Optimism associated with lowered risk of dying from heart disease:
Optimism associated with lowered risk of dying from heart disease
CHICAGO – Patients who described themselves as highly optimistic had lower risks of all-cause death, and lower rates of cardiovascular death than those with high levels of pessimism, according to an article in the November issue of The Archives of General Psychiatry, one of the JAMA/Archives journals.
According to the article, major depression is a known risk factor for cardiovascular death. However, the relationship between optimism and death has not received as much attention.
"'In conclusion, we found that the trait of optimism was an important long-term determinant of all-cause and cardiovascular mortality in elderly subjects independent of sociodemographic characteristics and cardiovascular risk factors,' the authors write. 'A predisposition toward optimism seemed to provide a survival benefit in elderly subjects with relatively short life expectancies otherwise.'
'Our results, combined with the finding that hopelessness was associated with an increased incidence or progression of disease, suggest that dispositional optimism affects the progression of cardiovascular disease,' the researchers state. 'Although optimism reduces the risk of cardiovascular death through mechanisms largely unaffected by baseline values of physical activity, obesity, smoking, hypertension, and lipid profile, pessimistic subjects may be more prone to changes across time in risk factors that affect the progression of cardiovascular disease (e.g., the development of smoking habits, obesity, or hypertension) than optimistic subjects. Dispositional optimism may also be associated with better coping strategies that are adhered to throughout life.'
Dispositional Optimism and All-Cause and Cardiovascular Mortality in a Prospective Cohort of Elderly Dutch Men and Women.Archives of General Psychiatry. 61(11):1126-1135, November 2004. Giltay, Erik J. MD, PhD; Geleijnse, Johanna M. PhD; Zitman, Frans G. MD, PhD; Hoekstra, Tiny PhD; Schouten, Evert G. MD, PhD
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Thursday, February 24, 2005
Wednesday, February 02, 2005
Wired News: Neurons Derived From Stem Cells
yes we can dreate all sorts with this, but is it the mix of chemicals and the timing, or the conscious choice that makes it???
Wired News: Neurons Derived From Stem Cells: "The conclusion, reported in the science journal Nature Biotechnology, is important for two reasons. First, stem-cell scientists have struggled to accomplish what researcher Su-Chun Zhang and his colleagues have just accomplished. It took Zhang's team two years of tedious trial-and-error experiments to direct stem cells to turn into motor neurons.
Perhaps more important, Zhang's recipe shows researchers that timing is everything when adding their chemical cocktails to stem-cell stews. Stem cells are vulnerable to successful human manipulation for only the briefest of moments -- and at different intervals depending on the results each researcher craves.
'This shows that you can't dump whatever growth factors you want in there,' Zhang said. 'It's not that simple. It's very specific. You have to have the right cocktail in the right amount at the right time.'
But with Zhang and others showing that the biological clock ticks differently in different animals and in each type of cell, it appears translating animal data to human terms is more about timing than biology.
"That is also somewhat reassuring," said Isacson, who has created dopamine-producing brain cells from stem cells. Parkinson disease patients lose dopamine cells, which help regulate body movement.
Embryonic stem cells are created in the first days after conception and ultimately turn into the 220 or so types of cells that make up the human body. Scientists believe they can someday control what stem cells become and when, using that power to replace damaged and dead cells that cause a wide range of suffering, from diabetes to Parkinson's.
But harnessing that power has proved elusive in all but a few cell types such as heart and two other types of brain cells.
'This is an important contribution because stem cell biology is difficult," Isacson said. "It helps decode the locks.'"
Wired News: Neurons Derived From Stem Cells: "The conclusion, reported in the science journal Nature Biotechnology, is important for two reasons. First, stem-cell scientists have struggled to accomplish what researcher Su-Chun Zhang and his colleagues have just accomplished. It took Zhang's team two years of tedious trial-and-error experiments to direct stem cells to turn into motor neurons.
Perhaps more important, Zhang's recipe shows researchers that timing is everything when adding their chemical cocktails to stem-cell stews. Stem cells are vulnerable to successful human manipulation for only the briefest of moments -- and at different intervals depending on the results each researcher craves.
'This shows that you can't dump whatever growth factors you want in there,' Zhang said. 'It's not that simple. It's very specific. You have to have the right cocktail in the right amount at the right time.'
But with Zhang and others showing that the biological clock ticks differently in different animals and in each type of cell, it appears translating animal data to human terms is more about timing than biology.
"That is also somewhat reassuring," said Isacson, who has created dopamine-producing brain cells from stem cells. Parkinson disease patients lose dopamine cells, which help regulate body movement.
Embryonic stem cells are created in the first days after conception and ultimately turn into the 220 or so types of cells that make up the human body. Scientists believe they can someday control what stem cells become and when, using that power to replace damaged and dead cells that cause a wide range of suffering, from diabetes to Parkinson's.
But harnessing that power has proved elusive in all but a few cell types such as heart and two other types of brain cells.
'This is an important contribution because stem cell biology is difficult," Isacson said. "It helps decode the locks.'"
Saturday, January 15, 2005
The Endocrine Regulation of Aging by Insulin-like Signals
Science -- Tatar et al. 299 (5611): 1346: "Pituitary Endocrine Deficiency in Mammals Of the half-dozen genetic models that retard murine aging, four involve deficiency of pituitary endocrine action. The mutations Prop1df (42) and Pit1dw impede pituitary production of growth hormone (GH), thyroid stimulating hormone (TSH), and prolactin; reduce growth rate and adult body size; and increase adult life-span by 40 to 60% (43, 44). Small adults with similar improvement in longevity are also produced by a knockout of growth hormone receptor (GHR-KO) (45). Expressed throughout life, these mutations produce many secondary alterations in endocrine systems. Without GH, the synthesis of circulating IGF-1 is suppressed, as is plasma insulin as a result of enhanced sensitivity in the liver combined with altered pancreatic islet development (46). Thyroid function is reduced in Prop1df and Pit1dw mutants deficient for TSH (45); GHR-KO mice are mildly hypothyroid, presumably as a result of impaired development (47). The challenge is to identify which of these hormones regulate aging and at which stage of life.
In invertebrates, reduced insulin/IGF signaling increases longevity, but it remains unclear whether or how reduction in GH and IGF-1 directly affects aging in rodents (Fig. 1C). In addition to its impact on IGF-1, GH influences somatic metabolism--for instance, by inducing adipocyte lipolysis. IGF-1 itself may affect aging in both beneficial and detrimental ways. In rodents as in humans, levels of GH and IGF-1 decline with adult age. Short-term GH supplementation in aged adults restores some aspects of body composition and cognition (48, 49). Thus, the withdrawal of GH and IGF-1 has been suggested to be a cause of senescence rather than a condition that retards aging. On the other hand, because it stimulates metabolism and cell growth, GH may hasten tissue pathology. Indeed, chronic treatment of GH-deficient dwarf rats with GH increased tumor incidence in response to a carcinogen (50). High IGF-1 titers in young wild-type animals may produce a trade-off between current benefits to reproduction and later costs in senescence (51).
Powerful evidence for the direct role of IGF-1 signaling in the control of mammalian aging was provided by mice mutant for the IFG-1 receptor Igf1r (52): Igf1r+/ females, but not males, live 33% longer than wild-type controls. These mutants exhibit minimal reduction in growth with no alterations in the age of sexual maturation, fertility, metabolism, food intake, or temperature. Life extension is associated with increased tolerance of oxidative stress and reduced phosphorylation of Shc, a gene previously implicated in the control of longevity and stress resistance in mice (53). Mouse longevity is also increased 18% by fat-specific disruption of the insulin receptor gene (54). These mice have normal caloric intake yet retain leanness and glucose tolerance with age. Multiple intriguing changes in adipocytes underlie these effects, including elevated plasma leptin relative to adipose tissue mass, reduced lipolysis, and polarization of adipocytes into populations with altered expression of fatty acid synthase (55). Thus, insulin at adipose tissue may affect aging through impacts on neural-targeted hormones as well as through regulation of intermediary metabolism."
Science, Vol 299, Issue 5611, 1346-1351 , 28 February 2003
In invertebrates, reduced insulin/IGF signaling increases longevity, but it remains unclear whether or how reduction in GH and IGF-1 directly affects aging in rodents (Fig. 1C). In addition to its impact on IGF-1, GH influences somatic metabolism--for instance, by inducing adipocyte lipolysis. IGF-1 itself may affect aging in both beneficial and detrimental ways. In rodents as in humans, levels of GH and IGF-1 decline with adult age. Short-term GH supplementation in aged adults restores some aspects of body composition and cognition (48, 49). Thus, the withdrawal of GH and IGF-1 has been suggested to be a cause of senescence rather than a condition that retards aging. On the other hand, because it stimulates metabolism and cell growth, GH may hasten tissue pathology. Indeed, chronic treatment of GH-deficient dwarf rats with GH increased tumor incidence in response to a carcinogen (50). High IGF-1 titers in young wild-type animals may produce a trade-off between current benefits to reproduction and later costs in senescence (51).
Powerful evidence for the direct role of IGF-1 signaling in the control of mammalian aging was provided by mice mutant for the IFG-1 receptor Igf1r (52): Igf1r+/ females, but not males, live 33% longer than wild-type controls. These mutants exhibit minimal reduction in growth with no alterations in the age of sexual maturation, fertility, metabolism, food intake, or temperature. Life extension is associated with increased tolerance of oxidative stress and reduced phosphorylation of Shc, a gene previously implicated in the control of longevity and stress resistance in mice (53). Mouse longevity is also increased 18% by fat-specific disruption of the insulin receptor gene (54). These mice have normal caloric intake yet retain leanness and glucose tolerance with age. Multiple intriguing changes in adipocytes underlie these effects, including elevated plasma leptin relative to adipose tissue mass, reduced lipolysis, and polarization of adipocytes into populations with altered expression of fatty acid synthase (55). Thus, insulin at adipose tissue may affect aging through impacts on neural-targeted hormones as well as through regulation of intermediary metabolism."
Science, Vol 299, Issue 5611, 1346-1351 , 28 February 2003
Monday, January 10, 2005
Sir2: scrambling for answers: researchers have yet to solidify links for the proposed longevity lynchpin.
The Scientist, Dec 6, 2004 v18 i23 p20(2)
(Research) Maria W. Anderson.
Full Text: COPYRIGHT 2004 Scientist Inc.
Low-calorie diets extend lifespan in almost every model tested, but scientists can't yet agree on what controls this phenomenon. biologist Leonard Guarente at Massachusetts Institute of Technology, contend that Sir2 is dependent on nicotinamide adenine di-nucleotide (NAD) and that CR activates Sir2 by reducing glucose metabolism, which increases the ratio of NAD to its reduced version, NADH. (2) Others, such as Harvard Medical School pathologist David Sinclair, hold that nicotinamide, not NAD, is the control switch for Sir2, and that the deaminase PncI converts nicotinamide to nicotinic acid, which in turn increases Sir2 activity.
"I think it's a push and a pull system," explains Sinclair. Work by Guarente and Shin-Ichiro Imai, a molecular biologist at Washington University, St. Louis, showed that increases in NAD activate yeast Sirz in vivo, while Sinclair's studies indicated that removing nicotinamide, a Sir2 inhibitor, can pull the reaction forward. "So we've got them pushing and us pulling, and [these mechanisms] probably work in concert with each other," says Sinclair.
In September, a group of researchers from Stan Fields' lab at the University of Washington (UW), Seattle, published a paper offering evidence that CR may work through a pathway not involving Sir2. In yeast lacking Sir2, CR did not extend lifespan
Matt Piper, a biologist at University College London, says he sees a role for Sir2 in lifespan extension by CR but notes that an organism's diet influences its physiology in multiple ways that might affect its lifespan. "Because diet is so complex, you have many different signaling pathways in the organism determining many different physiological processes, which result in lifespan extension or shortening," says Piper. "To put it all down to one gene in one pathway is a very big call." He explains that both the insulin-signaling pathway, which responds to sugar, and the TOR-signaling pathway, which is affected by dietary protein, probably play a role in CR-mediated longevity. Having at least two different signaling pathways for lifespan extension in flies and worms, Piper adds, "would suggest that there's probably a number of different feed-ins to get lifespan extension."
References
(1.) L.P. Guarente, "Forestalling the great beyond with the help of SIR2," The Scientist, 18:34-5, April 26, 2004.
(2.) S.J. Lin et al., "Calorie restriction extends yeast life span by lowering the level of NADH," Genes Dev, 18:12-6, 2004.
(3.) R.M. Anderson et al., "Nicotinamide and PNCl govern lifespan extension by calorie restriction in Saccharomyces cerevisiae," Nature, 423:181-5,2003.
(4.) M. Kaeberlein et al., "Sir2-independent life span extension by calorie restriction in yeast," PLoS Biology, 2:1381-87, September 2004.
(5.) H. Tissenbaum, L. Guarente, "Increased dosage of a sir-2 gene extends lifespan in Caenorhabditis elegans," Nature, 410:227-30, 200l.
(6.) K. Houthoofd et al., "Life extension via dietary restriction is independent of the Ins/IGF-1 signaling pathway in Caenorhabditis elegans," Exp Gemntol, 38:947-54, 2003.
(7.) B. Lakowski, S. Hekimi, "The genetics of caloric restriction in Caenorhabditis elegans," Proc Nat/Acad Sci, 95:13091-6, 1998.
(8.) B. Rogina, S.L. Helfand, "Sir2 mediates longevity in the fly through a pathway related to calorie restriction," Proc Natl Acad Sci, 101:15998-16003, Nov. 9, 2004.
(9.) D. Secko, "'Longevity' gene, diet linked," The Scientist Daily News, June 18, 2004, available online at www.biomedcentral.com/news/2005540618/01.
Maria W. Anderson (manderson@the-scientist.com)
(Research) Maria W. Anderson.
Full Text: COPYRIGHT 2004 Scientist Inc.
Low-calorie diets extend lifespan in almost every model tested, but scientists can't yet agree on what controls this phenomenon. biologist Leonard Guarente at Massachusetts Institute of Technology, contend that Sir2 is dependent on nicotinamide adenine di-nucleotide (NAD) and that CR activates Sir2 by reducing glucose metabolism, which increases the ratio of NAD to its reduced version, NADH. (2) Others, such as Harvard Medical School pathologist David Sinclair, hold that nicotinamide, not NAD, is the control switch for Sir2, and that the deaminase PncI converts nicotinamide to nicotinic acid, which in turn increases Sir2 activity.
"I think it's a push and a pull system," explains Sinclair. Work by Guarente and Shin-Ichiro Imai, a molecular biologist at Washington University, St. Louis, showed that increases in NAD activate yeast Sirz in vivo, while Sinclair's studies indicated that removing nicotinamide, a Sir2 inhibitor, can pull the reaction forward. "So we've got them pushing and us pulling, and [these mechanisms] probably work in concert with each other," says Sinclair.
In September, a group of researchers from Stan Fields' lab at the University of Washington (UW), Seattle, published a paper offering evidence that CR may work through a pathway not involving Sir2. In yeast lacking Sir2, CR did not extend lifespan
Matt Piper, a biologist at University College London, says he sees a role for Sir2 in lifespan extension by CR but notes that an organism's diet influences its physiology in multiple ways that might affect its lifespan. "Because diet is so complex, you have many different signaling pathways in the organism determining many different physiological processes, which result in lifespan extension or shortening," says Piper. "To put it all down to one gene in one pathway is a very big call." He explains that both the insulin-signaling pathway, which responds to sugar, and the TOR-signaling pathway, which is affected by dietary protein, probably play a role in CR-mediated longevity. Having at least two different signaling pathways for lifespan extension in flies and worms, Piper adds, "would suggest that there's probably a number of different feed-ins to get lifespan extension."
References
(1.) L.P. Guarente, "Forestalling the great beyond with the help of SIR2," The Scientist, 18:34-5, April 26, 2004.
(2.) S.J. Lin et al., "Calorie restriction extends yeast life span by lowering the level of NADH," Genes Dev, 18:12-6, 2004.
(3.) R.M. Anderson et al., "Nicotinamide and PNCl govern lifespan extension by calorie restriction in Saccharomyces cerevisiae," Nature, 423:181-5,2003.
(4.) M. Kaeberlein et al., "Sir2-independent life span extension by calorie restriction in yeast," PLoS Biology, 2:1381-87, September 2004.
(5.) H. Tissenbaum, L. Guarente, "Increased dosage of a sir-2 gene extends lifespan in Caenorhabditis elegans," Nature, 410:227-30, 200l.
(6.) K. Houthoofd et al., "Life extension via dietary restriction is independent of the Ins/IGF-1 signaling pathway in Caenorhabditis elegans," Exp Gemntol, 38:947-54, 2003.
(7.) B. Lakowski, S. Hekimi, "The genetics of caloric restriction in Caenorhabditis elegans," Proc Nat/Acad Sci, 95:13091-6, 1998.
(8.) B. Rogina, S.L. Helfand, "Sir2 mediates longevity in the fly through a pathway related to calorie restriction," Proc Natl Acad Sci, 101:15998-16003, Nov. 9, 2004.
(9.) D. Secko, "'Longevity' gene, diet linked," The Scientist Daily News, June 18, 2004, available online at www.biomedcentral.com/news/2005540618/01.
Maria W. Anderson (manderson@the-scientist.com)
Sunday, January 09, 2005
The Human Energy Field in Relation to Science, Consciousness, and Health
5000 years ago, ancient spiritual tradition of India spoke of a universal energy called prana. This universal energy is the source of all life. The breath of life moves through all forms to give them life. Yogis work with this energy with breathing techniques, meditation, and physical exercise to produce altered states of consciousness and longevity.
3,000 years ago, the ancient Qigong masters in China were practicing their meditative discipline to balance and invigorate the human energy field. They called this vital energy that pervades all forms, both animate and inanimate, Qi The Qi is the vital energy of the body; while gong means the skill of moving this Qi and working with it. Practitioners use mind control to move and control the Qi to not only improve health and longevity, but also to enhance awareness, psychic powers, and spiritual development.
The ancient Qigong masters also developed Tai Chi, Kung Fu, and the martial arts. In addition, they made the first model for acupuncture. Acupuncturists insert needles, or use moxa, or put magnets at specific acupuncture points to balance the yin and yang of the human energy field. When the Qi is balanced, the entity has good health. When the Qi is unbalanced, the entity has poor or impaired health.
The Kabbalah, the Jewish mystical teachings written about 538 B.C., calls these energies the astral light. Later on, Christian paintings and sculptures show a halo around the head of Christ and other spiritual leaders. Similarly, we see this halo on statues and paintings of Buddha, and also see energy or light coming from the fingers of many of the gods of India. In fact, there are references made to the phenomenon of the human energy field (HEF) or the aura of the body, in 97 different cultures, according to John White in his book "Future Science."
The history of medicine similarly reflects a fascination with the observation of the HEF and its study. Back in 500 B.C., the Pythagoreans believed that there is a universal energy pervading all of nature. They taught that its light could effect cures in sick patients.
In the 1100's, Liebault said that humans have an energy that can react on someone else's energy, either at a distance or close by. According to Liebault, a person can have either an unhealthy or a healthy effect on someone else -- just by being present. The HEF of one person may be harmonious, or it maye be discordant with another. The HEF of one person may be nurturing, or it may be draining to the HEF of another.
In the 1800's, Mesmer, the father of modern hypnotism, suggested that a field similar to an electromagnetic field might exist around the human body. Mesmer suggested that the power of this electromagnetic field, which he believed behaved as a fluid, might also be able to exert influence on the field of another.
In the mid-1800's, Count Von Reichenbach spent 30 years experimenting with the human energy field, whcih he called the odic field. He found that this field showed many properties which were similar to the electromagnetic field described by James Clark Maxwell in the early 1880's.
However, Von Reichenbach also showed that with the odic force, like poles attract. In other words, like attracts like. In his work, "Physico-physiological Researches on the Dynamics of Magnetism, Electricity, Heat, Light, Crystallization, and Chemism, In Their Relation to Vital Force", printed in New York in 1851, Von Reichenbach showed that electropositive elements gave his subjects feelings of warmth, and that this produced unpleasant feelings. In the reverse, electronegative elements produced cool and agreeable feelings.
He also found that the odic field could be conducted through a wire. It traveled slowly at 13 feet per second. This speed depended on the density of the wire rather than its conductivity. He showed that part of this odic field could be focused like a light through a lens, while another part of this odic field would flow around the lens, like a candle flame flows around something placed in its path. Air currents would also move this part of the odic field. This suggests a composition similar to a gas. Von Reichenbach's experiments suggest the odic or auric field is energetic, like a light wave, and also particulate, like a fluid. Also, he showed the right side of the body as being a positive pole, and the left as negative. This agrees with the ancient Chinese principles of yin and yang.
Copyright 1996, All Rights Reserved, Gloria Alvino, HeartGlo@aol.com
About The Author: Gloria Alvino, R.Ph., B.S. in Pharmacy, M.S. in Health & Human Sciences, is founder & president of Heart to Heart Associates, Inc. a charitable, educational, non-profit organization. HTHA is dedicated through education and the advocacy of research to help individuals improve their health and quality of life.
3,000 years ago, the ancient Qigong masters in China were practicing their meditative discipline to balance and invigorate the human energy field. They called this vital energy that pervades all forms, both animate and inanimate, Qi The Qi is the vital energy of the body; while gong means the skill of moving this Qi and working with it. Practitioners use mind control to move and control the Qi to not only improve health and longevity, but also to enhance awareness, psychic powers, and spiritual development.
The ancient Qigong masters also developed Tai Chi, Kung Fu, and the martial arts. In addition, they made the first model for acupuncture. Acupuncturists insert needles, or use moxa, or put magnets at specific acupuncture points to balance the yin and yang of the human energy field. When the Qi is balanced, the entity has good health. When the Qi is unbalanced, the entity has poor or impaired health.
The Kabbalah, the Jewish mystical teachings written about 538 B.C., calls these energies the astral light. Later on, Christian paintings and sculptures show a halo around the head of Christ and other spiritual leaders. Similarly, we see this halo on statues and paintings of Buddha, and also see energy or light coming from the fingers of many of the gods of India. In fact, there are references made to the phenomenon of the human energy field (HEF) or the aura of the body, in 97 different cultures, according to John White in his book "Future Science."
The history of medicine similarly reflects a fascination with the observation of the HEF and its study. Back in 500 B.C., the Pythagoreans believed that there is a universal energy pervading all of nature. They taught that its light could effect cures in sick patients.
In the 1100's, Liebault said that humans have an energy that can react on someone else's energy, either at a distance or close by. According to Liebault, a person can have either an unhealthy or a healthy effect on someone else -- just by being present. The HEF of one person may be harmonious, or it maye be discordant with another. The HEF of one person may be nurturing, or it may be draining to the HEF of another.
In the 1800's, Mesmer, the father of modern hypnotism, suggested that a field similar to an electromagnetic field might exist around the human body. Mesmer suggested that the power of this electromagnetic field, which he believed behaved as a fluid, might also be able to exert influence on the field of another.
In the mid-1800's, Count Von Reichenbach spent 30 years experimenting with the human energy field, whcih he called the odic field. He found that this field showed many properties which were similar to the electromagnetic field described by James Clark Maxwell in the early 1880's.
However, Von Reichenbach also showed that with the odic force, like poles attract. In other words, like attracts like. In his work, "Physico-physiological Researches on the Dynamics of Magnetism, Electricity, Heat, Light, Crystallization, and Chemism, In Their Relation to Vital Force", printed in New York in 1851, Von Reichenbach showed that electropositive elements gave his subjects feelings of warmth, and that this produced unpleasant feelings. In the reverse, electronegative elements produced cool and agreeable feelings.
He also found that the odic field could be conducted through a wire. It traveled slowly at 13 feet per second. This speed depended on the density of the wire rather than its conductivity. He showed that part of this odic field could be focused like a light through a lens, while another part of this odic field would flow around the lens, like a candle flame flows around something placed in its path. Air currents would also move this part of the odic field. This suggests a composition similar to a gas. Von Reichenbach's experiments suggest the odic or auric field is energetic, like a light wave, and also particulate, like a fluid. Also, he showed the right side of the body as being a positive pole, and the left as negative. This agrees with the ancient Chinese principles of yin and yang.
Copyright 1996, All Rights Reserved, Gloria Alvino, HeartGlo@aol.com
About The Author: Gloria Alvino, R.Ph., B.S. in Pharmacy, M.S. in Health & Human Sciences, is founder & president of Heart to Heart Associates, Inc. a charitable, educational, non-profit organization. HTHA is dedicated through education and the advocacy of research to help individuals improve their health and quality of life.
Tuesday, January 04, 2005
Meditation Gives Brain a Charge, Study Finds
Yes of course they are finding out how much people affect themselves, now we are almost ready to see how we can change our entire bodies... CONSCIOUSLY!!!
________________________________
Brain research is beginning to produce concrete evidence for something that Buddhist practitioners of meditation have maintained for centuries: Mental discipline and meditative practice can change the workings of the brain and allow people to achieve different levels of awareness
"Their mental practice is having an effect on the brain in the same way golf or tennis practice will enhance performance." It demonstrates, he said, that the brain is capable of being trained and physically modified in ways few people can imagine.
Davidson says his newest results from the meditation study, published in the Proceedings of the National Academy of Sciences in November, take the concept of neuroplasticity a step further by showing that mental training through meditation (and presumably other disciplines) can itself change the inner workings and circuitry of the brain.
The new findings are the result of a long, if unlikely, collaboration between Davidson and Tibet's Dalai Lama, the world's best-known practitioner of Buddhism. The Dalai Lama first invited Davidson to his home in Dharamsala, India, in 1992 after learning about Davidson's innovative research into the neuroscience of emotions. The Tibetans have a centuries-old tradition of intensive meditation and, from the start, the Dalai Lama was interested in having Davidson scientifically explore the workings of his monks' meditating minds. Three years ago, the Dalai Lama spent two days visiting Davidson's lab.
________________________________
Brain research is beginning to produce concrete evidence for something that Buddhist practitioners of meditation have maintained for centuries: Mental discipline and meditative practice can change the workings of the brain and allow people to achieve different levels of awareness
"Their mental practice is having an effect on the brain in the same way golf or tennis practice will enhance performance." It demonstrates, he said, that the brain is capable of being trained and physically modified in ways few people can imagine.
Davidson says his newest results from the meditation study, published in the Proceedings of the National Academy of Sciences in November, take the concept of neuroplasticity a step further by showing that mental training through meditation (and presumably other disciplines) can itself change the inner workings and circuitry of the brain.
The new findings are the result of a long, if unlikely, collaboration between Davidson and Tibet's Dalai Lama, the world's best-known practitioner of Buddhism. The Dalai Lama first invited Davidson to his home in Dharamsala, India, in 1992 after learning about Davidson's innovative research into the neuroscience of emotions. The Tibetans have a centuries-old tradition of intensive meditation and, from the start, the Dalai Lama was interested in having Davidson scientifically explore the workings of his monks' meditating minds. Three years ago, the Dalai Lama spent two days visiting Davidson's lab.
Thursday, December 23, 2004
Depression as a Risk Factor for Mortality in Patients With Coronary Heart Disease
Consciouness affects the complete human system
Depression as a Risk Factor for Mortality in Patients With Coronary Heart Disease: A Meta-analysis -- Barth et al. 66 (6): 802 -- Psychosomatic Medicine: "Depressive symptoms increase the risk of mortality in CHD patients. The risk of depressed patients dying in the 2 years after the initial assessment is two times higher than that of nondepressed patients (OR, 2.24; 1.37 3.60). This negative prognostic effect also remains in the long-term (OR, 1.78; 1.12 2.83) and after adjustment for other risk factors (HR [adj], 1.76; 1.27 2.43). The unfavorable impact of depressive disorders was reported for the most part in the form of crude odds ratios. Within the first 6 months, depressive disorders were found to have no significant effect on mortality (OR, 2.07; CI, 0.82 5.26). However, after 2 years, the risk is more than two times higher for CHD patients with clinical depression (OR, 2.61; 1.53 4.47). Only three studies reported adjusted hazard ratios for clinical depression and supported the results of the bivariate models. CONCLUSIONS: Depressive symptoms and clinical depression have an unfavorable impact on mortality in CHD patients. The results are limited by heterogeneity of the results in the primary studies. There is no clear evidence whether self-report or clinical interview is the more precise predictor. Nevertheless, depression has to be considered a relevant risk factor in patients with CHD. "
Depression as a Risk Factor for Mortality in Patients With Coronary Heart Disease: A Meta-analysis -- Barth et al. 66 (6): 802 -- Psychosomatic Medicine: "Depressive symptoms increase the risk of mortality in CHD patients. The risk of depressed patients dying in the 2 years after the initial assessment is two times higher than that of nondepressed patients (OR, 2.24; 1.37 3.60). This negative prognostic effect also remains in the long-term (OR, 1.78; 1.12 2.83) and after adjustment for other risk factors (HR [adj], 1.76; 1.27 2.43). The unfavorable impact of depressive disorders was reported for the most part in the form of crude odds ratios. Within the first 6 months, depressive disorders were found to have no significant effect on mortality (OR, 2.07; CI, 0.82 5.26). However, after 2 years, the risk is more than two times higher for CHD patients with clinical depression (OR, 2.61; 1.53 4.47). Only three studies reported adjusted hazard ratios for clinical depression and supported the results of the bivariate models. CONCLUSIONS: Depressive symptoms and clinical depression have an unfavorable impact on mortality in CHD patients. The results are limited by heterogeneity of the results in the primary studies. There is no clear evidence whether self-report or clinical interview is the more precise predictor. Nevertheless, depression has to be considered a relevant risk factor in patients with CHD. "
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