article contains supporting information online at www.pnas.org/lookup/suppl/doi:10.1073/pnas.1715687114/-/DCSupplemental.