Saturday, February 2, 2013

Does FAT scare you? - Operation Muffin Top - Connecticut News

I?m going to tell you a secret? something that the smartest, most cutting edge health professionals all know and have been talking about amongst themselves for a very long time. This information isn?t widely known or accepted yet, but it will be?at which point we will all be shaking our heads looking back on this period in medical history and saying ?What were we thinking??

Get ready to be shocked:

High cholesterol doesn?t cause heart disease.

Yes, you read that right, and before you recover completely, consider this: Fully half the people with heart disease have ?normal? cholesterol and fully half the people with elevated cholesterol are healthy as a horse.

Talk to people about living longer and living free from heart disease (or any of the other conditions that rob us of life and vitality) and you?ll invariably hear someone say, ?Yup, gotta do something about my cholesterol?.

Why are we so darn worried about cholesterol when it has practically nothing to do with living long and living well?

Well, for one thing it?s easy to measure. For another, lowering it is an extraordinarily profitable business. Zocor and Lipitor, two cholesterol-lowering drugs, remain in the top ten of every Forbes list of best-selling drugs, and bring in over 30 billion a year for their makers.

And for a third, the idea that high cholesterol causes heart disease is so embedded in our national consciousness that to dislodge it, even with the considerable amount of emerging scientific evidence that the cholesterol hypothesis is simply wrong, would be a massive undertaking. Heck, we?re still buying ?low-fat? cookies and margarine based on information that?s been out of date for 10 years.

So, if not cholesterol, what should we be paying attention to if we want to live longer and live healthier?

The Four Killers: The Real Dangers to Your Heart

  • Inflammation
  • Oxidation
  • Sugar
  • Stress

Inflammation, oxidation, sugar and stress will kill you. Cholesterol won?t.

Inflammation

Inflammation is a silent killer, a contributor to every major degenerative disease from Alzheimer?s to diabetes, from heart disease to cancer. It comes in two flavors- chronic and acute. Acute inflammation is the one we?re all familiar with?it?s what you feel when you stub your toe, get a toothache, pull a muscle or have an allergy attack.

But chronic inflammation is the killer and it flies beneath the radar. It?s your body?s response to small but continuous insults like exposure to toxins, bad diet, stress, cigarettes and the like, and it causes damage to your vascular system. In fact the body uses cholesterol to try to patch up that damage?so blaming cholesterol for the damage is like blaming a St. Bernard for an avalanche!

We can do a great deal to fight inflammation by eating anti-inflammatory foods (fruits and vegetables abound with natural anti-inflammatories like quercetin and other flavonoids and by taking anti-inflammatory supplements (top of the list: omega 3?s!)

Oxidation

Oxidation is another process that ages us. Oxidation is what you see when apple slices left in the air turn brown; that happens inside our bodies every day, the result of attacks on our cells and DNA by rogue molecules called free radicals. Diets high in antioxidants go a long way towards fixing the damage.

Sugar

Sugar is a risk factor for almost everything you don?t want to have?causes something called glycation. which happens when excess sugar in the bloodstream ?gums up the works.? Sugar gloms on to protein in the blood, making it too sticky to pass through small capillaries. It?s one reason why diabetics often have amputations in the extremities like toes and feet and problems in areas like the eyes and the kidneys which are served by small, narrow blood vessels. High blood sugar is far more damaging to the body and to life than cholesterol. And it?s relatively easy to ?fix?.

Stress

Finally, stress is one of the biggest killers on the planet, and, like sugar, far more of a danger to us than cholesterol ever was. Stress hormones age (and shrink) an important area of the brain called the hippocampus which is involved in memory and thinking.

Stress can exacerbate nearly any disease, not to mention that it can slow (or even prevent) recovery. And stress actually makes you fat- the major stress hormone, cortisol, causes the body to store weight around the middle.

In the ?Blue Zones?- areas around the globe where people routinely live to 100 in extraordinary health with all their faculties intact- no one worries about their cholesterol or their saturated fat intake. They don?t have to.

Their lives have built in stress-reducers like extended families and community events; they eat natural whole food diets filled with antioxidants and anti-inflammatories. And their sugar intake is naturally low, so they don?t have to worry about it gumming up the works and destroying their health.

Aging may be inevitable, but unhealthy aging is not. If you know what to do you truly can have an extraordinary life well into your 9th and 10th decade, filled with vitality, joy and purpose.

Best of all, it?s not all that hard to do.

The payoff is worth it!

Source: http://blog.ctnews.com/carozza/2013/02/01/does-fat-scare-you/

Usain Bolt 2012 Olympics Katie Ledecky Aaron Ross Sikh temple lollapalooza Nastia Liukin Gabby Douglas hair

Sin Chew Daily Education Fund Scholarships | Malaysia ...

Sorry, Readability was unable to parse this page for content.

Source: http://scholarships.malaysia-students.com/2013/02/sin-chew-daily-education-fund.html

affirmative action helicon zac efron and taylor swift real housewives of orange county bloom energy franklin graham jambalaya

Flight diverted after airline pilot passes out

By Alastair Jamieson, Staff writer, NBC News

A flight from Los Angeles to Seattle was diverted to Portland late Thursday after one of the pilots lost consciousness.

Alaska Airlines said Flight 473's first officer flew the Boeing 737-700 to Portland International Airport after the captain became ill over Oregon.

The plane landed safely at 9:05 p.m. local time (12:05 a.m. ET Friday) and paramedics took the pilot to the hospital, airline spokesman Paul McElroy said.

The Seattle Times reported that a doctor on board was able to tend to the captain at the front of the plane.

There were 116 passengers and five crew members on the flight, which had been due to arrive in Seattle at 9:30 p.m. local time (12.30 a.m. ET).

The captain has been flying with Alaska Airlines for 28 years, while the first officer has been with the airline 11 years, McElroy said.

NBC station KING5?said it was not known what caused the pilot to pass out.

About 20 passengers were re-accommodated on other flights to Seattle, while the rest took a flight scheduled to land in Seattle at 1:15 a.m. local time Friday (4:15 a.m. ET).

Related:

Full travel coverage from NBC News

?

?

Source: http://usnews.nbcnews.com/_news/2013/02/01/16802972-flight-diverted-after-alaska-airlines-pilot-passes-out?lite

red hook romney tax return the tree of life movie academy award nominees 2012 2012 oscar nominations kyle williams florida debate

Friday, February 1, 2013

Programming cells: Importance of the envelope

Feb. 1, 2013 ? In a project that began with the retinal cells of nocturnal animals and has led to fundamental insights into the organization of genomic DNA, researchers from Ludwig-Maximilians-Universitaet (LMU) in Munich show how the nuclear envelope affects nuclear architecture -- and gene regulation.

The double-stranded DNA molecules that make up the genetic material are wrapped around protein complexes to form compacted "chromatin." The active portion of the genome is less densely packed, and thus more easily accessible, than the inactive fraction, and is referred to as euchromatin. Euchromatin is typically located in the inner regions of the cell nucleus, while much of the inactive DNA in "heterochromatin" is associated with the inner face of the nuclear envelope. This type of chromatin organization is found in almost all higher organisms and may have been invented 500 million years ago.

But there is a curious exception to this generalization. In the retinal cells of nocturnal animals, the heterochromation is localized in the central area of the nucleus, as a research group led by LMU biologists Dr. Irina Solovei and Dr. Boris Joffe showed in a previous study. "This got us interested in the mechanisms that control the distribution of chromatin," says Professor Heinrich Leonhardt of LMU's Biozentrum. "How can the nuclear architecture in the rod cells of nocturnal animals be inverted in this way, and what determines the typical positioning of inactive chromatin on the outskirts of the nucleus in normal cells?" Leonhardt and his team have now completed an extensive study in search of the answers.

A fundamental principle unveiled

With the help of targeted genetic manipulations in the mouse, Joffe and Solovei together with their colleagues show for the first time that there are two independent mechanisms for fixing heterochromatin to the inner face of the nuclear envelope. These mechanisms make use of two different components of the inner nuclear membrane as clamps -- lamin A/C, and the so-called lamin-B receptor (LBR), which itself binds to B type lamins.

Normally the two components are used sequentially for this purpose. "In the course of differentiation, there is a switch from the LBR to lamin A/C, and there is always a least one type of tether available for attachment of heterochromatin to the nuclear periphery. But if both are missing, the inactive heterochromatin recoils like a severed elastic band and collapses in the center of the nucleus," explains Leonhardt. Moreover, the switch seems to be a fundamental principle of genome organization and cell differentiation in mammalian cells, as the researchers concluded from the study of 39 species and the analysis of diverse tissue types in nine genetic strains of mice.

Prospects for targeted therapies Lamin proteins not only have a structural function but also have an impact on gene regulation. Thus LBR binds B type lamins and regulates stem-cell populations by promoting the expression of genes that are important for the proliferation of rapidly dividing stem cells. The lamin A/C gene on the other hand codes for a structural component of the nuclear envelope, and regulates cellular differentiation programs like e.g. the expression of muscle-specific genes in muscle cells. Mutations in this gene result in so-called laminopathies -- rare genetic diseases that are associated with a broad spectrum of clinical symptoms, including muscular dystrophy and progeria, a premature aging syndrome.

Joffe and Solovei suspect that mutations in lamin A/C affect the expression of specific genes during the maturation and differentiation of cells, with deleterious results for their function and for tissue integrity. This notion could explain the highly diverse and complex symptoms seen in patients with mutations in the lamin A/C gene -- and it could open routes to the design of targeted therapies for laminopathies.

The new findings thus yield fundamentally new insights into how each of the many differentiated cell types in the body arises as the result of the precisely regulated expression of a specific complement of genes appropriate to each. "In the end, we have been brought from studies of night vision and an odd quirk of nature to the discovery of a fundamental regulatory mechanism: The nuclear envelope has a major say in development, and what kind of envelope our genetic material comes in makes a great deal of difference to our fate," Leonhardt concludes.

Share this story on Facebook, Twitter, and Google:

Other social bookmarking and sharing tools:


Story Source:

The above story is reprinted from materials provided by Ludwig-Maximilians-Universitaet Muenchen (LMU).

Note: Materials may be edited for content and length. For further information, please contact the source cited above.


Journal Reference:

  1. Irina Solovei, Audrey?S. Wang, Katharina Thanisch, Christine?S. Schmidt, Stefan Krebs, Monika Zwerger, Tatiana?V. Cohen, Didier Devys, Roland Foisner, Leo Peichl, Harald Herrmann, Helmut Blum, Dieter Engelkamp, Colin?L. Stewart, Heinrich Leonhardt, Boris Joffe. LBR and Lamin A/C Sequentially Tether Peripheral Heterochromatin and Inversely Regulate Differentiation. Cell, 2013; 152 (3): 584 DOI: 10.1016/j.cell.2013.01.009

Note: If no author is given, the source is cited instead.

Disclaimer: Views expressed in this article do not necessarily reflect those of ScienceDaily or its staff.

Source: http://feeds.sciencedaily.com/~r/sciencedaily/top_news/top_environment/~3/38_3gzFCTbw/130201114110.htm

kyla pratt justified season 3 custer scott walker restaurant week type 2 diabetes occupy congress

Louisville highlights FIU?s 2013 football schedule

The Miami Herald

A week after Conference USA got its final realignment for 2013 together, FIU was able to announce a football schedule that opens Aug. 31 at Maryland and closes Nov. 30 at FAU.

In between, FIU hosts Central Florida on Sept. 7 and Bethune-Cookman on Sept. 14 in non-conference games. Their non-conference schedule ends with a trip to Sugar Bowl-champion Louisville, Sept. 21.

FIU?s in C-USA?s East Division with FAU and Middle Tennessee State, both of which will leave the Sun Belt with FIU and North Texas this summer; Marshall; Southern Mississippi; East Carolina; and Alabama-Birmingham. Games against each of the other East schools and two games against the West Division, the Oct. 26 Louisiana Tech home game and a Nov. 16 road game at UTEP, comprise FIU?s conference schedule.

The Panthers open conference play Oct. 5 at Southern Mississippi. After that, there?s a run of home conference games against Alabama-Birmingham, Louisiana Tech and East Carolina. The Panthers fourth and last home conference game is against Marshall, Nov. 23.

The closing game, the Shula Bowl against FAU, has slowly been brought back from limbo. First, it was to be suspended indefinitely because FIU was leaving FAU in the Sun Belt Conference. Then, the game got put on hiatus for only 2013 once FAU accepted the invitation from Conference USA. Once FAU and Middle decided to leave the Sun Belt in 2013 instead of 2014, the game got its late season place back on both schedules.

Source: http://www.miamiherald.com/2013/01/31/3209135/louisville-highlights-fius-2013.html

abc glock earthquake abc news msnbc meteor shower 121212 Concert

Disease not a factor in Tasmanian Tiger extinction; Humans to blame for demise of extinct Australian predator

Jan. 30, 2013 ? Humans alone were responsible for the demise of Australia's iconic extinct native predator, the Tasmanian Tiger or thylacine, a new study led by the University of Adelaide has concluded.

Using a new population modelling approach, the study contradicts the widespread belief that disease must have been a factor in the thylacine's extinction.

The thylacine was a unique marsupial carnivore found throughout most of Tasmania before European settlement in 1803. Between 1886 and 1909, the Tasmanian government encouraged people to hunt thylacines and paid bounties on over 2000 thylacine carcasses. Only a handful of animals were located after the bounty was lifted and the last known thylacine was captured from the wild in 1933.

"Many people, however, believe that bounty hunting alone could not have driven the thylacine extinct and therefore claim that an unknown disease epidemic must have been responsible," says the project leader, Research Associate Dr Thomas Prowse, School of Earth and Environmental Sciences and the Environment Institute.

"We tested this claim by developing a 'metamodel' -- a network of linked species models -- that evaluated whether the combined impacts of Europeans could have exterminated the thylacine, without any disease."

The mathematical models used by conservation biologists to simulate the fate of threatened species under different management strategies (called population viability analysis or PVA) traditionally neglect important interactions between species. The researchers designed a new approach to PVA that included species interactions.

"The new model simulated the directs effects of bounty hunting and habitat loss and, importantly, also considered the indirect effects of a reduction in the thylacine's prey (kangaroos and wallabies) due to human harvesting and competition from millions of introduced sheep," Dr Prowse says.

"We found we could simulate the thylacine extinction, including the observed rapid population crash after 1905, without the need to invoke a mystery disease.

"We showed that the negative impacts of European settlement were powerful enough that, even without any disease epidemic, the species couldn't escape extinction."

The study 'No need for disease: testing extinction hypotheses for the thylacine using multi-species metamodels', which also involved Professors Corey Bradshaw and Barry Brook from the University of Adelaide's Environment Institute, Professor Chris Johnson from the University of Tasmania, and Dr Bob Lacy, Chicago Zoological Society, has been published online in the Journal of Animal Ecology.

Share this story on Facebook, Twitter, and Google:

Other social bookmarking and sharing tools:


Story Source:

The above story is reprinted from materials provided by University of Adelaide.

Note: Materials may be edited for content and length. For further information, please contact the source cited above.


Journal Reference:

  1. Thomas A. A. Prowse, Christopher N. Johnson, Robert C. Lacy, Corey J. A. Bradshaw, John P. Pollak, Michael J. Watts, Barry W. Brook. No need for disease: testing extinction hypotheses for the thylacine using multi-species metamodels. Journal of Animal Ecology, 2013; DOI: 10.1111/1365-2656.12029

Note: If no author is given, the source is cited instead.

Disclaimer: Views expressed in this article do not necessarily reflect those of ScienceDaily or its staff.

Source: http://feeds.sciencedaily.com/~r/sciencedaily/top_news/top_environment/~3/Y7FPxGmgdo4/130131095310.htm

haywire dog the bounty hunter tacoma narrows bridge weather nyc open marriage department of justice doj

Crossed wires this morning, Northwest Missouri State University is OPEN.

Sorry, Readability was unable to parse this page for content.

Source: http://www.facebook.com/DailyForum/posts/612154808800540

j.k. rowling j.k. rowling axl rose google earnings pat burrell hilary rosen grilled cheese