While the study is extremely interesting, it is important not to over-interpret the results. The authors suggest that there is a connection between prostate cancer and masturbation. But they do NOT prove that masturbation actually causes or protects against prostate cancer. It is quite possible that the level of hormones in a given man may determine both his frequency of masturbation and his chance of getting prostate cancer.
"...
"Frequent masturbation during men's 20s and 30s increased their risk of prostate cancer," Dimitropoulou tells WebMD. "But men in their 50s who masturbated frequently had decreased risk."
Of course, masturbation frequency is relative.
For men in their 20s, "frequent masturbation" was two to seven times per week. Compared to same-age men who reported masturbating less than once per month, 20-something frequent masturbators had a 79% higher risk of prostate cancer by age 60.
For men in their 50s, "frequent masturbation" was one or more times per week. Compared to same-age men who reported never masturbating, 50-something frequent masturbators had a 70% lower risk of prostate cancer...."
"...Meanwhile, Dimitropoulou, now at England's University of Cambridge, advises moderation for both younger and older men.
"It is kind of logical that a moderate level of masturbatory activity has to be maintained," she says. "Not too much, and not none at all.""
http://www.webmd.com/prostate-cancer/news/20090127/masturbation-and-prostate-cancer-risk
Sexual activity and prostate cancer risk in men diagnosed at a younger age.
Dimitropoulou P, Lophatananon A, Easton D, Pocock R, Dearnaley DP, Guy M, Edwards S, O'Brien L, Hall A, Wilkinson R, Eeles R, Muir KR; UK Genetic Prostate Cancer Study Collaborators; British Association of Urological Surgeons Section of Oncology.
Abstract
OBJECTIVE: To examine, in a case-control study, the association between the frequency of sexual activity (intercourse, masturbation, overall) and prostate cancer risk in younger men diagnosed at < or = 60 years old.
PATIENTS, SUBJECTS AND METHODS: In all, 431 prostate cancer cases and 409 controls participated and provided information on their sexual activity. In particular, the frequencies of intercourse and masturbation during the participants' different age decades (20s, 30s, 40s, 50s) were collected.
RESULTS: Whereas frequent overall sexual activity in younger life (20s) increased the disease risk, it appeared to be protective against the disease when older (50s). Alone, frequent masturbation activity was a marker for increased risk in the 20s and 30s but appeared to be associated with a decreased risk in the 50s, while intercourse activity alone was not associated with the disease.
CONCLUSION: These findings could imply different mechanisms by which sexual activity is involved in the aetiology of prostate cancer at different ages. Alternatively, there is a possibility of reverse causation in explaining part of the protective effect seen for men in their 50s
Monday, September 27, 2010
Sunday, September 26, 2010
Contagious Cancer
The common wisdom is that one can't "catch" cancer from another person. While this may be true for most cancers there are probably exceptions. One interesting case involves a type of cancer in dogs called Sticker's sarcoma. This cancer spreads from dog to dog during sex and when dogs byte or lick each other.
One fascinating point from the discovery published in the journal Cell is that the tumor is probably hundreds of years old (compare to the everage dog lifespan of 13 years)! The tumor is essentially immortal as it jumps from one animal to another.
"Robert A. Weinberg, a pioneer in the genetic underpinnings of cancer at the Whitehead Institute for Biomedical Research in Cambridge, Mass., said he was not surprised to learn that genetic studies had confirmed that Sticker's is a transmissible cancer, given the strength of earlier clues. But he agreed that the phenomenon raises difficult questions about why more cancers do not spread this way."
http://www.washingtonpost.com/wp-dyn/content/article/2006/08/10/AR2006081001535.html
Cell. 2006 Aug 11;126(3):477-87.
Clonal origin and evolution of a transmissible cancer.
Murgia C, Pritchard JK, Kim SY, Fassati A, Weiss RA.
MRC/UCL Centre for Medical Molecular Virology, Division of Infection and Immunity, University College London, 46 Cleveland Street, London W1T 4JF, UK.
Abstract
The transmissible agent causing canine transmissible venereal tumor (CTVT) is thought to be the tumor cell itself. To test this hypothesis, we analyzed genetic markers including major histocompatibility (MHC) genes, microsatellites, and mitochondrial DNA (mtDNA) in naturally occurring tumors and matched blood samples. In each case, the tumor is genetically distinct from its host. Moreover, tumors collected from 40 dogs in 5 continents are derived from a single neoplastic clone that has diverged into two subclades. Phylogenetic analyses indicate that CTVT most likely originated from a wolf or an East Asian breed of dog between 200 and 2500 years ago. Although CTVT is highly aneuploid, it has a remarkably stable genotype. During progressive growth, CTVT downmodulates MHC antigen expression. Our findings have implications for understanding genome instability in cancer, natural transplantation of allografts, and the capacity of a somatic cell to evolve into a transmissible parasite.
One fascinating point from the discovery published in the journal Cell is that the tumor is probably hundreds of years old (compare to the everage dog lifespan of 13 years)! The tumor is essentially immortal as it jumps from one animal to another.
"Robert A. Weinberg, a pioneer in the genetic underpinnings of cancer at the Whitehead Institute for Biomedical Research in Cambridge, Mass., said he was not surprised to learn that genetic studies had confirmed that Sticker's is a transmissible cancer, given the strength of earlier clues. But he agreed that the phenomenon raises difficult questions about why more cancers do not spread this way."
http://www.washingtonpost.com/wp-dyn/content/article/2006/08/10/AR2006081001535.html
Cell. 2006 Aug 11;126(3):477-87.
Clonal origin and evolution of a transmissible cancer.
Murgia C, Pritchard JK, Kim SY, Fassati A, Weiss RA.
MRC/UCL Centre for Medical Molecular Virology, Division of Infection and Immunity, University College London, 46 Cleveland Street, London W1T 4JF, UK.
Abstract
The transmissible agent causing canine transmissible venereal tumor (CTVT) is thought to be the tumor cell itself. To test this hypothesis, we analyzed genetic markers including major histocompatibility (MHC) genes, microsatellites, and mitochondrial DNA (mtDNA) in naturally occurring tumors and matched blood samples. In each case, the tumor is genetically distinct from its host. Moreover, tumors collected from 40 dogs in 5 continents are derived from a single neoplastic clone that has diverged into two subclades. Phylogenetic analyses indicate that CTVT most likely originated from a wolf or an East Asian breed of dog between 200 and 2500 years ago. Although CTVT is highly aneuploid, it has a remarkably stable genotype. During progressive growth, CTVT downmodulates MHC antigen expression. Our findings have implications for understanding genome instability in cancer, natural transplantation of allografts, and the capacity of a somatic cell to evolve into a transmissible parasite.
Sleep and Learning
One function of sleep is to help you learn. Scientists have found that sleep helps secure memories and improves certain types of learning. Therefore, to learn more one needs to sleep more.
"...a nap with REM (or “dream”) sleep improves people’s ability to integrate unassociated information for creative problem solving, and study after study has shown that sleep boosts memory. If you memorize a list of words and then take a nap, you’ll remember more words than you would without sleeping first. Even micronaps of six minutes—not including the time it takes to fall asleep, which is about five minutes if you’re really tired—make a difference."
http://hbr.org/web/2009/health/simplest-way-to-reboot-your-brain
"...a nap with REM (or “dream”) sleep improves people’s ability to integrate unassociated information for creative problem solving, and study after study has shown that sleep boosts memory. If you memorize a list of words and then take a nap, you’ll remember more words than you would without sleeping first. Even micronaps of six minutes—not including the time it takes to fall asleep, which is about five minutes if you’re really tired—make a difference."
http://hbr.org/web/2009/health/simplest-way-to-reboot-your-brain
Saturday, September 25, 2010
Interesting Testosterone Topics
Testosterone is an important hormone for both males and females. As testosterone level changes with age and for other reasons, it may have profound influence on the quality of adult life.
I find several effects of testosterone interesting and will blog about them:
Mental and physical energy
Maintenance of muscle tropism
Effects on prostate cancer
Cardiovascular health
Immune system
Fight-or-flight response
Falling in love
Risk-taking decisions
Fatherhood
I find several effects of testosterone interesting and will blog about them:
Mental and physical energy
Maintenance of muscle tropism
Effects on prostate cancer
Cardiovascular health
Immune system
Fight-or-flight response
Falling in love
Risk-taking decisions
Fatherhood
Friday, December 09, 2005
Sirt1 gene is required for the increase in physical activity induced by caloric restrictions
Caloric restriction (CR) is the best known approach to extend organism’s lifespan. It works remarkably well in various living beings, from yeast to mice. It is likely also to work in primates and humans. If an animal lives under CR, essentially semi-starving, one may think that it will try to preserve its energy by reducing physical activity. Apparently, this is not the case. For example, mice in reality move more and demonstrate increased foraging activity while on a restricted diet. This does make sense as far as individual’s survival is concerned. In the wild, mice confronted with food shortage are more likely to find more food when they try to search for it than if they simply sit there hoping for a piece of cheese to appear out of thin air.
I have recently written about Sir2, a gene critical for longevity in different organisms. Sir2 is multi-facet gene and may have opposite roles as far as longevity is concerned in different cell types. In the paper published this week in Science the authors add another evidence for Sir2 role in CR induced longevity in mammals. Sir2 homologue from mice, Sirt1, turns out to be needed for the increased activity induced by calorie restrictions in mice. The mice lacking Sirt1 demonstrate various biochemical changes triggered by CR (for example, reduction of blood glucose) just like the wild-type mice. But, starved Sirt1 animals are no more active than the animals fed to their full. Thus, Sirt1 is important for starvation induced physical activity. It will be very interesting to see if Sirt1 is also required for life-span extension. Apparently, because Sirt1 gene deletion has only been engineered recently, the mice missing Sirt1 gene are still too young to tell if Sirt1 is required for their longevity under calorie restriction.
Ok, calorie restricted mice demonstrate enhanced physical activity. But what about their sex lives? Are they as sexually active as their relatives who enjoy fuller plates? Could CR mice be in fact more sexually active just as they are more physically active? My guess is that most likely CR mice are less sexually active than their well-fed brothers and sisters. The reason for this is that while the mouse may not able to compromise its foraging activity when threatened with looming starvation, it can more easily forgo sexual activities to preserve the limited energy that is critically needed to hunt for food.
Reference
Science 9 December 2005:
Vol. 310. no. 5754, p. 1641
DOI: 10.1126/science.1118357
Increase in Activity During Calorie Restriction Requires Sirt1
Danica Chen, Andrew D. Steele, Susan Lindquist, Leonard Guarente
Sir2 (silent information regulator 2) is a nicotinamide adenine dinucletide-dependent deacetylase required for longevity due to calorie restriction in yeast and Drosophila. In mammals, calorie restriction induces a complex pattern of physiological and behavioral changes. Here we report that the mammalian Sir2 ortholog, Sirt1, is required for the induction of a phenotype by calorie restriction in mice.
I have recently written about Sir2, a gene critical for longevity in different organisms. Sir2 is multi-facet gene and may have opposite roles as far as longevity is concerned in different cell types. In the paper published this week in Science the authors add another evidence for Sir2 role in CR induced longevity in mammals. Sir2 homologue from mice, Sirt1, turns out to be needed for the increased activity induced by calorie restrictions in mice. The mice lacking Sirt1 demonstrate various biochemical changes triggered by CR (for example, reduction of blood glucose) just like the wild-type mice. But, starved Sirt1 animals are no more active than the animals fed to their full. Thus, Sirt1 is important for starvation induced physical activity. It will be very interesting to see if Sirt1 is also required for life-span extension. Apparently, because Sirt1 gene deletion has only been engineered recently, the mice missing Sirt1 gene are still too young to tell if Sirt1 is required for their longevity under calorie restriction.
Ok, calorie restricted mice demonstrate enhanced physical activity. But what about their sex lives? Are they as sexually active as their relatives who enjoy fuller plates? Could CR mice be in fact more sexually active just as they are more physically active? My guess is that most likely CR mice are less sexually active than their well-fed brothers and sisters. The reason for this is that while the mouse may not able to compromise its foraging activity when threatened with looming starvation, it can more easily forgo sexual activities to preserve the limited energy that is critically needed to hunt for food.
Reference
Science 9 December 2005:
Vol. 310. no. 5754, p. 1641
DOI: 10.1126/science.1118357
Increase in Activity During Calorie Restriction Requires Sirt1
Danica Chen, Andrew D. Steele, Susan Lindquist, Leonard Guarente
Sir2 (silent information regulator 2) is a nicotinamide adenine dinucletide-dependent deacetylase required for longevity due to calorie restriction in yeast and Drosophila. In mammals, calorie restriction induces a complex pattern of physiological and behavioral changes. Here we report that the mammalian Sir2 ortholog, Sirt1, is required for the induction of a phenotype by calorie restriction in mice.
Friday, November 25, 2005
Engineered yeast set a record in longevity. What are the implications for humans?
Restrict nutrient access, remove a couple of genes and one lives 5-fold longer than normal. This is not science fiction, this is the cutting edge science. But, of course, I am not talking about humans here. The research was done on a unicellular organism, yeast. In the paper published this month in Cell the authors state that they have created conditions that “causes one of the longest chronological lifespan extensions reported for any organism”.
Interestingly, the gene, called Sir2, that the scientists have removed to create the record longevity in yeast, is the same gene that was previously shown to extend longevity if its activity is INCREASED! Yes, Sir2, when overactivated, has been known to cause a longer life span in different organisms, from yeast to flies. How to reconcile these two opposite observations? It appears that Sir2 can play different roles in different cells. In the cells that are actively dividing extra Sir2 activity extends their capacity to divide. While in the cells that have stopped dividing, extra Sir2 activity appears to be harmful.
If Sir2 can have two opposite effects on life span depending on the cell state, which of the roles could be critical for human longevity? The most likely answer is “both”. Human body is made of billions of cells. Some of them are capable of dividing, the others are not, but we need them both. Therefore, provided that the human Sir2 similarly has dual function like its counterpart from yeast, simply turning Sir2 on or off may not be enough to extend our life span. If too much Sir2 is not good for dividing cells, while too little is not good for the post-mitotic ones, could it be that we have just the right amount?
Cell. 2005 Nov 18;123(4):655-67.
Sir2 blocks extreme life-span extension.
Fabrizio P, Gattazzo C, Battistella L, Wei M, Cheng C, McGrew K, Longo VD.Andrus Gerontology Center and Department of Biological Sciences, University of Southern California, 3715 McClintock Avenue, Los Angeles, California 90089.
Sir2 is a conserved deacetylase that modulates life span in yeast, worms, and flies and stress response in mammals. In yeast, Sir2 is required for maintaining replicative life span, and increasing Sir2 dosage can delay replicative aging. We address the role of Sir2 in regulating chronological life span in yeast. Lack of Sir2 along with calorie restriction and/or mutations in the yeast AKT homolog, Sch9, or Ras pathways causes a dramatic chronological life-span extension. Inactivation of Sir2 causes uptake and catabolism of ethanol and upregulation of many stress-resistance and sporulation genes. These changes while sufficient to extend chronological life span in wild-type yeast require severe calorie restriction or additional mutations to extend life span of sir2Delta mutants. Our results demonstrate that effects of SIR2 on chronological life span are opposite to replicatve life span and suggest that the relevant activities of Sir2-like deacetylases may also be complex in higher eukaryotes.
Interestingly, the gene, called Sir2, that the scientists have removed to create the record longevity in yeast, is the same gene that was previously shown to extend longevity if its activity is INCREASED! Yes, Sir2, when overactivated, has been known to cause a longer life span in different organisms, from yeast to flies. How to reconcile these two opposite observations? It appears that Sir2 can play different roles in different cells. In the cells that are actively dividing extra Sir2 activity extends their capacity to divide. While in the cells that have stopped dividing, extra Sir2 activity appears to be harmful.
If Sir2 can have two opposite effects on life span depending on the cell state, which of the roles could be critical for human longevity? The most likely answer is “both”. Human body is made of billions of cells. Some of them are capable of dividing, the others are not, but we need them both. Therefore, provided that the human Sir2 similarly has dual function like its counterpart from yeast, simply turning Sir2 on or off may not be enough to extend our life span. If too much Sir2 is not good for dividing cells, while too little is not good for the post-mitotic ones, could it be that we have just the right amount?
Cell. 2005 Nov 18;123(4):655-67.
Sir2 blocks extreme life-span extension.
Fabrizio P, Gattazzo C, Battistella L, Wei M, Cheng C, McGrew K, Longo VD.Andrus Gerontology Center and Department of Biological Sciences, University of Southern California, 3715 McClintock Avenue, Los Angeles, California 90089.
Sir2 is a conserved deacetylase that modulates life span in yeast, worms, and flies and stress response in mammals. In yeast, Sir2 is required for maintaining replicative life span, and increasing Sir2 dosage can delay replicative aging. We address the role of Sir2 in regulating chronological life span in yeast. Lack of Sir2 along with calorie restriction and/or mutations in the yeast AKT homolog, Sch9, or Ras pathways causes a dramatic chronological life-span extension. Inactivation of Sir2 causes uptake and catabolism of ethanol and upregulation of many stress-resistance and sporulation genes. These changes while sufficient to extend chronological life span in wild-type yeast require severe calorie restriction or additional mutations to extend life span of sir2Delta mutants. Our results demonstrate that effects of SIR2 on chronological life span are opposite to replicatve life span and suggest that the relevant activities of Sir2-like deacetylases may also be complex in higher eukaryotes.
Sunday, November 13, 2005
Time Magazine: Cloned Dog – the most amazing invention of 2005. Is the world running low on inventions?
Or is Time Magazine running low on brain power?
“NEW YORK (Reuters) - Snuppy, the first cloned dog, is the most amazing invention of 2005, Time magazine said on Sunday.” Surely, this cute little puppy makes a wonderful cover. But is it the most amazing invention of 2005? Really?
I understand why many would consider cloning of the first large mammal Dolly the sheep in 1997 as an important invention. But during the last 8 years we have seen much progress in the area of cloning. Many large mammals have been cloned since then: cows, pigs, rabbits, horses, and even such valuable pet as cat. These days anything but cloning human being can’t really be considered a huge break-through. So, where does the importance of dog cloning come from? Are dogs more important pets than cats? Or is it simply because a cute puppy picture is so more valuable to Time Magazine than anything more substantive?
Voluntary disclaimer: Health Filbert does not own any dogs or cats.
11/13/05 by Health Filbert
“NEW YORK (Reuters) - Snuppy, the first cloned dog, is the most amazing invention of 2005, Time magazine said on Sunday.” Surely, this cute little puppy makes a wonderful cover. But is it the most amazing invention of 2005? Really?
I understand why many would consider cloning of the first large mammal Dolly the sheep in 1997 as an important invention. But during the last 8 years we have seen much progress in the area of cloning. Many large mammals have been cloned since then: cows, pigs, rabbits, horses, and even such valuable pet as cat. These days anything but cloning human being can’t really be considered a huge break-through. So, where does the importance of dog cloning come from? Are dogs more important pets than cats? Or is it simply because a cute puppy picture is so more valuable to Time Magazine than anything more substantive?
Voluntary disclaimer: Health Filbert does not own any dogs or cats.
11/13/05 by Health Filbert
Friday, November 11, 2005
Herceptin may not be the "cure" for breast cancer
The Lancet questions if herceptin is indeed the "cure" for breast cancer: << ...As Victor Montori and colleagues advised in last week's JAMA, such analyses may “show implausibly large treatment effects”. They recommend that “clinicians should view the results of such trials with scepticism”. The two NEJM reports use different dosing regimens, making comparisons and conclusions additionally more difficult. It is especially hard to tease apart the results because one of the papers combines results from two trials sponsored by Genentech. Although the “joint analysis was developed and analysed” by both trial teams, it is not made clear whether this synthesis was planned in advance of the start of both trials...>>
Also not enough evidence has been presented in Lancet Editor's opinion about cardiovascular side effects: <<...Comparisons are further hampered by the omission of crucial overall and disease-free survival data, as well as information on cardiotoxicity. However, it is clear that Herceptin can precipitate severe heart failure in some patients. The best that can be said about Herceptin's efficacy and safety for the treatment of early breast cancer is that the available evidence is insufficient to make reliable judgments...>>
(The Lancet 2005; 366:1673 DOI:10.1016/S0140-6736(05)67670-2)
Also not enough evidence has been presented in Lancet Editor's opinion about cardiovascular side effects: <<...Comparisons are further hampered by the omission of crucial overall and disease-free survival data, as well as information on cardiotoxicity. However, it is clear that Herceptin can precipitate severe heart failure in some patients. The best that can be said about Herceptin's efficacy and safety for the treatment of early breast cancer is that the available evidence is insufficient to make reliable judgments...>>
(The Lancet 2005; 366:1673 DOI:10.1016/S0140-6736(05)67670-2)
Subscribe to:
Posts (Atom)