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Thursday 2 September 2010

God did not create the universe: Hawking



LONDON – God did not create the universe and the "Big Bang" was an inevitable consequence of the laws of physics, the eminent British theoretical physicist Stephen Hawking argues in a new book.
God did not create the universe: Hawking
File photo shows Canada's Prime Minister Stephen Harper applauds beside British physicist Stephen Hawking (R) after making an announcement at the Perimeter Institute for Theoretical Physics in Waterloo July 6, 2010. [Agencies] 
 
In "The Grand Design," co-authored with US physicist Leonard Mlodinow, Hawking says a new series of theories made a creator of the universe redundant, according to the Times newspaper which published extracts on Thursday.
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"Because there is a law such as gravity, the universe can and will create itself from nothing. Spontaneous creation is the reason there is something rather than nothing, why the universe exists, why we exist," Hawking writes.
"It is not necessary to invoke God to light the blue touch paper and set the universe going."
Hawking, 68, who won global recognition with his 1988 book "A Brief History of Time," an account of the origins of the universe, is renowned for his work on black holes, cosmology and quantum gravity.
Since 1974, the scientist has worked on marrying the two cornerstones of modern physics - Albert Einstein's General Theory of Relativity, which concerns gravity and large-scale phenomena, and quantum theory, which covers subatomic particles.
His latest comments suggest he has broken away from previous views he has expressed on religion. Previously, he wrote that the laws of physics meant it was simply not necessary to believe that God had intervened in the Big Bang.
He wrote in A Brief History ... "If we discover a complete theory, it would be the ultimate triumph of human reason - for then we should know the mind of God."
In his latest book, he said the 1992 discovery of a planet orbiting another star other than the Sun helped deconstruct the view of the father of physics Isaac Newton that the universe could not have arisen out of chaos but was created by God.
"That makes the coincidences of our planetary conditions -- the single Sun, the lucky combination of Earth-Sun distance and solar mass, far less remarkable, and far less compelling evidence that the Earth was carefully designed just to please us human beings," he writes.
Hawking, who is only able to speak through a computer-generated voice synthesizer, has a neuro muscular dystrophy that has progressed over the years and left him almost completely paralyzed.
He began suffering the disease in his early 20s but went on to establish himself as one of the world's leading scientific authorities, and has also made guest appearances in "Star Trek" and the cartoons "Futurama" and "The Simpsons."
Last year he announced he was stepping down as Cambridge University's Lucasian Professor of Mathematics, a position once held by Newton and one he had held since 1979.
"The Grand Design" is due to go on sale next week.

Link Between Everyday Stress and Obesity Strenthened With Study Using an Animal Model

ScienceDaily (Sep. 1, 2010) — Stress can take a daily toll on us that has broad physical and psychological implications. Science has long documented the effect of extreme stress, such as war, injury or traumatic grief on humans. Typically, such situations cause victims to decrease their food intake and body weight. Recent studies, however, tend to suggest that social stress--public speaking, tests, job and relationship pressures--may have the opposite effect--over-eating and weight gain. With the rise of obesity rates, science has increasingly focused on its causes and effects--including stress.


A recent study conducted by the Departments of Psychiatry and Biomedical Engineering at the University of Cincinnati College of Medicine, examined the effects of stress on the meal patterns and food intake of animals exposed to the equivalent of everyday stress on humans. The results suggest that, not only does stress have an impact on us in the short term, it can cause metabolic changes in the longer term that contribute to obesity.

The study was conducted by Susan J. Melhorn, Eric G. Krause, Karen A. Scott, Marie Mooney, Jeffrey D. Johnson, Stephen C. Woods and Randall R. Sakai at the University of Cincinnati College of Medicine, Cincinnati, OH. Their study was published in the American Journal of Physiology - Regulatory, Integrative and Comparative Physiology.

The Study

Previous studies have found that meal patterns (number, duration and size of meals) can affect metabolism. Studies of both humans and animals have shown that taking fewer and larger meals promotes the gain of fat mass and can increase triglycerides, lipids and cholesterol independent of total caloric intake. Conversely, weight gain--even while overeating--can be prevented by consuming smaller, more frequent meals. Whether social stress alters the microstructure of food intake, however, was unclear.

The current study used the visible burrow system (VBS), an animal model of chronic social stress, which has been shown to produce stress-associated behavioral, endocrine, physiological and neurochemical changes in animals. Long-Evans rats (90 days old) were individually housed for three weeks prior to the experiment. During this habituation time, they were briefly anesthetized and implanted with a unique subcutaneous microchip just behind their ears which allowed for identification and monitoring of feeding behavior. Meal pattern characteristics were measured for seven days during habituation. Data were calculated for each animal for each day and then averaged together to provide an overall habituation measure as a baseline for all of the conditions.

For the experiment, rats were formed into colonies, composed of four males and two females, and matched with a control group. Within a few days, all colonies formed a hierarchy which established the dominance of one male and the subordination of the other three males. Each colony had equal hours of light and darkness. Meal pattern characteristics were calculated for each animal on a daily basis. As documented by behavioral video analysis and microchip data, both subordinate and dominant rats reduced their initial food intake and body weight compared to the habituation period and as compared to the control group. After the hierarchy was stable, however, the dominant rats recovered their food intake relative to the control animals, while the subordinate rats continued to eat less by reducing their number of meals. Furthermore, although rats are nocturnal animals, the subordinate rats ate primarily during lighted periods, indicating a shift in circadian behavior.

The Result

After two weeks, the male rats were individually housed for a three-week recovery period and allowed to eat freely. Compared to the control group, both dominant and subordinate rats over- ate during the recovery period, but the dominant animals ate more frequently, while the subordinate animals ate larger meals, but less frequently. The dominant rats gained weight and lean mass, but only as comparable to the control group, while the subordinate rats gained significant fat in the visceral (belly) region. Throughout the recovery period, subordinate rats continued to overeat, eat longer meals and gain fat, suggesting long-term, deleterious metabolic changes.

Interestingly, the study results suggest that the signals controlling ingestive behavior become impaired or are overridden during social stress. Hypothalamic neuropeptide Y (NPY) is a well-known chemical messenger within the hypothalamus that stimulates food intake in times of negative energy balance, possibly by increasing meal size. In this case, NPY did not mediate the consumption patterns of the animals during the VBS period.

Conclusion

This is the first study of its kind to examine meal patterns in real-time during exposure to chronic social stress and during a subsequent recovery period, as well as to begin to evaluate the neuroendocrine and neurochemical underpinnings of the altered ingestive patterns observed. Stress and recovery induced changes in animals' body weight and composition and the alterations in meal patterns observed may have contributed to these physiological changes.

Stress is experienced by animals and humans on a daily basis and many individuals experience cycles of stress and recovery throughout the day. If, following stress, we consume larger and less frequent meals, the conditions are favorable for weight gain--especially in the abdomen. We know that belly fat, as well as stress, contributes to the development of cardiovascular disease, immune dysfunction and other metabolic disorders. Further studies using the VBS model will help us understand the relationship between stress and obesity and help us treat and prevent the development of these diseases.

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Wednesday 1 September 2010

Brain Exercises Can Delay Mental Decline, But Then Watch Out

By Jeanna Bryner, LiveScience Managing Editor

Brain exercises may keep cognitive decline at bay longer, but once dementia hits it mysteriously seems to progress faster than if it hadn't been postponed, according to an ongoing study that began in 1993. 

"Our results suggest that the benefit of delaying the initial signs of cognitive decline may come at the cost of more rapid dementia progression later on, but the question is: Why does this happen?" said study researcher Robert S. Wilson, of the Rush University Medical Center in Chicago. 

Mentally stimulating activities, such as crossword puzzles and reading, seem to keep the brain functioning relatively normally for a while despite the buildup of the plaques and tangles in the brain that are linked with dementia. However, there seems to be a threshold, after which a person's brainy lifestyle can't hold off the outward signs of dementia, the researchers say. 

How often do you read?
 
For their study, Wilson and his colleagues enlisted 1,157 people, all at least 65 years old and with no signs of dementia, and then evaluated their mental activities over the years. 

At the study's start, participants indicated on a 5-point scale how often they participated in seven  activities: viewing television, listening to radio; reading newspapers; reading magazines; reading books; playing games like cards or doing puzzles; and going to museums. (A rating of 5 meant a person did some of these activities about every day; 3 meant several times a month; 1 meant once a year or less.) 

About every three years, clinical evaluations were used to determine signs of dementia, mild cognitive impairment and Alzheimer's disease. (Dementia is a decline in mental capabilities, especially memory, which is primarily caused by Alzheimer's disease but also can be the result of Parkinson's disease, stroke, or infections in the brain.) 

During the first six years of the study, the researchers determined the number of individuals who had developed mild cognitive impairment, Alzheimer's, or no cognitive impairment. Then, they followed them for another six years and found that the rate of inevitable decline in those people still without cognitive impairment was reduced by 52 percent each subsequent year for each point they scored on the cognitive activity scale. 

But, perhaps surprisingly, for people who had developed Alzheimer's disease at the first six-year point (which accounted for about 90 percent of the dementia diagnoses), the average rate of decline per year actually increased by 42 percent for each point they scored on the cognitive activity scale. 

"Actually, the person with a cognitively active lifestyle has more severe disease than it appears when dementia is first diagnosed, and they decline more rapidly thereafter," Wilson said. 
 
Why reading delays brain decline
 
"There's been a long debate as to why people with a cognitively active lifestyle are less likely to experience cognitive decline," Wilson told LiveScience. One idea is that keeping the brain active protects against the decline, while another school of thought proposes that people who are less cognitively active are really showing early signs of the disease (and so decreasing cognitive activity is just a consequence of cognitive decline). In fact, past research has suggested people who have healthier brains are more likely to read and practice other mind-enhancing activities. 

The longitudinal study — meaning one in which participants are followed over time — is part of the Chicago Health and Aging Project, focusing on risk factors for Alzheimer's disease in four Chicago neighborhoods. 

The latest findings suggest the protective effect may be at work. Essentially, the plaques and tangles are still forming on the brain, but people who stay cognitively active don't show signs of those brain plaques until later.

The researchers aren't sure what's going on in the brain to keep decline at bay for cognitively active people. But past brain-imaging studies offer clues. 

One study over a three-year period of German medical students cramming for a sort of final exams found that their brains' hippocampus and neocortex had grown, Wilson said. Another study, focusing on jugglers, revealed corresponding changes in the parts of the brain devoted to juggling. 

The size increase in various brain regions means that some people will have an extra buffer for the cognitive decline that inevitably comes with age. Or as Wilson puts it, the beefed-up brain regions give you "a little more mileage out of what you have." 

Keeping your mind sharp
 
It's not too late for those who are creeping into old age to ward off the onset of mental deterioration, Wilson said. [Play brain-training games.] 

Wilson wouldn't recommend just mindless crossword puzzling; clues from neuro-imaging studies suggest the activities that make a difference in brain-boosting are the ones practiced regularly and intensively. 

"They need to be challenging activities and also intriguing or fun to the individual," Wilson said. He added:  "Any activity that involves reading is a good place to start." 

The study, supported by the National Institute on Aging and the National Institute of Environmental Health Sciences, was published online Sept. 1 in the journal Neurology.
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