Causes of weight loss

Tuesday, April 17, 2012

Lose weight on a budget

Gardening on A Budget - How to Design A Garden on A Budget Welcome Spring! The weather is warmer and the birds are singing. That can only mean one thing. It's planting season! Decisions, Decisions In order to plan your garden on a budget, you first need to decide how large you want your garden to be, how much space you have to… By: AJ in Finance > Budgeting Mar 11, 2012 13 Likes: 3

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Belly Fat! How Did I Get This Spare Tire?

After Christmas this year I was thinking, how did I get this spare tire? My spare tire didn't just arrive here overnight, it's taken years to accumulate here. Once I got married and started getting older I wasn't as active through sports. Something would always seem to come up, causing me to do chores, projects or being to tired to workout or eat right.

Here's some causes for my spare tire

1...Inactivity...I'm guilty of not working out enough or at all. I feel I'm fairly active with the duties of being a husband, a father and a home owner. The problem for me is to get in proper workouts regularly. As well as to get my heart rate up and sweat more during workouts. This inactivity is causing my bodies metabolism to remain idle.

2....Overeating....At meal times I tend to over eat, even when I'm trying to watch what I eat. Before supper or as I'm preparing supper I'll graze and sample the food. Then when I eat I'm already half full, but I still eat my full diner. Have you ever found yourself with a full stomach after a meal, then you wondered why you eat so much.

When you get older you find yourself eating for comfort. A release from whats going on in your life. The foods you eat are just as important as how much. Skimping on breakfast only to over eat at lunch. Not having healthy snacks in the afternoon and finding yourself starving. Then eating too much at supper time. I have a friend who doesn't eat all day except for a few cups of coffee and maybe a danish. Come supper time he eats a big supper and a few beers. This is usually late a night and then he goes to bed. This is not a healthy practice to maintain.

3....Stress.. today leads to over eating with our busy and hectic lifestyles. When stress is weighing you down your body releases stress hormones, including adrenaline which fires you up and contains Cortisol, which makes you fat. Cortisol is a powerful appetite stimulant. Thus people under stress make more trips to the fridge or cookie jar. Some people can handle stress better than others, resulting in some to secrete less cortisol during peak times. Elevated cortisol levels appear to stimulate growth in fat cells in the abdomen, producing the worst kind of weight gain, the dreaded spare tire around your mid section.

4....Sleep....Today it is estimated that only 25% of people are getting 7-8 hours of sleep a night. This scare's me to think that possibly 3/4 of the people are operating on less than optimal amounts of sleep. Operating on 5-7 hours or less of sleep a night can cause you to develop insulin resistance, which could result in weight gain. Operating on less sleep could explain why you munch on bad snacks. Your brain thinks your running low on energy and will increase your appetite.

5....Eating Processed or Refined Foods....Do you find yourself eating a lot of processed foods(pre packaged snacks,frozen dinners, meats and cheeses just to name a few). Refined foods are just as unhealthy for you. Some of the most popular products refined are flour. Flour is heated and striped of all it's nutrients and then it is bleached. White flour is found in a lot of the foods we eat(bagels,breads,cereals,snacks). These commercially produced foods are very high in simple carbohydrates and very low nutritional value.

Having a spare tire around your midsection is no laughing matter. It is very important to not except"I'm just going to stay fat" or "I'll never lose this weight". If you feel that you are losing your battle with weight loss. You need to think positive and know that you are going to change your situation. In doing so you will have already won half the battle. Remember that fat around your mid section is very serious and has major heart disease risks.

If you're looking to get rid of your spare tire check out my other article Belly Fat..Tips to get rid of that spare tire.

Article Source: http://www.streetarticles.com/weight-loss/belly-fat-how-did-i-get-this-spare-tire
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Rezidor announces the Park Inn by Radisson Sousse, Tunisia

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Apr
2012Rezidor, one of the fastest growing hotel companies worldwide and member of the Carlson Rezidor Hotel Group, announces its 4th hotel in Tunisia: The Park Inn by Radisson Sousse featuring 234 keys is scheduled to welcome the first guests in autumn 2013.

(1888PressRelease) April 13, 2012 - The existing property is currently undergoing a complete renovation before joining Rezidor's young, dynamic and colourful mid-market brand Park Inn by Radisson.

"We strongly believe in the Tunisian market, and aim to support the tourism sector that is stabilizing again after the Arab Spring. The country offers a fascinating culture, a favourable climate, and proximity to many European feeder markets", said Kurt Ritter, President & CEO of Rezidor. The group already operates a Radisson Blu- and a Park Inn by Radisson hotel in Djerba, and has a further Park Inn by Radisson hotel in Hammamet under development.

The Park Inn by Radisson Sousse is located in the heart of Sousse's city centre, Tunisia's 3rd largest city and situated between Hammamet and Monastir. Situated at the seaside and bordering the impressive medieval fortification of the UNESCO protected Medina, the Park Inn by Radisson Sousse will comprise 234 guest rooms, 3 restaurants (all-day dining,

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Nova Scotia luxury wilderness lodge lives up to Geotourism values: Successful local hiring effort results in 100% returning local employees

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Apr
2012 A successful Geotourism enterprise is all about expressing & sharing a sense of place. Trout Point Lodge of Nova Scotia--a Relais & Chateaux hotel-- has captured that spirit through hiring & training of purely local employees.

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Scientists use public-database search to identify novel receptor with key role in type 2 diabetes

ScienceDaily (Apr. 9, 2012) — Using computational methods, Stanford University School of Medicine investigators have strongly implicated a novel gene in the triggering of type-2 diabetes. Their experiments in lab mice and in human blood and tissue samples further showed that this gene not only is associated with the disease, as predicted computationally, but is also likely to play a major causal role.

See Also:Health & MedicineDiabetesObesityHypertensionDiet and Weight LossPersonalized MedicineHormone DisordersReferenceBlood sugarDiabetes mellitus type 1Diabetes mellitus type 2Hyperglycemia

In a study published online April 9 in Proceedings of the National Academy of Sciences, the researchers combed through freely accessible public databases storing huge troves of results from thousands of earlier experiments. They identified a gene never before linked to type-2 diabetes, a life-shortening disease that affects 4 percent of the world's population. These findings have both diagnostic and therapeutic implications.

The study's senior author is Atul Butte, MD, PhD, associate professor and chief of systems medicine in pediatrics; its first author is Keiichi Kodama, MD, PhD, a staff research scientist in Butte's group.

Ordinarily, cells throughout the body, alerted to the presence of sugar in the blood by insulin, hungrily slurp it up for use as an energy source. But excessive blood-sugar levels -- diabetes' defining feature -- eventually damage blood vessels, nerves and other tissues.

There are two broad categories of diabetes. In type-1 diabetes, a relatively rare autoimmune condition that typically begins in childhood, insufficient insulin is secreted by the pancreas. Type-2 diabetes, on the other hand, results from a phenomenon called insulin resistance: the tendency of cells in tissues throughout the body -- but especially in fat, liver and muscle -- to lose sensitivity and ignore the insulin's "gravy train" signal.

Drugs now used to treat insulin resistance can't reverse the progression to full-blown type-2 diabetes. "We don't really have a good grasp of the molecular pathology that makes people get it in the first place," said Butte, who is also director of the Center for Pediatric Bioinformatics at Lucile Packard Children's Hospital.

In searching for risk-increasing genes over the past 10 years, scientists have used two approaches to hunt them down. One way is to look for variations in genes' composition -- deviations in their chemical sequences that correlate with a higher likelihood of contracting a particular condition.

But genes don't change from one tissue to the next, and -- with the exception of mutations that accrue gradually over a lifetime in particular cells and can lead to cancer and other conditions -- they remain largely unaltered by disease and the aging process. What does change dynamically, from one tissue or state to another, is what all those genes are doing: how actively each of them is involved in cranking out the starting materials for the many thousands of proteins critical to each cell's or tissue's identity and to every organism's survival. In any given cell in a person's body, at any given time, some genes are switched off, others somewhat on and still others working overtime.

And so a second approach to understanding our genes has been devised. This latter method flags differences in genes' activity levels, for example in diseased vs. normal tissues, for each of the 20,000 genes in the entire genome.

Both types of approaches have generated staggering amounts of data -- far more than can fit onto the pages of standard, peer-reviewed journals, whose editors routinely demand (as do federal-government funding agencies) that researchers park their experiments' results in online, public repositories accessible to others. Now, investigators such as Butte are starting to reach in, drill down and pull out a treasure-trove of potentially valuable information.

In this study, the Stanford scientists wanted to know which genes showed especially marked changes in activity, as indicated in earlier comparisons of diabetic vs. healthy tissue samples (notably fat, muscle, liver and beta cells, the only cells in the body that release insulin). Mining public databases, they located 130 independent gene-activity-level experiments -- in rats, mice and humans -- comprising 1,175 separate individual samples in all. Then, integrating that data, they searched for those genes that showed activity-level differences in the most experiments.

They zeroed in on a single gene, called CD44, whose activity changed substantially in diabetic tissues compared with healthy tissues in 78 of the 130 experiments. The chance of this occurring "just due to dumb luck," Butte said, was vanishingly small: less than one in 10 million-trillion. The uptick in CD44's activity was especially pronounced in the fat tissue of people with diabetes, he said -- intriguing, because obesity is known to be a strong risk factor for type-2 diabetes.

The gene was interesting in itself. CD44 codes for a cell-surface receptor not found on fat cells, although those cells do have surface molecules that bind to it. Rather, this receptor sits on the surface of scavenger cells called macrophages (from the Greek words for "big eater") that can cause inflammation. In obese individuals, macrophages migrate to and take up positions in fat tissue. (Indeed, as many as half the cells in a big potbelly can be macrophages.) Recent medical research has strongly implicated inflammation in initiating type-2 diabetes.

CD44 was first identified more than a decade ago by immunologists looking for a possible connection to autoimmune disease. To test that connection, those immunologists created a strain of laboratory mouse lacking the gene. By chance, these "CD44 knockout" mice were derived from a lab-mouse strain that, if fed a high-fat diet, has a propensity for becoming obese, insulin-resistant and diabetic. With the exception of that missing gene, these two strains are identical.

Butte and his colleagues obtained these two strains of mice (one carrying the gene, the other lacking it) and divided them into two subgroups, which they fed either a normal or a high-fat diet, representative of today's increasingly common human diet. The team studied these mice using tests commonly applied to humans, for example measuring fasting blood sugar and measuring blood sugar after administering sugar or insulin. As anticipated, the mice on normal diets stayed slim and retained good insulin sensitivity. CD44-containing mice on high-fat diets, also as expected, got tubby and developed insulin resistance. But mice lacking the suspect gene never lost their sensitivity to insulin and didn't become diabetic on high-fat diets, although they became as plump as their CD44-carrying peers.

This suggested that knocking out CD44's function could improve insulin sensitivity, and that blocking CD44 with a drug might turn out to be an interesting new way to treat type-2 diabetes. So the team tested a prototype drug: antibodies that shut down the receptor's action in CD44-carrying mice fed a high-fat diet. Though these overfed mice didn't get any thinner, the prototype drug did reduce their blood-sugar levels within a week. Moreover, the number of macrophages in these mice's fat tissue plummeted.

Turning to human blood samples, Butte and his associates found that insulin-resistant people (those prone to developing type-2 diabetes) have higher levels of free-roving CD44-receptor molecules circulating in their blood than do people with normal insulin-processing capability. This suggests a potential early diagnostic test, or biomarker, that could help detect or predict insulin resistance. Plus, the antibody results suggest, a small molecule that blocked this receptor could have profound therapeutic potential for type-2 diabetes.

Funding for the study was provided by the Lucile Packard Foundation for Children's Health and the National Library of Medicine. Other Stanford co-authors of the study, done in collaboration with investigators at the University of Tokyo, Kitasato University, Keio University and RIKEN, all in Japan, were former graduate students Marina Sirota, PhD, and Alexander Morgan, PhD; and former staff bioinformatics programmer Rong Chen, PhD, all then in Butte's lab.

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Less sleep, disrupted internal 24-hour clock means higher risk of diabetes and obesity

ScienceDaily (Apr. 11, 2012) — A study by researchers at Brigham and Women's Hospital (BWH) reinforces the finding that too little sleep or sleep patterns that are inconsistent with our body's "internal biological clock" may lead to increased risk of diabetes and obesity. This finding has been seen in short-term lab studies and when observing human subjects via epidemiological studies. However, unlike epidemiological studies, this new study provides support by examining humans in a controlled lab environment over a prolonged period, and altering the timing of sleep, mimicking shift work or recurrent jet lag.

See Also:Health & MedicineSleep Disorder ResearchInsomnia ResearchDiabetesMind & BrainSleep DisordersInsomniaObstructive Sleep ApneaReferenceCircadian rhythm sleep disorderJet lagCircadian rhythmSleep deprivation

The study will be electronically published on April 11, 2012 in Science Translational Medicine.

Researchers hosted 21 healthy participants in a completely controlled environment for nearly six weeks. The researchers controlled how many hours of sleep participants got, as well as when they slept, and other factors such as activities and diet. Participants started with getting optimal sleep (approximately 10 hours per night). This was followed by three weeks of 5.6 hours of sleep per 24-hour period and with sleep occurring at all times of day and night, thereby simulating the schedule of rotating shift workers. Thus, during this period, there were many days when participants were trying to sleep at unusual times within their internal circadian cycle-the body's "internal biological clock" that regulates sleep-wake and many other processes within our bodies. The study closed with the participants having nine nights of recovery sleep at the usual time.

The researchers saw that prolonged sleep restriction with simultaneous circadian disruption decreased the participants' resting metabolic rate. Moreover, during this period, glucose concentrations in the blood increased after meals, because of poor insulin secretion by the pancreas.

According to the researchers, a decreased resting metabolic rate could translate into a yearly weight gain of over 10 pounds if diet and activity are unchanged. Increased glucose concentration and poor insulin secretion could lead to an increased risk for diabetes.

"We think these results support the findings from studies showing that, in people with a pre-diabetic condition, shift workers who stay awake at night are much more likely to progress to full-on diabetes than day workers," said Orfeu M. Buxton, PhD, BWH neuroscientist and lead study author. "Since night workers often have a hard time sleeping during the day, they can face both circadian disruption working at night and insufficient sleep during the day. The evidence is clear that getting enough sleep is important for health, and that sleep should be at night for best effect."

This research was supported by the National Institute on Aging; National Heart, Lung and Blood Institute; National Center for Research Resources; Center for Clinical Investigation of the Harvard Clinical and Translational Science Center; Joslin Diabetes and Endocrinology Research Center Service Specialized Assay Core; the National Space Biomedical Research Institute; and Natural Sciences and Engineering Research Council of Canada.

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8 Tips to See Your Doctor Quickly

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Obesity is a Bigger Threat to Health Care Than Obamacare

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Italian player's death sparks probes into ambulance delay

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View the Original article

Causes of weight loss

Tuesday, April 17, 2012

Lose weight on a budget

Belly Fat! How Did I Get This Spare Tire?

Rezidor announces the Park Inn by Radisson Sousse, Tunisia

Nova Scotia luxury wilderness lodge lives up to Geotourism values: Successful local hiring effort results in 100% returning local employees

Scientists use public-database search to identify novel receptor with key role in type 2 diabetes

Less sleep, disrupted internal 24-hour clock means higher risk of diabetes and obesity

8 Tips to See Your Doctor Quickly

Obesity is a Bigger Threat to Health Care Than Obamacare

Italian player's death sparks probes into ambulance delay

Looking for a Rush, Kids Play the Deadly Choking Game

Mom's caffeine not linked to infant sleep problems: study

India's Piramal buys Bayer's potential Alzheimer drug