Saturday, August 12, 2017

fiat is very reliable

what nonsense! I have Fiat Palio for 15 years, still runs like a charm and better than modern competition

Friday, August 11, 2017

toyota stopped in rain 79k miles

Junior Member
Joined:Sep 5, 2014


Vehicle:2009 Prius

2009 Prius stopped in rain 79K mi

After 400 mi of driving, 2009 Prius stopped in rain 200 mi from home.
How to tell model of second generation Prius ??
Lots of red and amber lights on on the dash, what means what ??
12.6v battery reading, disconnect 12v battery and car will move
100 yards before red and amber lights on on the dash.
Does the 2009 Prius have a problem with the elect connections some
where that water will get into ??
Not impressed with this car !!

valentino rossi beats marquez by 0.018s in Brno MotoGP test

Rossi beats Marquez by 0.018s in Brno MotoGP test

Thursday, August 10, 2017

반딧불은 애벌레도 빛을낸다.

반딧불이 입은 퇴화 한 것입니다. 인간을 포함한 모든 생물들이 마찬가지겠지만, 잘 사용하지 않고 필요가 없는 기능은 퇴화하게 되잖아요 반딧불이는 몸 자체에 생활사에 의해서 양분섭취가 필요가 없어요 보통 15일 안팍으로 생존을 하는데요~ 체내에 저장해 놓은 에너지로만 활동한답니다. 15일동안 배우자 찾아다니고 후손남기는데에만 에너지를 쓰기 때문에 먹이를 먹을 시간이 없다고 해요 반딧불이만이 가지고 있는 고유한 생활사인것이죠! 그리고 입이 없어서 내장기관이 없다고 생각하시는 분들이 많던데...... 체내에 수분이 효율적으로 전달되게 하기 위해 내장기관은 있어요 [ 반딧불 ] 반딧불이는 애벌레 때는 우렁이나 다슬기를 먹고사는 육식성이며, 어른 일때에는 이슬을 먹고 삽니다 (어른 반딧불이는 잘 보이지 않은 입을 가지고 있습니다 그래서 사람들이 입이 없는것으로 착각 할수 있습니다) 1) 특징 - 반딧불이는 개똥벌레라고도 하며, 몸빛깔은 검은색이며 앞가슴 등판은 붉은색 바탕에 한가운데 선은 검은색으로 되어 있습니다 - 그리고 배마디 배면 끝에서 2-3째 마디는 연한 노란색이며 빛을내는 기관이 있습니다 2) 활동과 먹이 - 어른벌레는 짝찟기를 한후 4-5일뒤에 이끼위에 300-500개의 알을 낳습니다 - 그리고 알은 20-30일만에 부화하며, 특히 애벌레는 얕은 하천에 서식하는 우렁이나 다슬기를 먹이로 수중생활을 하면서 15-20mm까지 자랍니다 ( 애벌레는 우렁이나 다슬기를 먹고 사는 육식성 입니다 ) - 반딧불이는 알, 애벌레, 번데기 과정을 거쳐서 6월경에 어른벌레가 되는데 어른벌레를 볼려면 6,7월경에 어른 벌레를 볼수 있습니다 어른벌레가 된후에는 빛을 내며 밤에 활동을 시작 합니다 - 어른 벌레는 암퀏이 크고 수컷이 조금 작으며, 수명은 2주 정도로 이슬을 먹고 사는데, 알을 낳고 11-13일 뒤에는 자연적으로 죽습니다 - 반딧불이는 어른벌레 뿐만아니라 알, 애벌레, 번데기도 빛을 냅니다 빛은 보통 노란색 또는 황록색이며, 한국에는 환경오염 등으로 점차적으로 거의 사라져 가는 형태이며 쉽게볼수 없습니다 - 반딧불이는 전북 무주군 설천면 일대가 서식지인데 이곳을 보호구역으로 지정하여 반딧불이를 보호하고 있습니다 (서식지를 천연 기념물 제 322호로 보호를 받고 있습니다. 특히 무주 일원은 반딧불이의 먹이 서식지로서, 먹이(다슬기) 서식지가 천연기념물로 되어 있습니다 ) 3) 분포지역은 한국, 일본 입니다 4) 종류로서는 파파리반딧불이,늦반딧불이,애반딧불이,꽃반딧불이...등이 있습니다 출처 : 다음 신지식 & 네이버 백과사전

해외축구리그가 우리나라 최고 인기 스포츠다.

나삐졌다(whitehouse92)2017-08-10 19:44:24112.187.***.***
요즘 epl누가보냐
MAMA무솔라(tottenhamno7)2017-08-10 19:50:32222.239.***.***
잡혀사는지코(kl3695)2017-08-10 20:14:58175.192.***.***
너빼고 다
스포츠운영자(afreecasport)2017-08-10 23:30:18222.121.***.***
안녕하세요 저도 잘 안봤는데... 올 시즌부터 보려고 합니다 감사합니다^^

Tuesday, August 8, 2017

renault has better engineering than honda

Honda aims to overtake Renault before end of 2017

Honda can leapfrog Formula 1 engine rival Renault before the end of the current season, says its motorsport chief Yusuke Hasegawa.

The Japanese manufacturer has been fourth in the engine pecking order, behind Mercedes, Ferrari and Renault, since rejoining F1 in 2015.
After changing its engine concept over the winter, Honda has struggled for performance and reliability this year, which in turn has put a strain on its relationship with McLaren.
But Honda has shown progress in recent races, with the team scoring its first points in June’s Azerbaijan Grand Prix - where it introduced ‘spec 3’ - followed by a double-points finish in Hungary last time out.
“I think we can keep the same ratio of the increasing of the power but it is difficult to catch up Mercedes or Ferrari,” Hasegawa told
“I really want to move ahead of Renault in terms of performance before the end of the season.”
When asked if he believed that would be a genuine possibility, given the Japanese manufacturer’s horsepower deficit to its rivals, Hasegawa replied: “Yes, I can see that on the data. I will not tell you the number, but we are closing the gap.”

Hasegawa added he felt this was the closest Honda has been to its rivals since rejoining F1 in 2015.
This comes after he said the Hungarian Grand Prix weekend was the first in 2017 where Honda was not plagued by reliability concerns.
Fernando Alonso finished sixth with teammate Stoffel Vandoorne 10th to enable McLaren to rise above Sauber into ninth in the constructors’ championship.
Speaking about the engine performance in Hungary, Hasegawa said: “The drivability was OK but still the drivers highlighted a lack of power.
“They are very confident with the car, which is good, but it is still difficult to challenge the top three teams.”
Honda is pushing on with development of its 2017 engine at its bases at Sakura and Milton Keynes and intends to introduce ‘spec 4’ as soon as it can verify gains on the dyno.

Monday, August 7, 2017

in japan, greek foot is appreciated

Wisepersonsay10개월 전
In Japan, Greek toes are appreciated.  The Japanese saying goes those with Greek toes surpass their parents for more success.  Every culture has a different myth and superstitions.  If what the narrator says is true about Greek toes, I have them and am so thankful I have intelligence and charm.  Thank everything good and bad.

Sunday, August 6, 2017

andre ward lost to kovalev twice. american judges allows andre ward cheating his entire career.

Maxwell Baer
Maxwell Baer4 months ago
Not that it's a real offer, when has Ward ever made any concession for anyone? , but even if it was..... Ward is a overrated boxer. The entire sport of boxing should duck his scumbag fake Christian ass. The guy fouls his way through every fight and never fights on a level playing field. Golovkin would have to KO him and he'd be dealing with a referee that allows Ward to get away with anything he wants. Headbutts, holds, hit and hold, elbow, whipping the elbow.....theirs no depths to which the guy won't sink.

Saturday, August 5, 2017

volkswagen jetta has the best fuel efficiency by far, much better than japanese cars

2015 Volkswagen Jetta Sedan 2.0L TDI SE w/Connectivity – Sedan – Black

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2.0L TDI SE w/Connectivity
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31 City MPG / 46 Hwy MPG †

Wednesday, August 2, 2017

Do Glasses Weaken Your Eyes?

Do Glasses Weaken Your Eyes?

When you take them off you feel “blind”. Have the glasses weakened your eyes? Rest assured the answer is no. Since getting your new glasses you probably see better than ever. But now it seems you can’t get along without them. When you take them off you feel “blind”. The obvious thought strikes: have the glasses weakened your eyes? Rest assured the answer is no.

Think about what your vision was like before you had these glasses. Though you were getting along okay you actually had gotten used to your poor vision and whatever effort it took to see—squinting your eyes to see more clearly (especially if you are nearsighted) or moving reading material farther away (if you are over 40).

Once you put on your new glasses the struggle ended; seeing became effortless and far more satisfying. But when you took the glasses off the struggle to see returned only now it seemed even worse than before.

Why Do Your Eyes Seem Weaker?

Let’s look at an analogy. What if you had to live with a 20-pound knapsack strapped to your back. It was heavy but after a while you go used to it and didn’t even notice it anymore. Similarly what if you saw poorly without glasses. But after a while you got used to it and barely noticed the effort required.

Now suppose that someone came along and removed the knapsack. (What a relief!) Or suppose someone gave you glasses that made it easier for you to see.

Time passes and you put the knapsack on again. It feels a lot heavier than you remember partly because past memories are not perfect but mostly because you’re used to the freedom of not being weighed down by it. In the same way once you are used to seeing better with glasses a return to the old struggle to see without them becomes intolerable. This does not mean that the glasses have worsened you basic eye condition.

But…..Haven’t You Become Dependent on the Glasses? Wearing your glasses makes you no more dependent on them than living without the knapsack. In each case you are more comfortable and you function with less effort.

Yes you depend on your glasses for ease of vision but isn’t that why you got them? You depend on them the same way you depend on a good tool. The fact is glasses are the proper tool for the job of seeing. You are no more or less dependent on them than you are on having the proper hammer or screwdriver for a carpentry job.

Glasses Do Not Cause Eye Changes

There are many conditions affecting the eye that progress (get worse) on their own whether you wear glasses or not. Glasses are sometimes blamed for the worsening but they are not at fault.

One such condition is presbyopia the eye problem everyone experiences around age 40 or so. Having presbyopia means that because of normal aging changes our eyes start losing the ability to focus up close. At first you only notice it when you try to read small print but over time everything at close range loses clarity. You attempt to adjust by holding the material farther away. When you finally need to hold things so far away that your “arms are too short ” you get glasses that let you see again at the normal reading distance.

The glasses work well….for a time. Then one sad day you realize that your eyes are gradually getting “worse.” Just like before you are beginning to have difficulty reading. What is happening however has nothing to do with the glasses. You are only experiencing the natural progression of the presbyopia which is a normal part of life.

Another eye condition that changes on its own independent of glasses is myopia (nearsightedness). Children who have myopia are commonly subject to its progression especially during adolescence when glasses are worn to sharpen vision. But here too the myopia progression if it is going to occur will do so even without wearing glasses. To learn more about factors causing myopia progression click here.

Tuesday, August 1, 2017

even in japan, japanese people buy benz, bmw and audi but not lexus

2015 (Full Year) Japan: Best-Selling Car Brands and Manufacturers

January 8, 2016 by Henk Bekker in Japan

In 2015, Japan’s largest car manufacturers and brands were Toyota, Honda and Suzuki. The Japanese market shrank by 9% to just over 5 million vehicles. Japanese car manufacturers generally experienced sharp sales losses in Japan in 2015 but heavy and commercial vehicle sales were mostly stronger indicating some growth potential in the Japanese economy. Mercedes Benz replaced Volkswagen as the favorite imported car brand in Japan.

The Japanese New Vehicle Market in 2015 (Full Year)

New vehicle registrations in Japan decreased by 9.3% in 2015 to 5,045,511 vehicles. This figure includes cars (including Kei or minicars), trucks and buses.

The Japanese vehicle market was over half a million units smaller in 2015 than in 2014. Although sales remained above five million vehicles, 2015 was the weakest for four years.

Japanese New Vehicle Registrations per Year

Japanese new vehicle registrations, including cars, Kei cars, trucks and buses were as follows per calendar year according to JADA figures:

Year Vehicle Sales % Change
2015 5,046,511 -9.3
2014 5,562,888 3.5
2013 5,375,513 0.1
2012 5,369,721 27.5
2011 4,210,220 -15.1
2010 4,956,136 7.5
2009 4,609,255 -9.3
2008 5,082,235
Best-Selling Car Manufacturers in Japan in 2015

The top-selling vehicle manufacturers and brands in Japan in 2015 according to new vehicle registration figures released by JADA were as follows:

Manufacturer Sales 2015 Sales 2014 % Change
Total 5,046,511 5,562,887 -9.3
1 Toyota 1,449,067 1,509,149 -4
2 Honda 726,928 848,753 -14.4
3 Suzuki 636,360 787,361 -19.2
4 Daihatsu 610,396 708,179 -13.8
5 Nissan 589,099 670,315 -12.1
6 Mazda 245,437 224,359 9.4
7 Subaru 162,254 169,552 -4.3
8 Mitsubishi 102,009 125,083 -18.4
9 Isuzu 74,730 74,556 0.2
10 Mercedes-Benz 65,162 60,839 7.1
11 Hino 61,173 57,422 6.5
12 VW 54,766 67,438 -18.8
13 Lexus 48,231 44,246 9
14 BMW 46,229 45,645 1.3
15 Mitsubishi Fuso 44,230 42,509 4
16 Audi 29,414 31,413 -6.4
17 BMW MINI 21,083 17,596 19.8
18 Volvo 13,786 13,520 2
19 UD Trucks 11,001 11,072 -0.6
20 Jeep 7,132 6,692 6.6
Best-Selling Car Brands in Japan in 2015

Although there were wide swings in the performances of various marques in Japan in 2015, the only change in the order of the top-ten largest car manufacturers was Mercedes Benz’s entry at 10 in place of Volkswagen. Truck and commercial vehicle manufacturers generally had stronger sales, which indicate some growth potential in the Japanese economy in coming months.

Toyota easily remained the largest vehicle manufacturer in Japan in 2015. Although Toyota sales were down 4%, this was solidly above the market average. Toyota was helped the popularity of new models but also its large commercial vehicle business.

Honda remained Japan’s second largest carmaker but sales were down by 15% leaving Honda almost exactly half the size of Toyota. Honda suffered from an aging model range – Japanese buyers generally prefer very new models,

Suzuki, like Honda, suffered from the absence of a major commercial vehicle operation. Suzuki sales were down by a fifth – the worst decline of all top carmakers. Daihatsu and Nissan sales were similarly down by double digits.

Mazda was the best performer of the top brands in Japan in 2015 by increasing sales by 9.4%. Of the 20 largest carmakers in Japan, only Mini improved more.

Subaru sales were down 4.3% allowing it to gain some market share while Mitsubishi lost nearly a fifth of sales. Isuzu sales were flat.

Mercedes Benz increased sales by 7.1% and entered the top-ten list at the expense of Volkswagen that was for years the top foreign car brand in Japan. Volkswagen slipped from tenth to twelfth with the second weakest performance of the top brands.

The only other changes in the order of the top-20 best-selling car brands in Japan were Lexus again overtaking BMW and Jeep entering the list at the expense of Fiat.

Sports and Exotic Car Sales in Japan in 2015

Japan remained an important market for expensive sports and exotic cars in 2015. These expensive brands did not suffer any of the declines common among the mass brands.

A small selection from the JADA statistics of new passenger vehicle registrations in Japan in 2015:

Manufacturer Sales 2015 Sales 2014 % Change
Maserati 1,449 1,407 3
Ferrari 720 561 28.3
Bentley 370 317 16.7
Lamborghini 349 187 86.6
Rolls Royce 156 154 1.3
McLaren 90 88 2.3
Bugatti 5 2 150

The three German players BMW, Audi and Mercedes-Benz account for approximately 80% share of the global luxury car market

Global Luxury Car Market Report 2017 - Research and Markets

Research and Markets
19 Jun, 2017, 12:30 BST

Research and Markets has announced the addition of the "A Study of the Global Luxury Car Market 2017" report to their offering.
A Study of the Global Luxury Car Market 2017'highlights key dynamics of the global luxury car market. The growing opportunity in the sector has been investigated along with analysis of the five markets of luxury cars: United States, Europe, China India and Middle East.
The Initiatives and performance of key global players including Volkswagen AG, Daimler AG, Bayerische Motoren Werke AG (BMW), Tata Motors Limited and General Motors Company along with current market scenario has also been studied. The report contains latest industry leaders verbatim.
The global luxury car market has seen been relatively untouched by the financial crisis and has been posting growth driven by the emerging markets. The three German players BMW, Audi and Mercedes-Benz account for approximately 80% share of the global luxury car market. BMW is the global leader in the luxury car segment, followed by Mercedes-Benz and Audi. World over while mass automobile manufacturers are struggling with margins, high end manufacturers are enjoying steadily increasing sales.
In the United States luxury car market, over the past few years, it is the crossovers and SUVs, which have been experiencing growth in sales. In 2016, the two leading players in the market, Mercedes-Benz and Lexus did not see any of its non-SUV models experience growth in sales. The luxury car market in the US is now diverging into two clear categories, the budget cars and the ultra luxury cars. There is clustering of new purchases in the two extreme categories of budget and ultra luxury.
Demand for luxury cars in Europe had been at a low for nearly two decades and started recovering gradually from 2014. Even though challenging economic conditions still prevail in many European markets, players such as BMW have been able to maintain volumes of their higher end models. In Europe, there is greater demand for high-end models as compared to the emerging markets such as China where the entry-level luxury markets are seeing greater growth. New players in the market such as Hyundai have big plans for Europe even though traditionally the foreign players have not been able to match the big 3 German brands which account for approximately 4 out of 5 luxury cars in the market.
In 2017, the luxury car segment in China is seeing strong growth. The millionaires in China increased by 10% in 2016 year-on-year. Despite the government's austerity drive, sales of super-luxury and supercar sales have not slowed down in China. Mercedes-Benz witnessed its best ever month in terms of sales in China in March 2017.
India is one of the largest passenger vehicle markets in the world and vehicle manufacturers both in the passenger and luxury segment see a huge potential for sales growth in the country. While the luxury car penetration level in the country is low but leading luxury car manufacturers are betting on the market's potential. Luxury car penetration in India currently stands at 1.1%. Launch of multiple strategically priced models at various price points coupled with smart financing schemes and a robust dealer network is boosting the sales of luxury cars in India.
In the GCC region, the United Arab Emirates is the second-largest automotive market after Saudi Arabia. U.A.E. is heavily dependent upon imports and almost the entire supply of car as well as light vehicles is imported. The low oil prices and global macroeconomic factors are affecting the luxury goods market in the Middle East. While over the last 10 years the personal luxury goods market witnessed an annual growth of 8-10%, it is projected to drop to approximately 4-5% over the next few years. Even amidst the economic slowdown globally, the sales of luxury cars per capita are still the highest in the Middle East.
Key Topics Covered:

1. Analyst Opinion

2. Global Luxury Car Market

3. United States Luxury Car Market

4. Europe Luxury Car Market

5. China Luxury Car Market

6. India Luxury Car Market

7. Middle East Luxury Car Market

8. Key Player Profiles

Bayerische Motoren Werke AG (BMW)
Daimler AG
General Motors Company
Tata Motors Limited
Volkswagen AG
For more information about this report visit

Media Contact:

Research and Markets
Laura Wood, Senior Manager

For E.S.T Office Hours Call +1-917-300-0470
For U.S./CAN Toll Free Call +1-800-526-8630
For GMT Office Hours Call +353-1-416-8900

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SOURCE Research and Markets
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Friday, July 21, 2017

german cars are much more reliable than japanese car

Шевери Венто
Шевери Венто7시간 전하이라이트 답글
German cars are only known to be fast, not reliable? You must live in some very contemporary culture not having heard of the half-a-million mile Mercedes- diesels? Now compare them to the utter pieces of shit asian diesels, like the Toyota AD- engine family. Your comment is as subjective as they come.

Wednesday, July 12, 2017

arrogant nadal is a whiner even when he buys a fixed draw

Is Rafael Nadal in Danger of Being Labeled a Whiner?

Rafael Nadal, the tennis king of idiosyncrasies, might be adding another ritual to his routine: whining.

In case you haven't heard, Nadal hated the tennis balls used at the China Open in Beijing. He thinks those things are freaking dangerous.

He told The Associated Press (via, "This week we are playing with one ball. Next week we are playing with a different ball. That's dangerous for the shoulder, dangerous for the elbow."

Oh, Rafa, Rafa, Rafa. What now?

Sometimes it seems the Spaniard is always complaining about something.

Nadal certainly wasn't the only player to raise questions about the balls. Andy Murray complained too. It's just that Nadal's beef with the balls lands on a growing list of grievances.

You see, this week, it was the balls. Every year he grumbles about the number of hard-court tournaments and the impact it has on his knees

In November 2013, Nadal complained about the ATP finals being played on indoor hard courts. He told, “During these nine years the Masters Cup was on indoor, a surface that was not the best for me ... I understand, but I think this is unfair.”

You think Roger Federer wishes a few French Opens could be played on grass? But every year, the same thing...clay. That's just wrong.

Oh, Rafa, Rafa, Rafa.

Sometimes he acts like the world is against him. Like last year, at the French Open. That's when he slammed the French for their scheduling and called it unfair, according to the AP (h/t

Nadal thinks many things are unfair.

Two years ago, he was unhappy about the blue clay in Madrid. He and Novak Djokovic threatened to skip the tournament the next year if the blue clay came back. It didn't.

There’s nothing wrong with a professional athlete speaking his mind. However, instead of appearing outspoken, Nadal comes across as a whiner.

He avoids bombastic outbursts like those from Richard Sherman. Yet, there's something about the way in which Nadal states his case. It rubs folks the wrong way.

Perhaps it’s the tone of his voice, which sometimes barely rises above a mumble? Maybe it’s his shoulder-shrugging demeanor in press conference?

Whatever it is, it’s beginning to grate. Like fingernails across a chalk board, Nadal’s constant complaining irks.

It's unfortunate too because otherwise, Nadal is considered humble. He's gracious in defeat and has been an excellent ambassador for the sport. Just this week, he carried roses out to Li Na at her retirement celebration in Beijing. He was one of the few ATP players to make an appearance.

But oh Rafa, Rafa, Rafa. Complaining about the balls?

What used to be mere fodder for Rafa haters has spilled over into editorials and tweets. A recent headline by USA Today asked: “Did Rafa Nadal’s whining set him up for Beijing Open collapse?”

After Nadal went on and on about the experimental blue clay in Madrid, veteran tennis writer Peter Bodo devoted an entire column for Tennis Magazine to questioning Nadal's persistent whining. Bodo wrote (via NBC Sports):

Most of you are familiar with his dissatisfactions: The engorged calendar, the ranking system (he lobbied to have it transformed into one that was based on 24 months or results, rather than 12), his seemingly never quite right knees, the blue clay. . . Rafa isn't the only player to complain about such things, but none of his peers at the top of the game seems to have quite as many issues, or appear to take them so personally (to the point where he quit the ATP player council, seemingly because his fellow pros just didn't understand).
Whether or not the whiner label is justified, the fact that it's coming up more often speaks to the prevalence of the perception.

Nadal's talent and accomplishments have already earned him a future spot in the Hall of Fame and probably a few pages in the record books. That's why the whining seems beneath him.

Oh Rafa, Rafa, Rafa. It's OK to remain conscientious and opinionated. Just pick your battles better, or else earn a new nickname: "Rafaree."

arrogant whiner excuse king nadal yet again whine even when everything was corrupt for him

Rafael Nadal questions Wimbledon officials' decision after Roger Federer gets Centre Court nod
Roger Federer and Rafael Nadal: The greatest tennis rivalry of all time Reuters
Rafael Nadal apologised to his supporters on Wimbledon's Court One after his shock fourth round defeat to Gilles Muller on Monday (10 July). And, apart from his disappointment of losing, he also addressed the tournament officials' decision to move him to Court One and give the nod to Roger Federer to play on Centre Court.

The Spaniard was one of the pre-tournament favourites to make it to the latter stages, admitted that he put all his effort into the game, which ended 15-13 in favour of the Luxembourg's 16th seed in the fifth set. Nadal's loss is unlikely to overshadow his strong first-half of the campaign, which saw him play in seven finals and pick up four titles, including a 15th Grand Slam title at the French Open.

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"Great feeling. Great atmosphere. I put everything on the court. I played with all my passion," Nadal said after his loss, as quoted by NDTV "The crowd normally appreciate that. Sorry for the crowd that were supporting me."

Apart from his defeat, Nadal was unhappy about the tournament officials' decision to move him to Court One for his fourth round clash to accommodate Roger Federer on Centre Court and admitted that they should distribute matches in the main court evenly rather than always choose the same players.

The 31-year-old, however, made it clear that his statements are no indication about his future participation at SW19 and vowed to make a comeback as he desires to play many more matches on Centre Court.

"I never said I not going to come back. Yeah, I want to come back because I want to play more times in the Centre Court," Nadal added, as quoted on Sport360.

"I like playing more on Centre Court. Someone has to play on Centre, and it's almost always the same players here. This is the reality. Here, there are many of us who have won a lot in our careers, who have a lot of important history behind us.

"A tournament that wants to be as traditional and as special as Wimbledon has to distribute the number of matches scheduled on Centre Court and that not always the same people play there, and when there are doubts, the others are sent to other courts," the Spaniard said.

Rafael Nadal
Rafael Nadal suffered a shock fourth round defeat at the hands of Gilles Muller at Wimbledon on MondayGetty
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Tuesday, July 11, 2017

how to reduce number of fat cells

How to make a fat cell less not thin: the lessons of fat flux

I do still plan to finish the third, and perhaps a fourth, part on the “Ketosis – advantaged or misunderstood state?” mini-series.  However, a question I get often makes me realize a tiny bit of housekeeping is in order before we go there.  The question is basically a variation on this theme: Does being in ketosis automatically translate to fat loss?
For those too busy to read ahead, let me give you the punch line: No. For those who want to understand why, keep reading (hopefully this is still everyone). This topic is — surprise, surprise — very nuanced, and almost always bastardized when oversimplified, which I’m about to do, though hopefully less than most.  Without oversimplifying, though, this will turn into a textbook of 1,000 pages.
From the ketosis series, or at least the first and second part, along with the video in this previous post, you should have taken away that ketosis is not some ‘magical state of mystery.’  It’s simply a state of physiology where our liver turns fatty acid (both ingested and stored) into ketones. In part III (and possibly a part IV) of that series, I’ll go more into the actions of ketones and why you may or may not want to consider putting yourself into a state where your liver makes them.
There seems to be great confusion around ‘nutritional’ ketosis (a term we use to distinguish ‘dietary-induced’ ketosis from the other 2 forms of ketosis: starvation ketosis and ketoacidosis, the latter a serious complication of type I diabetes). But, before I try to dispel any of the confusion, we need to go through a little primer on what I like to call “fat flux.”
One point before diving in, please do not assume because I’m writing this post that I think adiposity (the technical term for relative amount of fat in the body) is the most important thing to worry about.  On the contrary, I think the metabolic state of the cell is far more important. While there is a correlation between high adiposity (excessive fat) and metabolic dysfunction, that correlation is far from perfect, and, as I’ve discussed elsewhere, I think the arrow of causation goes from metabolic dysfunction to adiposity, not the reverse.  But, everyone wants to lose fat, it seems, so let’s at least get the facts straight.
Let’s start with an assertion: Barring the presence of scientific evidence I’m unaware of, and barring surgical intervention (e.g., liposuction), reducing the adiposity of a person is achieved by reducing the adiposity of individual adipose cells, collectively. In other words, the number of adipocytes (fat cells) we have as an adult does not change nearly as much as their size and fat content.  So, for a person to reduce their fat mass, their fat cells must collectively lose fat mass. 

Fat flux 101

According to “An Etymological Dictionary of Modern English,” the word flux comes from the Latin word fluxus and fluere, which mean “flow” and “to flow,” respectively. While the term has a clear mathematical meaning in physics, defined by a dot product I promise I won’t speak of, you can think of flux as the net throughput which takes into account positive and negative accumulation.
If we start with a bucket of water and put a hole in the bottom, the result, needless to say, is an efflux of water, or negative water flux.  Conversely, if we start with a bucket – no hole – and we pour water in, that’s an influx of water, or positive water flux.
If that makes sense, then the idea of fat flux is pretty straight forward.  If more fat enters a fat cell (called an adipocyte) than leaves it, the fat cell is experiencing a net influx – i.e., positive fat flux.  And, if more fat leaves a fat cell than enters, the reverse is true: it is experiencing a net efflux, or negative fat flux.
Not surprisingly, a fat cell is more complicated than a bucket.  Basically, though, there are two “inputs” and one “output.” The figure below shows this in some detail. (TAG stands for triacylglycerol, which is another word for triglyceride, which is the storage form of fat.)  The first thing you may appreciate, especially since I’ve highlighted it, is the role insulin plays in regulating the process of fat flux.  Insulin does the following:
  1. Upregulates lipoprotein lipase (LPL), an enzyme that breaks down TAG so they can be transported across cell membranes. Since TAG are too big to bring across cell membranes, they need to be “hydrolyzed” first into free fatty acids, then re-assembled (re-esterified) back into TAG.
  2. Translocates GLUT4 transporters to the plasma membrane from endosomes within the cell.  In other words, insulin moves the GLUT4 transporter to the cell surface to bring glucose into the cell.
  3. Facilitates lipogenesis, that is, facilitates the conversion of glucose into acetyl CoA which gets assembled into fatty acids along with glycerol.
  4. Facilitates esterification, that is, facilitates the process of assembling fatty acids into TAG (3 fatty acids per TAG).
  5. Inhibits hormone-sensitive lipase (HSL) and adipose triglyceride lipase (ATGL), two important enzymes that breaks down TAG into fatty acids and glycerol such that the fatty acids can be released from the fat cell. Once bound to albumin the free fatty acids are free to travel elsewhere in the body for use (e.g., to the liver for conversion to ketones, to the heart muscle or skeletal muscles for conversion to ATP).
  6. Though not shown in this figure, insulin appears to indirectly act on malonyl-CoA, a potent inhibitor of CPT I, one of the most important mitochondrial enzymes that facilitates the oxidation of fatty acids. (CPT I is what enables fatty acids to be shuttled into the mitochondria for oxidation, the process which releases or liberates their energy through electron transport.)
Adipose cell - detailed
Other hormones and enzymes in the body also play a role.  For example, under a sympathetic response, the so-called “fight or flight” response, adrenaline and noradrenaline (i.e., epinephrine and norepinephrine) activate HSL and ATGL to combat the effect of insulin as an inhibitor of lipolysis, thereby increasing lipolysis, or liberating stored energy from the fat cell.  Glucagon may also play a role in this process, though the exact role is not as well understood, at least not in humans.
So in summary, insulin is indeed the master hormone that regulates the flow of fat (and glucose) into and out of a fat cell.  There are other players in this game, to be sure, but insulin is The General. High levels of insulin promote fat storage and inhibit fat oxidation, and low levels of insulin promote fat mobilization or release along with fat oxidation.
If this sounds crazy – the notion that insulin plays such a crucial role in fat tissue — consider the following two clinical extremes: type 1 diabetes (T1D) and insulinoma. In the former, the immune system destroys beta-cells (the pancreatic cells that make insulin) – this is an extreme case of low insulin.  In the case of the latter, a tumor of the beta-cell leads to hypersecretion of insulin – this is an extreme case of high insulin.  Prior to the discovery of insulin as the only treatment, patients who developed T1D would become emaciated, if the other complications of glycosuria and dehydration didn’t harm them first. They literally lost all fat and muscle.  Conversely, patients with insulinoma often present looking not just obese, but almost disfigured in their adiposity.  Because Johns Hopkins is a high volume referral center for pancreatic surgery, it was not uncommon to see patients with insulinoma when I was there.  As quickly as we would remove these tumors, the patients would begin to return to their previous state and the adipose tissue would melt away.
For the purpose of our discussion, I’ve simplified the more detailed figure above into this simplified figure, below. I’ve tried to size the arrows accordingly to match their relative contributions of each input and output.
The first figure, below, shows a state of fat balance, or zero net fat flux.
Neutral fat flux
Input #1: De novo lipogenesis, or “DNL” – Until the early 1990’s there was no way to measure this directly, and so no one really had any idea how much this process (i.e., the conversion of glucose to fat) contributed to overall fat balance.  Without going into great technical detail, Marc Hellerstein, arguably one of the world’s foremost authorities on metabolomics and DNL, developed a tracer technique to directly measure this process.* If I recall correctly, the original report was in 1991, but this paper is a great summary.  Published in 1995 in the Journal of Clinical Investigationthis paperwould go on to become the “citation classic.” This study demonstrated that under eucaloric feeding conditions, with about 50% of energy coming from CHO, DNL did not represent a significant contribution to fat flux. It was about 5%, hence the tiny red arrow under a state of fat balance (i.e., a state where fat entering the fat cell is equal to fat leaving the fat cell). A very important point to be mindful of, however, is this: this represents an average throughout the body and does not differentiate specifically between, say, DNL in the liver and DNL in the periphery (i.e., fat cells). This limitation is not trivial, but rather than focus on the very specific details of this paper, I’d rather use it as a framework for this discussion. (This paper is really interesting, and were it not for the fact that this post is going to be long enough, I would say much more about it.  As such, I will probably do a full post on this paper and related topic in the future. The 1995 paper also examined what happened to DNL during periods of over- and under-feeding CHO and fat.)
(*) Marc is on the Scientific Advisory Board for NuSI, so perhaps I’m biased in my admiration of him and his work.
Input #2: Re-esterification, or “RE” – In a state of fat balance, RE is largely composed of dietary fat sources that are not immediately used, but rather stored for later use.  (Nuanced point: RE also includes fatty acids that were previously liberated from adipocytes, not oxidized, and are now being recycled back into TAG.  This is a normal consequence of fat liberation.  The fat cell probably ‘deliberately overdoes it’ by liberating more fatty acid from TAG just to be safe; that which is not oxidized is re-esterified.  The exact balance of RE composed from dietary sources versus recycled fatty acids will depend on fat consumption and energy demands of the person. For the purpose of simplicity, this diagram does not show some portion of the L fraction returning to the RE fraction, though this is exactly what is happening in ‘real life.’)
Obviously, though, the relative size of the blue arrow depends on how much fat one is consuming and how many metabolic demands are in place for fatty acids.  The latter is highly determined by dietary composition (see the discussion on RQ, or respiratory quotient, at about minute 31 in this video).
For the real aficionado, there is another wee bit of nuance here. This study, published in 1991 in the Journal of Lipid Research, suggested that the RE process is a bit more complicated than simply re-assembling fatty acids on a glycerol backbone inside an adipocyte.  Based on these experiments, which used a similar* tracer method to the one used by Hellerstein et al. to evaluate DNL, the authors (which included Rudy Leibel, the co-discoverer of leptin) suggested that RE requires an intermediate step outside of the adipocyte in the interstitial and capillary space (figure 8 of the paper demonstrates this very well schematically).
(*) Technically, Hellerstein et al. used a heavy isotope; Leibel et al. used radioactive isotopes.
Output: Lipolysis, or “L” – Finally, in a state of fat balance, lipolysis must be equal to the sum of DNL and RE.  This is true if we are talking about tiny little fat cells or giant ones.  Remember, it’s the balance that matters.
I hope it’s clear from this summary that there are an infinite number of physiologic states that can satisfy the equation of fat balance: DNL + RE = L. For example, someone like me who is in fat balance (i.e., I’m neither gaining nor losing fat mass at this point), has virtually zero DNL, but quite high RE, especially after meals.  Consequently, I have very high L.  If you took a person on a very low-fat diet (e.g., 20% fat, but 65% CHO), they would have modest DNL and low RE, but they would have low L.  We would both be in fat balance, but we satisfy the equation DNL + RE = L by very different means.
Ok, so let’s turn our attention to the non-equilibrium states: Net fat influx and net fat efflux.

Fat influx

In a state of net fat influx – accumulation of fat within a fat cell – the following condition must be met (on average): DNL + RE > L.  (I say “on average” because, of course, a fat cell is a dynamic system with constant changes in these parameters.  So, at any moment in time the balance can shift, but over a period of time the equation is correct.)
The next (overly simplistic) figure below gives you a representative state of what fat influx or ‘positive fat flux’ probably looks like.  DNL is higher, but still relatively small, unless overfeeding CHO.  RE is larger than it was in a balanced state, but not necessarily ‘huge.’  Most cases of net fat influx are probably governed by low L.  In other words, fat accumulation is probably more governed by a failure to mobilize (breakdown TG into fatty acids for export and use) TAG than anything else.
Have you ever spoken with someone who is trying desperately to lose weight (fat) who says, “I don’t understand what’s happening…I hardly eat any fat, and yet I can’t lose a pound (of fat)!”  The skinny people in the group scoff, right? Well, not so fast.  It’s quite possible, if the hormones that regulate fat tissue are not working in your favor, to do such a poor job mobilizing fat from fat cells, and oxidizing that fat (see below), that you can be in fat balance, or even fat imbalance with accumulation, despite small DNL and small RE.
If you think about it, lipolysis (L), or liberating fat from a fat cell is a necessary, but not sufficient condition to actually generate the free energy inherent or stored within it.  One more major step is necessary – oxidizing the fatty acid via the process of beta-oxidation. This is where one actually gets the energy (ATP) from fatty acids. The same hormones and enzymes that promote L, directly or indirectly act on other intermediaries that promote oxidation, more or less. The converse is also largely true.
Brief digression: I’m always troubled by folks who have never tried to take care of someone who is struggling to lose weight (fat), and who themselves have never been overweight, but who insist obesity is ‘simply’ an energy balance problem – people eat too many calories.  When eternally lean people preach about the virtues of their ‘obvious’ solutions to obesity – just eat less and exercise more – I’m reminded of a quote (source unknown to me), “He was born on the finish line, so he thinks he won the race.”  You only need to meet one woman with PCOS, or one person with hypothyroidism, or one child with Cushing’s disease to know that adiposity can – and is – largely regulated by hormones.  The fact that such patients need to create a positive energy balance (i.e., eat more calories than they expend) to allow it does not seem to provide a meaningful insight into the mechanism of why.
Fat influx

Fat efflux

In a state of net fat efflux – reduction of fat within a fat cell – the following condition must be met (on average): DNL + RE < L (same caveat as above on the idea of “on average”).   Again, looking at the figure, you can see one physiologically common way this occurs, the setting of carbohydrate restriction.  DNL is reduced (probably even to immeasurable levels, depending on the extent of restriction), but RE actually goes up.  The net efflux, however, results from the greater increase in L.
A person in nutritional ketosis, if experiencing fat loss, probably looks like this. (Don’t worry, I have not forgot the opening questions: Does being in nutritional ketosis automatically put you in this state?).  Certainly another state of net fat efflux is starvation.  DNL and RE are both very small, especially DNL, and lipolysis is quite large. This is probably the most rapid state of negative fat flux a human can experience.
Fat efflux

So what we do about it?

I do not believe there is only one state, shy of total starvation, which will assuredly put you in state of negative fat flux.  Of course, starvation is not sustainable, and therefore should be taken off the table as a viable long term eating strategy.
What about profound caloric restriction? Yup, this is probably (though not necessarily) going to work, depending on how “profound” is defined.  If defined as a 40% reduction of energy stable intake, it’s probably going to work.  If defined as a 10% reduction, it would be difficult to know without knowing at least two other things:
  1. Baseline level of insulin resistance;
  2. RQ of pre- and post-diet.
What about dramatic alterations in macronutrient composition? This is where the discussion gets really interesting.  Many people, myself included, advocate a diet low in the type of carbohydrates that result in the greatest insulin secretion.  In other words, a diet that overall reduces insulin secretion. The rationale, of course, is provided by the first figure above (from the textbook) and a slew of clinical studies which I will not review here (see Gardner JAMA 2007, Ludwig JAMA 2012, and Shai NEJM 2008 to name a few).
But, the bigger question is why? Why do most (but not all, by the way) people with excess fat to spare who are on well-formulated carbohydrate-reduced diet lose fat? (Notice, I did not say weight, because the initial – and often rapid — weight loss achieved by many is actually water loss.)
Is it because of a physiologic change that leads them to reduce overall intake?
Is it because of a physiologic change that, despite the same intake in overall calories, increases their energy expenditure?
Is it some combination of these?
I wish I knew the answer, but I don’t (universally).  I believe we will know the answer to this question in a few years, but until then, I’m left to offer the best my limited intuition can offer.  In other words, what I suggest below is my best interpretation of the literature, my personal experience that I’ve had with hundreds of other people, and my discussions with some of the most thoughtful scientists in the world on this topic:
Thought #1: I suspect that many people who reduce simple carbohydrates and sugars end up eating fewer calories.  This observation, however, may confound our understanding of why they lose weight.  Do they lose weight because they eat less? Or, do they eat less because they are losing weight? I suspect the later.  In this state, lipolysis — and by extension, given the hormonal milieu, oxidation — are very high, certainly relative to their previous state.  By definition, L > DNL + RE, so there is ample ATP generated by oxidation of the fatty acid.  If you believe (as I do*) that the liver is the master organ of appetite regulation, increases in ‘available energy’ (i.e., ATP) would naturally reduce appetite (though I don’t think we know if ATP per se is the driver of this feedback loop).  But don’t confuse what’s happening. They are not giving up fat from their fat cells because they are eating less.  They are eating less because they are giving up fat from their fat cells.  Big difference.
(*) The especially astute reader will note that this is the first time I have made reference to this point.  I have been heavily influenced recently by the work of Mark Friedman, and a discussion of this point is worth an entire post, which I promise to deliver at some point in the future. If you can’t wait, which I can understand, I highly encourage you to start scouring the literature for Mark’s work.  It’s simply remarkable.
Thought #2: I also suspect that some fraction of people who follow this eating strategy lose fat without any appreciable reduction in their total caloric intake, at least initially. What?, you say, doesn’t this violate the First Law of Thermodynamics? Not at all.  If L > DNL + RE, and the increase in lipolysis (i.e., fatty acid flux out of the fat cell) results in increased oxidation of fatty acids, energy expenditure (EE) would be expected to rise.  A rise in EE, in the face of constant input, is a sign of fat loss. What differentiates those in this camp (I was in this camp) from those above (point #1), is unclear to me.  It may have to do with concomitant exercise.  I have seen unpublished data, which I can’t share, suggesting non-deliberate EE rises more in a low RQ (high fat, low carb) environment when a person is exercising significantly (as I do). I’m not stating the obvious – that the deliberate EE is higher – that is clearly true. I’m suggesting resting EE is for some reason more likely to rise in this setting.  Since I’m taking the liberty of hypothesizing, I would guess this effect (if real) is a result of the body trying to keep up with a higher energy demand and making one trade-off (generating more free ATP via more lipolysis) for another (ensuring a constant supply of available energy to meet frequent demands). It is also possible that this increase in free/available energy results in an increase in deliberate EE (i.e., the person who suddenly, in the presence of a cleaned up diet feels the desire to walk up the stairs when they previously took the elevator).  Finally, and perhaps most importantly, whether or not this up-regulation of energy takes place may be dependent on the other hormones in the body that also play a role in fat regulation, including cortisol, testosterone, and estrogen. They could be partly or mostly responsible for this. The literature is quite dilute with respect to this question, but in my experience (feel free to dismiss), it is not uncommon to see a reduction in cortisol and an increase in testosterone (I experienced about 50% in free and total testosterone) with a dietary shift that improves food quality.  The same may be true of estrogen in women, by the way, though I have less clinical experience with estrogen.
Thought #3: As a subset to the point above (point #2), in an ‘extreme’ state of carbohydrate restriction, i.e., — nutritional ketosis — there is an energy cost of making the ketones from fatty acids.  I referred to this as the “Hall Paradox” after Kevin Hall, who first alerted me to this last year, in this post (near the bottom of the post).  What is not clear (to me, at least) is if this effect is transient and if so, how significant it is.  I recall that during the first three months of my foray into nutritional ketosis, I was eating between 4,000 and 4,500 kcal/day for a 12-week period, yet my weight reduced from 176 lb (about 9.5% bf by DEXA) to 171 lb (about 7.5% bf by DEXA), which means that of the 5 pounds I lost in 12 weeks, 4 were fat tissue. Today, however, I don’t consume this much, closer to 3,800 kcal/day, and one reason may be that two years later my body is more efficient at making ketones and this so-called “metabolic advantage” is no longer present.
(I have always found the term “metabolic advantage” to be misleading, though I’m guilty of using it periodically.  It’s really a metabolic disadvantage if your body requires more energy to do the same work, but nevertheless, people refer to – and argue vehemently about – this phenomenon. The question is not, does it exist?  One look at individual summary data from David Ludwig’s JAMA paper on this topic makes that clear. The questions are, why does it only exist in some people, what relevance does it have to fat loss – is it cause or effect? – and, for how long does it persist?)
Thought #4: For reasons I have yet to fully understand, some people can only lose fat on a diet that restricts fat (and by extension a diet that is still high in carbohydrate, since I’m excluding starvation and profound caloric restriction from this discussion). In my experience (and Gardner’s A TO Z trial seems to validate this, at least in pre-menopausal women), about 20% of people aspiring to reduce adiposity seem to do it better in a higher RQ environment. Using the Ornish diet as the example from this paper, I suspect the reason is multifactorial.  For example, the Ornish diet restricts many things, besides fat. It restricts sugar, flour, and processed carbohydrates.  Much of the carbohydrate in this diet is very low in glycemic index and comes primarily from vegetables. So, I don’t really know how likely it is to lose weight on a eucaloric diet that is 60% CHO and 20% fat, if the quality of the carbohydrates is very poor (e.g., cookies, potato chips).  The big confounder in these observations is that most low-fat diets, though still modestly high in RQ relative to a low-carb diet, reduce greatly the glycemic index and glycemic load, as well as the fructose.

Which brings us to the point…

Does being in nutritional ketosis ensure negative fat flux (i.e., fat loss, or L > DNL + RE)?
Being in ketosis tells us nothing about this equation!  Let me repeat this: It is metaphysically impossible to infer from a measurement of B-OHB in the blood if this equation is being satisfied.  It just tells us that our body is using some fraction of our dietary fat and stored fat (once it undergoes lipolysis) to make ketones, given that glucose intake is very low and protein intake is modest (net effect = minimal insulin secretion).
If you look at the figure below, you see this point (It’s simplified, obviously, and for example, does not show that fat from fat cells can be used directly by skeletal muscles).  Nothing in this figure implies a reduction in the size of the cells at the bottom right of the figure. It’s quite possible, of course, since ketosis results in a large L and implies a very small DNL.  But, if (small) DNL + (very large) RE is greater than (large) L, guess what? Fat flux is net positive.  Fat is gained, not lost. Still in ketosis, by the way (quantified loosely by fasting levels of B-OHB greater than about 0.5 to 1 mM), but not losing fat. (I hope the first attempt at a solution in this setting is obvious by now, notwithstanding the fact that I’ve seen this situation dozens of times with more than one solution, including the ‘obvious’ one — reducing fat intake.)
Ketone pathways
The other myth worth addressing is that the higher the level of B-OHB, the more “fat burning” that is going on.  This is not necessarily true at all.  As you can tell, I love equations, so consider this one:
B-OHB (measured in blood) = B-OHB produced (from dietary fat) plus B-OHB produced (from lipolysis of TAG) less B-OHB consumed by working muscles, heart, brain.
How does knowing one of these numbers (B-OHB measured in blood) give definitive answers to another (B-OHB produced from lipolysis of TAG)? It can’t. That’s the problem with multivariate algebra (and physiology).
Many people who enter nutritional ketosis do so, I worry, because they believe it “guarantees” fat loss. I hope I have convinced you that this is not true.  Nutritional ketosis is one eating strategy to facilitate negative fat flux, and it works very well if done correctly. It comes with some advantages and some disadvantages, just like other eating strategies.  When I get back to the series on ketosis, I will address these, but for now I felt it was very important to put things in perspective a bit.  Furthermore, I am convinced that it is not the ideal eating strategy for everyone.
And, most importantly, I hope at least someone appreciated my reference to the flux capacitor.