A new study from Ohio State University reveals that the much-mythologized 'Freshman 15' is just that -- a tall tale.
College students do gain an average of 2 to 3 pounds in their first year of school, according to OSU researcher Jay Zagorsky.
The Houston Chronicle has more:
Zagorsky's study used data from more than 7,000 young Americans who as part of the National Longitudinal Survey of Youth 1997 were interviewed between the ages of 13 and 17 in 1997 and then interviewed each year since.
Only 10 percent of respondents gained 15 or more pounds during their freshmen years, while one-quarter of the study participants lost weight during their college years.
Zagorsky also said that college wasn't the culprit of late-teenage weight gain. "Most students don't gain large amounts of weight. And it is not college that leads to weight gain - it is becoming a young adult," he said, according to Psych Central.
Read the report's abstract here.
What do you think? Did you gain the freshman 15? Share your thoughts in the comments section.
ScienceDaily (Oct. 31, 2011) ? Fifty years after participating in studies of pentosuria, an inherited disorder once mistaken for diabetes, 15 families again welcomed medical geneticists into their lives. Their willingness to have their DNA analyzed with advanced genomics technologies has solved a mystery more than a hundred years old.
Researchers from the University of Washington, Israel, and Switzerland reported the solution in the Oct. 31 Early Edition of the Proceedings of the National Academy of Sciences.
Their findings may help elucidate historical and geographical patterns of genetic mutations -- when and how human mutations appear and are carried over generations and with migration of human populations. Pentosuria occurs almost exclusively in Ashkenazi Jews, whose ancestors trace back to the Middle Ages in Central or Eastern Europe. Traditionally, Ashkenazi Jews have married within their religious and ethnic group.
Dr. Arno Motulsky, professor emeritus of medicine, Division of Medical Genetics, and of genome sciences at the UW, and one of the founders of the discipline of medical genetics, was the senior author of the study. He was among the geneticist sleuths who tracked down the families and the genetic mutations responsible for the metabolic condition that ran in their families.
In the early and mid 20th century, clinical testing methods did not distinguish between pentosuria and diabetes mellitus. The confusion resulted in potentially dangerous treatment errors. Diabetic patients have problems with increased levels of glucose, a six-carbon sugar, whereas pentosuria causes high levels of a five-carbon sugar, xylulose, in urine and blood. Pentosuria itself is completely harmless. But when pentosuria patients were misdiagnosed with diabetes and received insulin, their blood glucose levels plummeted and they suffered insulin reactions.
The diagnostic errors motivated New York City biochemist Margaret Lasker to devise an accurate urine test for the five-carbon sugar that is characteristic of pentosuria. This test, and accurate tests for glucose in the urine, resolved the issue.
"People with pentosuria, which needs no treatment, no longer came to clinical attention," Motulsky said.
Lasker also conducted extensive family pedigree and survival studies of people with pentosuria. She concluded that pentosuria, which has no effect on lifespan and no clinical symptoms, was inherited as an autosomal recessive condition: a person had to inherit a causative gene sequence from both parents to have the disorder.
Pentosuria remained the last of Garrod's four inborn errors of metabolism for which the responsible DNA mutations were unknown. In 1904 Dr. Archibald Garrod of the Royal College of London had introduced the idea that certain inherited metabolic conditions were caused by a disease-specific genetic error. He surmised that the mutation disrupted a specific chemical reaction. He gave as examples albinism, cystinuria, alkaptonuria,[KL1] and pentosuria. The underlying mutations for three of these traits have since been discovered.
By 2002, researchers had identified the gene that codes for the enzyme that normally rids the body of excess xylulose. Still no mutations were identified in pentosuria.
However, in the course of sequencing DNA, the UW genomics laboratory of Dr. Mary-Claire King,serendipitously discovered a deletion in this gene in an individual of Ashkenazi Jewish background. King is a professor of medicine, Division of Genetics, and of genome sciences.
King and Motulsky hypothesized that, because the mutated gene led to a protein missing about 50 amino acids, it couldn't produce the right sugar-busting enzyme.
King, Motulsky, their team, and colleagues from Israel and Switzerland set about to determine whether this mutation caused pentosuria. Other UW researchers involved in the study were Sarah Pierce, Cailyn Spurrell, Ming Lee, and Sunday Stray of the Department of Genome Sciences and the Division of Medical Genetics, Department of Medicine; Jessica Mandell of the Division of Medical Genetics, and Michael MacCoss and Michael Bereman of the Department of Genome Sciences.
The problem in connecting the mutation to pentosuria was that people with the condition were no longer identified in their doctors' offices. Current urine tests do not check for this trait. Fortuitously, before her death in 1976, Lasker had entrusted Motulsky with her extensive research archives on the disorder. She had hoped that in the future Motulsky or his colleagues might be able to carry out new studies to determine the genetic cause of pentosuria.
Motulsky called and wrote to the families named in the Lasker records. Participants with pentosuria from the original studies or the children of deceased individuals with pentosuria agreed to the new study. Fifteen families enrolled.
Genetic analysis of DNA samples from the families led to the discovery of two different DCXR mutations linked to loss of function of the xylulose-breaking enzyme. In nine unrelated people with pentosuria, six had one type of mutation, one had the other, and two had both. None had the active enzyme in question in their blood cells, and all had high levels of xylulose in their blood. This confirmed the relationship between the mutations and the metabolic error.
Studies of the frequency of the two mutations in 1,067 Ashkenazi Jews showed that one mutation is more common than the other and suggested that pentosuria occurs in about 1 in 3,330 people of this ancestry. Pentosuria has also been found in a large Lebanese family, a Japanese family, and an Athabascan Canadian Indian in British Columbia, but the mutations in these individuals are not known.
The frequency of the two DCXR mutations causing pentosuria in Ashkenazi Jews follows a pattern of other rare recessive mutations in this population. The Israeli National Genetic Database shows that for most of the "Jewish genetic diseases," including Tay Sachs disease, Canavan syndrome, maple syrup urine disease and Gaucher disease, two or more mutations in the same gene have been found, with one mutation more common than the other, according to the researchers. For conditions like cystic fibrosis and a certain inherited hearing loss that are common in Jews and other groups, two or more mutations in the same gene have been discovered, with the more common mutation found throughout Europe and the less common one specific to the European Jewish population.
Other studies have suggested that many of the "founder" mutations for Ashkenazi Jewish genetic diseases date back to three time periods: the expansion of the Jewish population in the Middle East about 100 generations ago, the entry of the Jewish population into Central Europe about 50 generations ago, and their movement into Lithuania and the Pale of the Settlement about 12 generations ago. (A human generation is about 30 years).
"It will be interesting to determine the ages of the newly identified pentosuric mutations relative to Jewish history in Europe," the researchers on the current PNAS paper noted.
Although previous studies of pentosuria indicate that it is entirely benign, animal studies on the DCXR enzyme suggest that mutations that result in a loss of enzyme function could play a role in kidney damage. If so, patients with both pentosuria and diabetes could be more susceptible to diabetic kidney disease.
Other researchers on the PNAS paper, "Garrod's fourth inborn error of metabolism solved by the identification of mutations causing pentosuria," were Ephrat Levy-Lahad and Sharon Zeligson of the Shaare Zedek Medical Center in Jerusalem, and Siv Fokstuen of Genetic Medicine at the University Hospitals of Geneva, Switzerland.
The project was funded by unrestricted gifts to the Mary-Claire King Laboratory and by grants from the National Institutes of Health.
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The above story is reprinted from materials provided by University of Washington. The original article was written by Leila Gray.
Note: Materials may be edited for content and length. For further information, please contact the source cited above.
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For Halloween, I thought it would be fun to hear about your investing horror story. We all brag about how we have made a great move (as I always boast that I bought my first house with the trading profit from a leveraging Manoeuvre!). But we rarely talk about our worst trade, the one that made all our profits vanish within a few months? So I want to know if you are like me; I want to know if you have some skeletons hidden in your investing closet!
?
I won?t let you down and will start first! Here?s my story? be ready ?cause this one is pretty scary!
?
We are at the end of summer 2006. I had been trading since 2003 with great success and especially that year. I?m up 71% with my portfolio and I feel that everything I trade turns into gold. While I?m having great success with my trades, I?m also having great success in real estate. I just successfully sold my house and I?m going to buy another one in November. Everything is going smoothly ;-D
?
But there is this stock: Northern Shield Resources (CVE: NRN). I?ve been making a few plays on it and making some really good profit. I?m well aware that it?s a speculative mining stock but until then I had made a lot of money on it. I actually bought my shares at $0.38 the first time and the stock went up to $1.40 a few months later. In August, I decided to use part of the down payment for my future house to average up and buy more stock at $1,00 or so. In September, I then had $15,000 invested in NRN with an average price of $0.76. I?m still making profit but holding my position as the company will announce results of their latest prospecting in a few weeks.
?
I already made plans as to how I will spend my extra profits. I truly believe the stock will rise to a few bucks (maybe $5 if I?m lucky!) and that I will have enough money to not only buy my house, but a? BMW and a nice trip down south at the same time? my wife is going to be so proud of me!
?
So I go for lunch with a few friends on a casual day at work. I always look at my positions when I come back from lunch. Not that it ever changes anything but I like to see where my portfolio is at in the middle of the day . It was a sunny day, lunch was great and we laughed a lot; it was just another great day in my life? until I looked at my computer screen and saw my portfolio.
?
The stock value went from $1,00 to $0.45 during my lunch hour!
In a heartbeat, I lost about $8,000 (remember, that was my down payment money!). I started suffocating? I had to leave my office and take a walk. Eight Thousand Dollars. This is the only sound ringing in my head?. Until a worse sound crossed my mind like an axe chopping off my head:
?Mike, you?ve got to tell your wife about that?.Oh and Mike, you also have to figure how you will still put 20% cash down on your house now that you don?t have it anymore??
?
Ugh!
?
That was one of the most painful experiences I have ever had and definitely the worst investing story I have to tell. In the end, I told my wife with a pitiful face and borrowed the missing amount for my down payment from my parents and repaid them a few months later with my year-end bonus.
?
I learned a lot from this trade:
?
#1 I must play with money that I can actually lose and not with cash that needs to be used shortly for something else!
?
#2 I?ve also learned that investing is not gambling and I should not combine greed with ambition. These are 2 very bad ingredients for an investor?s soup!
?
#3 When you are lucky enough to make a lot of money in a short time, don?t be greedy, just cash in your profit and find another stock to buy (I should have sold this stock at $1.43 and made it one of my best investment stories instead!)
?
#4 Finally, investing in mining stocks is just a bad idea. Invest in real businesses generating real profits; hope is cute but will not report any gains on an investment statement
?
So I hope you appreciated reading how I failed and hope that you never have? but we both know that?s not true Now it?s your turn; what is your investment horror story?
?
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?
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Modern genetics answers age-old question on Garrod's fourth inborn error of metabolismPublic release date: 31-Oct-2011 [ | E-mail | Share ]
Contact: Leila Gray leilag@u.washington.edu 206-685-0381 University of Washington
Findings in Ashkenazi Jews may help elucidate historical and geographical patterns of human mutations in diasporic populations
Fifty years after participating in studies of pentosuria, an inherited disorder once mistaken for diabetes, 15 families again welcomed medical geneticists into their lives. Their willingness to have their DNA analyzed with advanced genomics technologies has solved a mystery more than a hundred years old.
Researchers from the University of Washington, Israel, and Switzerland reported the solution in the Oct. 31 Early Edition of the Proceedings of the National Academy of Sciences.
Their findings may help elucidate historical and geographical patterns of genetic mutations -- when and how human mutations appear and are carried over generations and with migration of human populations.
Pentosuria occurs almost exclusively in Ashkenazi Jews, whose ancestors trace back to the Middle Ages in Central or Eastern Europe. Traditionally, Ashkenazi Jews have married within their religious and ethnic group.
Dr. Arno Motulsky, professor emeritus of medicine, Division of Medical Genetics, and of genome sciences at the UW, and one of the founders of the discipline of medical genetics, was the senior author of the study. He was among the geneticist sleuths who tracked down the families and the genetic mutations responsible for the metabolic condition that ran in their families.
In the early and mid 20th century, clinical testing methods did not distinguish between pentosuria and diabetes mellitus. The confusion resulted in potentially dangerous treatment errors.
Diabetic patients have problems with increased levels of glucose, a six-carbon sugar, whereas pentosuria causes high levels of a five-carbon sugar, xylulose, in urine and blood. Pentosuria itself is completely harmless. But when pentosuria patients were misdiagnosed with diabetes and received insulin, their blood glucose levels plummeted and they suffered insulin reactions.
The diagnostic errors motivated New York City biochemist Margaret Lasker to devise an accurate urine test for the five-carbon sugar that is characteristic of pentosuria. This test, and accurate tests for glucose in the urine, resolved the issue.
"People with pentosuria, which needs no treatment, no longer came to clinical attention," Motulsky said.
Lasker also conducted extensive family pedigree and survival studies of people with pentosuria. She concluded that pentosuria, which has no effect on lifespan and no clinical symptoms, was inherited as an autosomal recessive condition: a person had to inherit a causative gene sequence from both parents to have the disorder.
Pentosuria remained the last of Garrod's four inborn errors of metabolism for which the responsible DNA mutations were unknown. In 1904 Dr. Archibald Garrod of the Royal College of London had introduced the idea that certain inherited metabolic conditions were caused by a disease-specific genetic error.
Garrod surmised that the mutation disrupted a specific chemical reaction. He gave as examples albinism, cystinuria, alkaptonuria, and pentosuria. The underlying mutations for three of these traits have since been discovered.
By 2002, researchers had identified the gene that codes for the enzyme that normally rids the body of excess xylulose. Still no mutations were identified in pentosuria.
However, in the course of sequencing DNA, the UW genomics laboratory of Dr. Mary-Claire King serendipitously discovered a deletion in this gene in an individual of Ashkenazi Jewish background. King is a professor of medicine, Division of Medical Genetics, and of genome sciences at the UW.
King and Motulsky hypothesized that, because the mutated gene led to a protein missing about 50 amino acids, it couldn't produce the right sugar-busting enzyme.
King, Motulsky, their team, and colleagues from Israel and Switzerland set about to determine whether this mutation caused pentosuria. Other UW researchers involved in the study were Sarah Pierce, Cailyn Spurrell, Ming Lee, and Sunday Stray of the Department of Genome Sciences and the Division of Medical Genetics, Department of Medicine; Jessica Mandell of the Division of Medical Genetics, and Michael MacCoss and Michael Bereman of the Department of Genome Sciences.
The problem in connecting the mutation to pentosuria was that people with the condition were no longer identified in their doctors' offices. Current urine tests do not check for this trait.
Fortuitously, before her death in 1976, Lasker had entrusted Motulsky with her extensive research archives on the disorder. She had hoped that in the future Motulsky or his colleagues might be able to carry out new studies to determine the genetic cause of pentosuria.
Motulsky called and wrote to the families named in the Lasker records. Participants with pentosuria from the original studies or the children of deceased individuals with pentosuria agreed to the new study. Fifteen families enrolled.
Genetic analysis of DNA samples from the families led to the discovery of two different DCXR mutations linked to loss of function of the xylulose-breaking enzyme. In nine unrelated people with pentosuria, six had one type of mutation, one had the other, and two had both. None had the active enzyme in question in their blood cells, and all had high levels of xylulose in their blood. This confirmed the relationship between the mutations and the metabolic error.
Studies of the frequency of the two mutations in 1,067 Ashkenazi Jews showed that one mutation is more common than the other and suggested that pentosuria occurs in about 1 in 3,330 people of this ancestry. Pentosuria has also been found in a large Lebanese family, a Japanese family, and an Athabascan Canadian Indian in British Columbia, but the mutations in these individuals are not known.
The frequency of the two DCXR mutations causing pentosuria in Ashkenazi Jews follows a pattern of other rare recessive mutations in this population. The Israeli National Genetic Database shows that for most of the "Jewish genetic diseases", including Tay Sachs disease, Canavan syndrome, maple syrup urine disease and Gaucher disease, two or more mutations in the same gene have been found, with one mutation more common than the other, according to the researchers.
For conditions like cystic fibrosis and a certain inherited hearing loss that are common in Jews and other groups, two or more mutations in the same gene have been discovered, with the more common mutation found throughout Europe and the less common one specific to the European Jewish population.
Other studies have suggested that many of the "founder" mutations for Ashkenazi Jewish genetic diseases date back to three time periods: the expansion of the Jewish population in the Middle East about 100 generations ago, the entry of the Jewish population into Central Europe about 50 generations ago, and their movement into Lithuania and the Pale of the Settlement about 12 generations ago. (A human generation is about 30 years).
"It will be interesting to determine the ages of the newly identified pentosuric mutations relative to Jewish history in Europe," the researchers on the current PNAS paper noted.
Although previous studies of pentosuria indicate that it is entirely benign, animal studies on the DCXR enzyme suggest that mutations that result in a loss of enzyme function could play a role in kidney damage. If so, patients with both pentosuria and diabetes could be more susceptible to diabetic kidney disease.
###
Other researchers on the PNAS paper, "Garrod's fourth inborn error of metabolism solved by the identification of mutations causing pentosuria," were Ephrat Levy-Lahad and Sharon Zeligson of the Shaare Zedek Medical Center in Jerusalem, and Siv Fokstuen of Genetic Medicine at the University Hospitals of Geneva, Switzerland.
The project was funded by unrestricted gifts to the Mary-Claire King Laboratory and by grants from the National Institutes of Health.
[ | E-mail | Share ]
?
AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert! system.
Modern genetics answers age-old question on Garrod's fourth inborn error of metabolismPublic release date: 31-Oct-2011 [ | E-mail | Share ]
Contact: Leila Gray leilag@u.washington.edu 206-685-0381 University of Washington
Findings in Ashkenazi Jews may help elucidate historical and geographical patterns of human mutations in diasporic populations
Fifty years after participating in studies of pentosuria, an inherited disorder once mistaken for diabetes, 15 families again welcomed medical geneticists into their lives. Their willingness to have their DNA analyzed with advanced genomics technologies has solved a mystery more than a hundred years old.
Researchers from the University of Washington, Israel, and Switzerland reported the solution in the Oct. 31 Early Edition of the Proceedings of the National Academy of Sciences.
Their findings may help elucidate historical and geographical patterns of genetic mutations -- when and how human mutations appear and are carried over generations and with migration of human populations.
Pentosuria occurs almost exclusively in Ashkenazi Jews, whose ancestors trace back to the Middle Ages in Central or Eastern Europe. Traditionally, Ashkenazi Jews have married within their religious and ethnic group.
Dr. Arno Motulsky, professor emeritus of medicine, Division of Medical Genetics, and of genome sciences at the UW, and one of the founders of the discipline of medical genetics, was the senior author of the study. He was among the geneticist sleuths who tracked down the families and the genetic mutations responsible for the metabolic condition that ran in their families.
In the early and mid 20th century, clinical testing methods did not distinguish between pentosuria and diabetes mellitus. The confusion resulted in potentially dangerous treatment errors.
Diabetic patients have problems with increased levels of glucose, a six-carbon sugar, whereas pentosuria causes high levels of a five-carbon sugar, xylulose, in urine and blood. Pentosuria itself is completely harmless. But when pentosuria patients were misdiagnosed with diabetes and received insulin, their blood glucose levels plummeted and they suffered insulin reactions.
The diagnostic errors motivated New York City biochemist Margaret Lasker to devise an accurate urine test for the five-carbon sugar that is characteristic of pentosuria. This test, and accurate tests for glucose in the urine, resolved the issue.
"People with pentosuria, which needs no treatment, no longer came to clinical attention," Motulsky said.
Lasker also conducted extensive family pedigree and survival studies of people with pentosuria. She concluded that pentosuria, which has no effect on lifespan and no clinical symptoms, was inherited as an autosomal recessive condition: a person had to inherit a causative gene sequence from both parents to have the disorder.
Pentosuria remained the last of Garrod's four inborn errors of metabolism for which the responsible DNA mutations were unknown. In 1904 Dr. Archibald Garrod of the Royal College of London had introduced the idea that certain inherited metabolic conditions were caused by a disease-specific genetic error.
Garrod surmised that the mutation disrupted a specific chemical reaction. He gave as examples albinism, cystinuria, alkaptonuria, and pentosuria. The underlying mutations for three of these traits have since been discovered.
By 2002, researchers had identified the gene that codes for the enzyme that normally rids the body of excess xylulose. Still no mutations were identified in pentosuria.
However, in the course of sequencing DNA, the UW genomics laboratory of Dr. Mary-Claire King serendipitously discovered a deletion in this gene in an individual of Ashkenazi Jewish background. King is a professor of medicine, Division of Medical Genetics, and of genome sciences at the UW.
King and Motulsky hypothesized that, because the mutated gene led to a protein missing about 50 amino acids, it couldn't produce the right sugar-busting enzyme.
King, Motulsky, their team, and colleagues from Israel and Switzerland set about to determine whether this mutation caused pentosuria. Other UW researchers involved in the study were Sarah Pierce, Cailyn Spurrell, Ming Lee, and Sunday Stray of the Department of Genome Sciences and the Division of Medical Genetics, Department of Medicine; Jessica Mandell of the Division of Medical Genetics, and Michael MacCoss and Michael Bereman of the Department of Genome Sciences.
The problem in connecting the mutation to pentosuria was that people with the condition were no longer identified in their doctors' offices. Current urine tests do not check for this trait.
Fortuitously, before her death in 1976, Lasker had entrusted Motulsky with her extensive research archives on the disorder. She had hoped that in the future Motulsky or his colleagues might be able to carry out new studies to determine the genetic cause of pentosuria.
Motulsky called and wrote to the families named in the Lasker records. Participants with pentosuria from the original studies or the children of deceased individuals with pentosuria agreed to the new study. Fifteen families enrolled.
Genetic analysis of DNA samples from the families led to the discovery of two different DCXR mutations linked to loss of function of the xylulose-breaking enzyme. In nine unrelated people with pentosuria, six had one type of mutation, one had the other, and two had both. None had the active enzyme in question in their blood cells, and all had high levels of xylulose in their blood. This confirmed the relationship between the mutations and the metabolic error.
Studies of the frequency of the two mutations in 1,067 Ashkenazi Jews showed that one mutation is more common than the other and suggested that pentosuria occurs in about 1 in 3,330 people of this ancestry. Pentosuria has also been found in a large Lebanese family, a Japanese family, and an Athabascan Canadian Indian in British Columbia, but the mutations in these individuals are not known.
The frequency of the two DCXR mutations causing pentosuria in Ashkenazi Jews follows a pattern of other rare recessive mutations in this population. The Israeli National Genetic Database shows that for most of the "Jewish genetic diseases", including Tay Sachs disease, Canavan syndrome, maple syrup urine disease and Gaucher disease, two or more mutations in the same gene have been found, with one mutation more common than the other, according to the researchers.
For conditions like cystic fibrosis and a certain inherited hearing loss that are common in Jews and other groups, two or more mutations in the same gene have been discovered, with the more common mutation found throughout Europe and the less common one specific to the European Jewish population.
Other studies have suggested that many of the "founder" mutations for Ashkenazi Jewish genetic diseases date back to three time periods: the expansion of the Jewish population in the Middle East about 100 generations ago, the entry of the Jewish population into Central Europe about 50 generations ago, and their movement into Lithuania and the Pale of the Settlement about 12 generations ago. (A human generation is about 30 years).
"It will be interesting to determine the ages of the newly identified pentosuric mutations relative to Jewish history in Europe," the researchers on the current PNAS paper noted.
Although previous studies of pentosuria indicate that it is entirely benign, animal studies on the DCXR enzyme suggest that mutations that result in a loss of enzyme function could play a role in kidney damage. If so, patients with both pentosuria and diabetes could be more susceptible to diabetic kidney disease.
###
Other researchers on the PNAS paper, "Garrod's fourth inborn error of metabolism solved by the identification of mutations causing pentosuria," were Ephrat Levy-Lahad and Sharon Zeligson of the Shaare Zedek Medical Center in Jerusalem, and Siv Fokstuen of Genetic Medicine at the University Hospitals of Geneva, Switzerland.
The project was funded by unrestricted gifts to the Mary-Claire King Laboratory and by grants from the National Institutes of Health.
[ | E-mail | Share ]
?
AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert! system.
Twitter / CultureMap Houston: Halloween stats that scare ...Halloween stats that scare: Texas is the No. 1 state in the country for pet costumes ? and really loves candy corn Il y a 30 minutesvia SocialFlow
This week things got magical. China staged an unreal fashion week, castles appeared in the Doha sand, and Sinead O'Connor ate her dinner in a fancy restaurant.
?? BACK TO ARTICLE
"Hotel Lux" Premiere - 6th International Rome Film Festival
ROME, ITALY - OCTOBER 29: Actress Thekla Reuten attends the 'Hotel Lux' premiere during the 6th International Rome Film Festival on October 29, 2011 in Rome, Italy. (Photo by Christine Pettinger/Getty Images)
For Halloween, I thought it would be fun to hear about your investing horror story. We all brag about how we have made a great move (as I always boast that I bought my first house with the trading profit from a leveraging Manoeuvre!). But we rarely talk about our worst trade, the one that made all our profits vanish within a few months? So I want to know if you are like me; I want to know if you have some skeletons hidden in your investing closet!
. It was a sunny day, lunch was great and we laughed a lot; it was just another great day in my life? until I looked at my computer screen and saw my portfolio.
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Public release date: 31-Oct-2011
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