Sunday, November 30, 2008

Schizophrenia Risk Rises with Father’s Age

Schizophrenia Risk Rises with Father’s Age
ISLAMABAD: Children fathered by older men have an increased risk of schizophrenia in later life, possibly because of mutations in their father’s DNA, according to a new study from Sweden.

A link between paternal age and schizophrenia has been reported before but scientists were not sure whether this was due to increasing mutations with advancing age or the result of inherited personality traits.

To find out, researchers at the University of Wales College of Medicine in Cardiff and Gothenburg University in Sweden examined the medical records of 50,087 Swedish army conscripts recruited between 1969 and 1970.

Their findings, reported in the British Journal of Psychiatry, show that 362 of the former soldiers had been diagnosed with schizophrenia by 1996.

Their fathers’ ages varied between 19 and 65. In a control group of men without schizophrenia, the fathers’ ages ranged from 15 to 75.

The study found that the odds of developing schizophrenia increased by 30 percent for each 10-year increase in paternal age.

Adjusting for poor social integration had only a minimal effect on the findings, suggesting personality traits were not a major factor.

"This supports the hypothesis that accumulating germ cell mutations may lead to an increase in genetic liability to schizophrenia in the offspring," Dr Stanley Zammit, from the University of Wales, said.

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Tuesday, November 25, 2008

2. DNA damage is significantly related to age

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Sperm DNA Damage: Correlation To Severity Of Semen Abnormalities
Main Category: Fertility
Also Included In: Urology / Nephrology; Genetics
Article Date: 24 Nov 2008 - 1:00 PST

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SAN FRANCISCO, CA, USA (UroToday.com) - Evaluation of male fertility includes assessment of the standard semen parameters (SSP) and may include assessment of DNA damage. However, the relationship between DNA damage and SSP remains controversial. This study examined the the relationship of DNA damage to SSP in patients presenting for infertility evaluation.

The authors conducted an IRB approved retrospective review of semen samples from 2586 unselected non-azoospermic patients underwent computer-assisted semen analysis and flow cytometry based sperm DNA damage assessment expressed as the DNA Fragmentation Index (DFI). DFI was significantly negatively correlated to sperm concentration, motility, and normal morphology and positively correlated to age (P<0.001). DNA damage increased in relationship to the number of abnormalities in the SSP (P <0.001).

The authors concluded:

1. DNA damage is significantly related to standard parameters of semen analysis
2. DNA damage is significantly related to age
3. The degree of DNA damage increases with the number of abnormal parameters in a sample and is most severe in patients with oligo-astheno-teratospermia (OAT).

Editorial Comments:

The authors demonstrate the relationship between progressively more abnormal semen parameters and abnormal DFI. This is consistent with clinical observations and does not appear to demonstrate any incremental value to DFI assessment, in clinical practice, in the initial assessment of the infertile male.

Presented by S. I. Moskovtsev, J. Willis, and J. White, et al., at the 64th Annual Meeting of the American Society for Reproductive Medicine - November 8 - 12, 2008 - San Francisco, California

Reported by UroToday.com Contributing Editor Harris M. Nagler, MD

UroToday - the only urology website with original content written by global urology key opinion leaders actively engaged in clinical practice.

To access the latest urology news releases from UroToday, go to: www.urotoday.com

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Saturday, November 22, 2008

Radio Host Has Drug Company Ties, Drug Companies Supress the Knowledge that autism schizophrenia and bipolar are caused de novo by older fathers

Radio Host Has Drug Company Ties

By GARDINER HARRIS
Published: November 21, 2008
An influential psychiatrist who was the host of the popular NPR program “The Infinite Mind” earned at least $1.3 million from 2000 to 2007 giving marketing lectures for drugmakers, income not mentioned on the program.

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Don Hogan Charles/The New York Times
Dr. Frederick K. Goodwin in 2001 during taping of “The Infinite Mind,” his public radio program.

Related
Conflicts of Interest May Ensnare Journalists, Too (November 22, 2008) The psychiatrist and radio host, Dr. Frederick K. Goodwin, is the latest in a series of doctors and researchers whose ties to drugmakers have been uncovered by Senator Charles E. Grassley, Republican of Iowa. Dr. Goodwin, a former director of the National Institute of Mental Health, is the first news media figure to be investigated.

Dr. Goodwin’s weekly radio programs have often touched on subjects important to the commercial interests of the companies for which he consults. In a program broadcast on Sept. 20, 2005, he warned that children with bipolar disorder who were left untreated could suffer brain damage, a controversial view.

“But as we’ll be hearing today,” Dr. Goodwin told his audience, “modern treatments — mood stabilizers in particular — have been proven both safe and effective in bipolar children.”

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Friday, November 21, 2008

Roche NimbleGen launches microarrays for analysis of DNA copy number variation

Roche NimbleGen launches microarrays for analysis of DNA copy number variation

Published: Thursday, 20-Nov-2008
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Devices/Technology


Roche NimbleGen, Inc. has launched NimbleGen Comparative Genomic Hybridization (CGH) microarrays in a 12x135K format for analysis of DNA copy number variation.
NimbleGen CGH 12x135K arrays allow simultaneous analysis of 12 independent sample pairs on a single microarray slide, each with 135,000 empirically tested long oligonucleotide probes. This new array format will enable rapid and cost-effective analysis of DNA copy number variation associated with human genetic disease, genomic disorders, cancer, and other complex diseases for research purposes.

Similar to the NimbleGen 2.1 million feature (2.1M) arrays, the 12x135K arrays are manufactured on Roche NimbleGen's new HD2 platform, a next generation light-directed microarray synthesizer with increased system contrast providing improved sensitivity and reproducibility compared to the earlier 385K and 4x72K arrays. The launch of NimbleGen CGH 12x135K arrays is further supported with a new release of Roche NimbleGen's NimbleScan v2.5 software that includes an Experimental Metrics Report and enhanced analysis features for NimbleGen CGH arrays.

A single catalog array design, Human CGH 12x135K Whole-Genome Tiling v2.0, is available and enables genome-wide detection of copy number gains and losses down to ~100kb in size. Similar to the NimbleGen human whole-genome designs currently available in 2.1M, 385K, and 4x72K array formats, the Human CGH 12x135K Whole-Genome Tiling v2.0 array has enhanced probe coverage of segmental duplication regions that are often associated with pathogenic chromosomal rearrangements.

For researchers interested in targeted analysis of chromosomal regions, genes, or copy number variants (CNVs), Roche NimbleGen offers rapid and cost-effective creation of custom arrays for any eukaryotic organism. Custom CGH array designs consisting of either uniform or mixed-density probe spacing can be created for all available array formats (12x135K, 2.1M, 385K, 4x72K) and may include whole genomes, single chromosomal regions, or multiple loci of interest.

The release of NimbleGen CGH 12x135K arrays follows the launch earlier this year of our CGH 2.1M feature arrays. NimbleGen CGH 2.1M arrays offer ultra-high resolution detection of CNVs, down to ~5kb resolution using a single Human CGH 2.1M Whole-Genome Tiling v2.0 array. Gerd Maass, CEO of Roche NimbleGen, stated: "The launch of NimbleGen CGH 2.1M and 12x135K arrays positions Roche NimbleGen as a leading provider of CGH microarrays and services offering both ultra-high resolution discovery and large-scale validation of CNVs on a single platform. These tools will facilitate the identification of genetic variants associated with a variety of rare and common diseases including diabetes, cancer, psychiatric disorders, and autoimmune disease."

http://www.roche.com

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The unexpected association with paternal age may be the result of an increased risk of accumulating germ cell mutations among older men.

Epidemiology. 2004 Nov;15(6):717-23. Links
Parental age, family size, and risk of multiple sclerosis.Montgomery SM, Lambe M, Olsson T, Ekbom A.
Clinical Epidemiology Unit, Department of Medicine, Karolinska Hospital, Karolinska Institutet, SE-171 76Stockholm, Sweden. Scott.Montgomery@medks.ki.se

BACKGROUND: Family structure, such as having siblings, provides proxy measures for a variety of characteristics relevant to disease risk. The etiology of multiple sclerosis (MS) is not well defined and analysis of family structure may provide etiologic clues. We conducted a case-control study to examine possible associations. METHODS: Using the Swedish Inpatient Register, we identified 4443 patients with a diagnosis of MS. From the general Swedish population, using birth and death registers, we selected 24,194 controls with similar characteristics for year, county of birth, and survival until at least age at diagnosis of the matched cases. The Multi-Generation Register linked data on siblings and parents. The Census provided father's social class based on occupation. RESULTS: Having 3 or more younger siblings, compared with none, produced an adjusted odds ratio (OR) for MS (with 95% confidence interval) of 0.80 (0.70-0.92) (adjusting for number of siblings, twins, maternal and paternal age, parental MS, sex, father's social class, county and year of birth). With 3 or more older siblings, the adjusted OR was 0.83 (0.72-0.96). Different-sex twin pairs compared with singletons had an OR of 0.59 (0.37-0.95) for MS. The risk of MS increased steadily with father's age but not mother's age, up to 2.00 (1.35-2.96) for 51- to 55-year-old fathers (compared with 21- to 25-year-old fathers). CONCLUSIONS: Parents who have offspring with MS may have subtly impaired fertility. The unexpected association with paternal age may be the result of an increased risk of accumulating germ cell mutations among older men.

PMID: 15475721 [PubMed - indexed for MEDLINE]

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In our study, the development of type 1 diabetes mellitus was associated with higher paternal age

Eur J Pediatr. 1999 May;158(5):362-6. Links
Risk factors for type I diabetes mellitus in children in Austria.Rami B, Schneider U, Imhof A, Waldhör T, Schober E.
University Children's Hospital Vienna, Austria.

The aim of this study was to investigate environmental risk factors in the development of type 1 diabetes mellitus in a population-based case-control study. Parents of all patients with manifestation of type 1 diabetes between 1989 and 1994 in Vienna were asked to complete a questionnaire (n = 114). Control children (n = 495), matched for age and sex, were randomly recruited from all schools in Vienna. Fathers of diabetic children were significantly older at the time their children were born than fathers of control children (P = 0.015). Children with diabetes were more likely to be second- or third-born children (P<0.05) and fewer went to kindergarten than the control group children (P = 0.007). No significant difference in duration of gestation, percentage of delivery by caesarean section, birth weight or length was found. Neonatal jaundice was more often observed in the patient group (P = 0.038). Breast feeding was reported by 82.7% of mothers of diabetic children and by 81% of mothers of control children, and the duration of breast feeding was longer in patients than in controls (n.s.). CONCLUSION: In our study, the development of type 1 diabetes mellitus was associated with higher paternal age and neonatal jaundice. No correlation could be found with dietary intake of cow's milk products in early infancy, vaccination and other environmental factors.

PMID: 10333115 [PubMed - indexed for MEDLINE]

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Alzheimer's link to older fathers

Alzheimer's link to older fathers
Independent, The (London), Sep 17, 1998 by Charles Arthur Technology Editor
E-mail Print Link CHILDREN BORN to fathers who are approaching middle age have a higher than average risk of developing Alzheimer's disease in later life, a study suggests.

A retrospective investigation of 206 people who have the degenerative illness, but no history of it occurring in the family, revealed a statistically significant link with the age of their father when they were born.

Some genes are known to contibute to the chance of developing Alzheimer's, but the new study, carried out by Lars Bertram at the Technical University of Munich, suggests that simply having an older father - average age 35.7 - can be a risk factor even in the absence of those genes. For those where there was a family history of Alzheimer's, the average age of the father was 31.3 years.

Though the sample is comparatively small, it is in line with the knowledge that ageing is associated with genetic damage to the sperm, which carry the father's genetic contribution to the child. That might eventually lead to Alzheimer's in the offspring. "There's an accumulation of environmental factors which somehow alter the genome of the father," Dr Bertram told New Scientist magazine.

Similar effects are already known to occur in women, where mothers over 35 have a far higher chance of giving birth to babies with Down's syndrome, which is caused by a genetic defect in the embryo. People with Down's syndrome are also more likely eventually to develop Alzheimer's.

Copyright 1998 Newspaper Publishing PLC
Provided by ProQuest Information and Learning Company. All rights Reserved.

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Tuesday, November 18, 2008

Working Dad: An Unauthorized Guide to Parenting

Older dads have their own biological clocks
Can you hear it? Men's biological clocks are ticking louder than ever.

I keep stumbling across evidence that older men bring their own share of problems to baby-making, just like women. I've written about connections between old sperm, schizophrenia, bipolar disorder and autism. Recently, I read about a possible connection to miscarriages in "Yo, dude, check your bio clock -- now."

A French study released in July found that women's pregnancy rates drop and miscarriages increase when the mother is over 35 and the father is over 40. Another study suggests that a man's fertility begins to decrease as early as his 20s. Researchers from the University of California at Berkeley and the Lawrence Livermore National Laboratory tested men between the ages of 22 and 80, and found that semen volume and sperm motility were both significantly compromised by aging.


-- The Ottawa Citizen. (The story came out this summer, but I haven't seen it in the United States.)

Don't get me wrong, I am not saying dads hold more responsibility for any of these problems. It is just that moms carried the biological clock on their own for a long time, and we all know it takes a man and woman to make babies.


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de.licio.usDiggFacebookNewsvineRedditStumbleUponGoogle BookmarksYahoo MyWebTwitterPosted by Paul Nyhan at November 18, 2008 3:17 p.m.
Categories: Autism, Health news and research, News, pregnancy

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'I'm 41 and childless. Is it too late to become a father?'


(Ian Tucker is a wise and compassionate man) concerned heart


'I'm 41 and childless. Is it too late to become a father?'The latest science claims older dads can cause autism, schizophrenia and Down's Syndrome - and their fertility fades with age. Ian Tucker consults his biological clockComments
(47)
Ian Tucker guardian.co.uk, Sunday November 16 2008 00.01 GMT The Observer, Sunday November 16 2008 Article history
Ian Tucker ponders fatherhood and fertility. Photograph: Ellis Parrinder

Last night I ate a large bowl of beetroot from my garden. This morning my urine is the colour of rosé wine and I'm worried that my semen might have taken on a similar hue. The colour of my semen is a concern because someone will be studying it in a short while. I'm considering this while sitting in the top floor 'specimen room' of the London Fertility Centre on Harley Street. Later on, when I mention where I've been to friends and colleagues they seem really interested in the interior design details of a room set aside for masturbation. So if you're planning one, here's some decorating tips. The room is on the second floor and it has two notices on its door: one saying 'Quiet Please' (in case passers-by are inclined to cheer or clap, I guess) and a sliding sign with 'Vacant/Occupied' options - I've opted for 'occupied' although I'm not, so far. Inside, the room is about 6ft x 12ft and painted in various pale non-colours. It is equipped with an ensuite shower, light-green vinyl-covered daybed and a fudge-coloured bathroom suite (including bidet). There is a sash window - which isn't overlooked. The atmosphere is more Carry On than Casualty. On one side of the sink there is a small empty plastic beaker (with my name on it). On the other a DVD player, screen and a remote. I consider all the hands that have touched the remote. Using one of the many tissues provided I pick it up and inspect it; it appears to be clean. The television doesn't show any of the normal channels.

I'm here because I'm concerned about my sperm. Not that they might be beetroot coloured, but rather that they might not be fit for purpose. That they might not be as athletic, plentiful and perfectly formed as they need to be. I'm 41 and childless, and although I'm not involved in a 'trying-for-a-baby'-type scenario I've been reading the papers and the news for fortysomething men and their sperm isn't great.

'Scientists warn that biological clock affects male fertility' warned the Guardian in July - well, scientists are always saying stuff aren't they? 'Risk of miscarriage soars once the father reaches 35' (Daily Mail) - that sounds worrying. 'Blokes going infertile aged 35' (Sun). Must have sex, pronto! The papers were all reporting in their own particular ways on the research of Dr Stephanie Belloc from the Eylau Centre for Assisted Reproduction in Paris. Dr Belloc had studied the records of 12,000 couples who visited her clinic and separated out the influence of the mother's and father's ages on the chances of conception and miscarriage.

Belloc and her team found that women whose partners were 35 or older had more miscarriages than those who were with younger men, regardless of their own age. The risk of miscarriage was on average 16.7 per cent when the men were aged 30-34, but it doubled to 33 per cent in men over 40. Moreover, her research showed that men's ages also affected pregnancy rates, which were lower in the over-40s. As the Mirror summed it up, 'Over-35? You're a dad loss.'

I can remember ridiculing my own father for being 40, so how did I end up childless at 41? To start with I went to university and became middle-class. It seems only people from council estates and people who own estates have kids young these days. The middle classes are too busy in their twenties establishing careers, climbing the property ladder and going on snowboarding holidays.

Although lack of one doesn't stop some people, I feel you need to be in a reasonably stable relationship before having kids - and I haven't been in one of those of late. But of late, many of my peers are reproducing, some are already on to their third. Even the ones who had drug problems are conceiving and, meanwhile, gay friends are cutting breeding deals with lesbians. I wonder if time is running out.

It's an easy thought to have because I can't act on it, but sometimes I think I should have had some children in my twenties. I had more energy and didn't have many material comforts to give up or much of a lifestyle to compromise. I'd be packing them off to university around now, thumbing sports car brochures and thinking about buying a peach farm in Spain. Frankly, I can't remember that much of my twenties, so maybe it would have put this decade of void to good use. I don't recall any of my peers having kids; maybe it was a hangover from the Aids era - people seemed pretty conscientious about birth control, there were no 'accidents'. So now, at 41, I wonder if I've skipped the whole kids thing.

I seem to be developing the hobbies and pastimes of a senior citizen - golf, growing beetroot, buffing my classic car. But the reality is I've got 19 years until I qualify for my bus pass - which is just enough time to raise at least one human being. So should I be worried about or believe in the 'male biological clock'?

Back in 2001, Professor Dolores Malaspina, of Columbia University College of Physicians and Surgeons, concluded that men aged 50 or over are three times more likely to father a child with schizophrenia compared with men of 25 or under. Four years later, epidemiologist Jorn Olsen at the University of California, Los Angeles, found a fourfold rise in Down's syndrome among babies born to men aged 50 and older. And in 2006 scientists from the Institute of Psychiatry at King's College, London and Mount Sinai School of Medicine in New York found that children born to fathers aged 40 and over were nearly six times more likely to suffer from autism than those with a father under 30. Meanwhile, other researchers have suggested patterns between older fathers and increased chances of bipolar disorder, dwarfism and Apert syndrome - whose unlucky sufferers have a malformed skull and webbed hands and feet, among other disfigurements. A report in 2006 even suggested 'a modest effect of advanced paternal age on the Apgar score'. And after finding out what an Apgar score is I now know this to be less than good. The evidence appeared to be stacking up.

Yet are these findings as scary as they sound? Dr Belloc's sample was made up entirely of couples presenting for infertility treatment. 'It is not evident that we can extrapolate these conclusions to a fertile population,' she tells me. And many of the incidences in the other studies are minute; so a fivefold increase is still only a five-times-minute chance of some disorder or other. Moreover, these studies only show patterns, rather than direct causal links - finding a direct link would probably require examining DNA at a detail beyond most researchers' budgets or ability. Some commentators have speculated that if a man first becomes a father in his forties or fifties that may indicate he has had trouble forming relationships earlier in his life, which may mean in a mild, undiagnosed kind of way he's a carrier of problems like bipolar disorder or autism which have a genetic element - so his paternal age is irrelevant to the outcome.

Which isn't exactly comforting, but it suggests the 'male biological clock' doesn't tick as loudly as the headlines suggest. For Dr Allan Pacey, senior lecturer in andrology at Sheffield University, the clock is nothing more than ageing. As you grow older, you lose a bit of hair and experience the odd 'senior moment', so you shouldn't be surprised if your sperm isn't as sprightly as it used to be. 'In terms of numbers it's the same, but what tends to happen is that the sperm isn't as good.' If their biological clock is ticking, men are pretty deaf to it. The age of fatherhood is creeping up: the latest figures from the Office of National Statistics show that the average age of married fathers rose from 29.1 in 1971 to 34.1 in 2003 - getting close to the 35-year point where some of the problems are alleged to kick in. I ask Dr Pacey if this is a worrying trend. 'The problem is couples are waiting until they are older. To wait until the woman is approaching 40 is the wrong time to be starting, and that will be exasperated by any problem that he has due to ageing.' Dr Pacey's advice to me is not to hang about: 'You will be more successful having a child naturally at an earlier age; it will be cheaper for you and it will be much more fun than waiting until you're well into your forties, going to an infertility clinic and having it done artificially. What we're finding are lots of people attending infertility clinics in their forties who would have succeeded in getting pregnant at 25. Rather than waiting for technology to sort it out, if you are in a position to have children early, then go ahead and do it.'

What Dr Pacey and others are quick to point out is that there's definitely a female biological clock. Women are born with a finite number of eggs and at some point they will run out. According to the Human Fertilisation and Embryology Authority (HFEA), a woman is half as fertile at 35 as she is at 25, and half as fertile again at 40.

You might be thinking, 'Why is he bothering to spell that out, everyone knows that?' Well, before researching this piece I was only vaguely aware of those blunt facts, but, more surprisingly, when chatting to single and married thirtysomething childless women about this article they start saying things like: 'My gran had my mother at 45,' 'What about Madonna?' or, most biologically incorrect: 'I'm not ready yet.' They seemed about as informed as I was. 'With the Madonnas and all the rest who seem to have children quite naturally, no one mentions IVF or egg donors, and celebrity miscarriages don't make the pages of Heat,' says Dr Pacey. 'This silence reinforces the myth that these miracle births happen, when often there's a medical intervention.' And IVF isn't a safety net: according to the HFEA, IVF has only a 12 per cent success rate for a 40-year-old woman. And it will cost you: the NHS, on the advice of the National Institute of Clinical Excellence (Nice), doesn't fund IVF for women over 40 because of the low success rate. The average cost of a cycle is £4,000-£8,000. Is it chauvinistic to question the sense of delaying having kids for the sake of a career if you're going to spend most of the extra income on fertility treatment?

However it's not only career building that is nudging the maternal age up; those commitment-phobic, nappy-changing-averse partners make a contribution, too - people like me. One could argue that this male biological clock business is providing men with another excuse to avoid having kids - we move from 'I'm not ready yet' to 'It's too dangerous now' in the time it takes to power up a Nintendo Wii. Or maybe you could blame the introduction of Viagra - which has engendered the idea that men can stay virile forever, so why rush? - as most men think the difference between virility and fertility is latex thin. But if you're looking for something that's really obscuring the hands of the male biological clock, look to famous people. When it comes to fertility, biology tells us one thing, but celebrities tell us another: ie, no matter how superannuated you are, getting your girlfriend up the duff is child's play. Middle-aged famous fellas love a baby shower.

Dr Pacey isn't impressed: 'The John Humphrys thing does distort the picture. There'll be lots of men who will read this piece and say, "I was 50 and I had a child," and it's really difficult to argue against that because they do, but statistically you are less likely to succeed and more likely to have problems. For the individual who has been successful it will seem stupid that I'm saying that, but for every 50-year-old father there'll be 10 times more thinking, "I had a lot of problems."'

Even if you, your sperm and your wife from a younger generation manage to buck the stats, there are other non-bio reasons against fathering kids late. Most obviously you might die before they graduate - if you're 65 now, on average you'll die at 82 - although for how much longer you will be capable of having a kick-about, helping them with their homework or visiting the lavatory without their assistance isn't recorded. And while it's embarrassing to be mistaken occasionally for their grandfather, it's thoughtless not to meet your grandchildren.

Am I being too hard on the older dad? I call Charlie Lewis, professor of family and developmental psychology at Lancaster University. Should we give middle-aged men the snip? 'Some men claim to be better fathers when older, but I don't see this in the majority of men. I find them saying, "I'm clapped out, I've done my bit at work, I've provided a house and comfortable living, now let me vegetate." They think it's their right to sit in front of the telly and not take part in any interaction. It's almost autistic. Older fathers tend to do less of the stereotypical activities than younger fathers do, less childcare and less kicking footballs - for fear of snapping a tendon. They think, "I'm much too old for this."'

Surprisingly, Lewis is more relaxed about the dying thing. 'I don't want to put fathers down, but if you look at the majority of evidence on loss, it does point to losing a mother before 11 being more predictive of later social/psycho disorders than losing a father. These effects are most often caused by the child absorbing the surviving partner's grief. So if the mother can manage the grieving process, the predictable death of an older father needn't be a life-changing trauma.'

Dads dead or alive, we should be more concerned about the kids, says Lewis. 'You do get studies that say old dads feel closer to their kids, but I'm not aware that kids feel closer to their older fathers.'

I wonder if I would become one of these dead-beat, distant dads. I like to think not. I don't quite understand how

that could happen. What kind of an individual would tune into a Top Gear repeat rather than read to their child or even relieve them of a shitty nappy? Maybe I'm being naive. I talk to some dad friends.

Gary, 45, first became a father when he was 23, but then remarried and had three more children, the oldest of whom is five. Would he like to compare and contrast? 'Obviously becoming a father young was a bit of a shock, it made me grow up quickly. I'm not sure at that age if you're responsible enough to look after yourself let alone a little child.' So how is it second time around: does older dad mean better dad? 'When my second wife first wanted children I did have slight panic attacks, because I had this memory of it being a total whirlwind, but this time it's completely different, it doesn't seem half as stressful as when I was in my twenties.' Gary says this isn't just because he's been a parent before - 'No, it's mainly because I'm more grown-up, more patient, more financially settled. I'm far more chilled out this time around.' So you'd advise an older option? 'It's better to have children at a later date, but myself, I'm worried about getting older. First time round I was one of the youngest parents in the playground; now I'm one of the oldest. My youngest is 10 months, so I'll be at retirement or grandfather age in her late teens. You hope to be running around in the park, doing those things that children want you to do and provide as parents. Hopefully I'll be one of those who manages it, but I will have to wait and see.'

The energy issue: I've heard this raised before. People talk about the nuclear-like amounts of energy you need to bring up a child, but I suspect it's similar to the stamina needed to squire a girlfriend half your age. Because down-ageing your just-broody girlfriends each time they start describing a new frock as 'a bit maternity' is really the only alternative to producing offspring.

Jonathan, 49, had two sons when he was 23 and 27. He says the early months were 'terrifying', and both he and his girlfriend had to abandon their career plans: 'Our embryonic lives together as a couple were entirely transformed into a fully fledged proper adult relationship. And we didn't have much money - I even used to scavenge skips for firewood.' But for all the foraging the relatively small age difference means he's closer to his kids. 'We can go to the cinema together, appreciate some of the same music, go out for a beer, they call me by my first name.' He got divorced and, a couple of years ago, he remarried. He isn't keen to become a father again: 'I'm interested in the relationship with my wife rather than with anyone else. The relationship I have with my children is established, I like the marriage and lifestyle we have, and because of my previous experience I can see how that could be compromised.'

What is his advice for someone like me, thinking of becoming a father in my forties? 'I think, you're not going to get a lot of sleep. And by the time you're my age, when you take your kids to a restaurant they'll be running around banging their heads, stealing food, whereas I'll be discussing the amount of oak in the Sauvignon with mine. I'd think about that quite carefully.'

So that's what I should have done. Bred early. Guess there's no point in crying over spilled, er, milk.

The trouble with this when-to-procreate business is it's personal. Apologies, it's not much of an insight but everyone is different. They earn lots of money, earn not much money, like kids, don't like kids, have live-in help, are still looking for The One, are given a babies-or-else ultimatum by their partners, had a shit childhood themselves, don't feel the need to have babies to preserve their relationship, are worried they'll pass on a condition, feel they've established their career, don't want a career, haven't been to Patagonia yet - the list of caveats and factors that make it the 'right time' for someone is as long as the waiting list for a Doctor Who Dalek Electronic Voice Changer Helmet.

So, to borrow a phrase from a Dragon: 'Let me tell you where I am.' For me, I think 45 is the cut-off. For biological reasons - you can't donate sperm past 45 - there must be something in those scary reports. And financially, I'd like to retire on time, if indeed I'm lucky enough to still have a career by then. Which doesn't give me much time, I guess, to meet someone, fall in love, imagine being with this person for the foreseeable future - if that's not over-romantic, delusional, too-much-like-a-John-Cusack-movie. But I'm getting ahead of myself: maybe I'm firing blanks anyhow.

For the 20-minute wait while my sperm is being tested, I chat to Dr Magdy Asaad, clinical director, in his office about the problems with semen. Mine is being tested for volume, viscosity, concentration, mobility, morphology and antibodies.

Dr Asaad uses the gold standard WHO criteria which are surprisingly generous - only 50 per cent of your sperm needs to move, for instance, and you're allowed up to 80 per cent with an abnormal form, such as funny-shaped heads or two tails, 'because 20 per cent of 20m is considered enough, it's a lot of sperm,' Dr Asaad chuckles.

I'm curious: do anxious men often pop in on their own for a lunchtime sperm test, check everything is wriggling right? 'It's not common, but when men present on their own, it's normally a problem with their ability to have an erection or ejaculation.'

Well as you can tell I have no problems in that area, I say.

'But some men don't like to give a sample,' he continues. 'They find all kinds of excuses: maybe they are worried it will not be good, or that it's an artificial thing, to press a button [is he talking about the remote control?]. I don't know how it was for you, I'm not asking. Sometimes a gentleman will have difficulty preparing manually.' Unbelievable.

The walls and desk of the doctor's office are smothered with framed photographs of beaming parents with their children - patients he's helped to fashion a bundle of joy for over the years. In your experience, I ask Dr Asaad, when is a good age for procreation? 'You're mature enough by your late twenties, early thirties, responsible enough, you probably have a job, a partner. I don't think it's a very serious problem waiting to 40-45, but beyond that you have to think about time with the child.'

With that, Dr Asaad prints off a piece of A4 containing all my sperm's vital statistics. 'It's a good sample,' he says, 'so you're all right.' I'll spare you the details.

On one hand this is a relief, but on the other it means I've no alibi, no excuses, I'm ready to breed. All I need now is a woman.

Paternity frights: ten bus-pass fathers
Julio Iglesias Sr, a dad at 89

Nobody could accuse the gynaecologist father of Julio and grandfather of Enrique, and who was head of a Madrid family-planning unit, of not taking his work home with him. After having two children with his first wife, he remarried and, at 89, when his wife was 40, produced another son. Barely out of the maternity ward, Ronna signed up for IVF and within a few months was pregnant again. Tragically, filling a test-tube turned out to be the former Franco supporter's last significant act: two months later he was muerto. His daughter Ruth was born posthumously seven months later in July 2006.

Dad-speak: 'At my age, a child is marvellous. I felt just like Abraham. It was an act of generosity towards her [Ronna]. I leave her part of my blood, of my life.'

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Sunday, November 16, 2008

— Contrary to our previous beliefs, identical twins are not genetically identical

Science News Share Blog Cite Print Email BookmarkIdentical Twins Not As Identical As Believed
ScienceDaily (Feb. 20, 2008) — Contrary to our previous beliefs, identical twins are not genetically identical. This surprising finding may be of great significance for research on hereditary diseases and for the development of new diagnostic methods. How can it be that one identical twin might develop Parkinson's disease, for instance, but not the other? Until now, the reasons have been sought in environmental factors. The current study complicates the picture.



The researchers studied 19 pairs of monozygotic, or identical, twins and found differences in copy number variation in DNA. Copy number variation (CNV) occurs when a set of coding letters in DNA are missing, or when extra copies of segments of DNA are produced.

Humans receive one chromosome from their mother and one from their father, providing for two copies of the genome. In some cases, bits of DNA are missing from a chromosome, leaving the offspring with just one copy of that bit of DNA. In other instances, mutations may produce three, four or more copies of a particular bit of DNA. In most cases, variation in the number of copies likely has no impact on health or development. But in others, it may be one factor in the likelihood of developing a disease.

Researchers at UAB( University of Alabama), Leiden University Medical Center and VU University, The Netherlands; and Uppsala University and Karolinska Institutet, Sweden recently published their findings.*

“The presumption has always been that identical twins are identical down to their DNA,” said Carl Bruder, Ph.D. and Jan Dumanski, Ph.D., of UAB’s Department of Genetics and the study’s lead authors. “That’s mostly true, but our findings suggest that there are small, subtle differences due to CNV. Those differences may point the way to better understanding of genetic diseases when we study so-called discordant monozygotic twins….a pair of twins where one twin has a disorder and the other does not.”

Bruder points out that one twin might develop a particular disease…Parkinson’s, for example…while the other does not. Previously, it was thought that environmental factors were the likely culprits, not genetics. Bruder and Dumanski think their findings indicate that CNV may play a critical role and this can be efficiently studied in identical twins.

“More importantly, changes in CNV may tell us if a missing gene, or multiple copies of a gene, are implicated in the onset of disease,” Bruder said. “If twin A develops Parkinson’s and twin B does not, the region of their genome where they show differences is a target for further investigation to discover the basic genetic underpinnings of the disease.”

The UAB lab is one of the few worldwide that can make the full genome BAC (bacterial artificial chromosome) arrays that are used to find the changed DNA regions.


The findings were published Feb. 14 online in the American Journal of Human Genetics.http://eproofing.dartmouthjournals.com/pdfproofing/ajhg0069r.pdf

The research was funded by support from UAB, the Swedish Cancer Society, the Swedish Children’s Cancer Foundation, the U.S. Army Research and Material Command, National Institutes of Health, The Netherlands Genomics Initiative and the National Institutes of Health.


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Friday, November 14, 2008

What is the most irrefutable finding that you and your colleagues have made?

Dolores Malaspina, MD, MSPH, interviewed by Norman Sussman, MD
Primary Psychiatry. 2006;13(7):33-36


This interview took place on April 26, 2006, and was conducted by Norman Sussman, MD.






What is the most irrefutable finding that you and your colleagues have made?
The most irrefutable finding is our demonstration that a father’s age is a major risk factor for schizophrenia. We were the first group to show that schizophrenia is linearly related to paternal age and that the risk is tripled for the offspring of the oldest groups of fathers.7 This finding has been born out in every single cohort study that has looked at paternal age and the risk for schizophrenia. The only other finding that has been as consistently replicated in schizophrenia research is that there is an increased risk associated with a family history of schizophrenia. Since only 10% to 15% of schizophrenia cases have a family history, family history does not explain much of the population risk for schizophrenia. However, we think that approximately one third or one quarter of all schizophrenia cases may be attributable to paternal age. Paternal age is the major source of de novo genetic diseases in the human population, which was first described by Penrose8 in the 1950s. He hypothesized that this was due to copy errors that arose in the male germ line over the many cycles of sperm cell replications. These mutations accumulate as paternal age advances. After the Penrose report, medical researchers identified scores of sporadic diseases in the offspring of older fathers, suggesting that these could occur from gene mutations. Particular attention was paid to conditions in last-born children. In the 1960s, an excess of schizophrenia in last-born children was also reported. However, rather than entertaining the main medical hypothesis being explored at that time, the finding of more schizophrenia in later-born children nourished the idea that schizophrenia could be caused by an unavailable mother, soon to be called a schizophenigenic mother, rather than showing its genetic nature. This perception was a result of the unfortunate idea that psychiatric disorders did not have the same types of biologic underpinnings as other chronic diseases prevalent in the United States from the 1940s through the 1970s. Another rationale for those ideas, which I do not fault, was that if schizophrenia was caused by dysfunctional families, perhaps it could be cured with good treatment. Genetic conditions were seen as being too hopeless and off limits in the years following the Nazi genocide.

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Tuesday, November 11, 2008

Older parents, epigenomics and psychiatric illness

Older parents, epigenomics and psychiatric illness
2008-11-11 — Dave Bath
Nature’s British Journal of Pharmacology has (for free!) an editorial that is getting my nose twitching, and pushes me to speed up a Balneus post that has been brewing for a while. The growing literature on the diseases of children caused by advanced parental age suggests that the societal pattern of people building their careers before having children needs to be reviewed by social policy makers.
"Epigenetic biomarkers in psychiatric disorders" British Journal of Pharmacology (2008) 155, 795–796; doi:10.1038/bjp.2008.254; published online 23 June 2008 (also as PDF is yet another paper stressing the importance of epigenetics in pathogenesis, and introduces a new word, "epigenomics" that relates to testing and markers.
Basically, the older the person (male or female) when conceiving a child, the more likely something epigenetic has gone awry and will cause problems.
Another relatively recent paper highlighted the relationship between advanced parental age and schizophrenia: "Aberrant Epigenetic Regulation Could Explain the Relationship of Paternal Age to Schizophrenia" Schizophrenia Bulletin doi:10.1093/schbul/sbm093 (advance publication 2007-08-21) contains the following:
In 2001, Malaspina et al showed that the incidence of schizophrenia increased progressively with increasing paternal age, the risk being 2-fold and 3-fold for offspring of fathers aged 45–49 and 50 or more years, compared with those of fathers aged less than 25 years.
It’s not just schizophrenia: autism, cognitive and learning difficulties, longevity … the list gets longer every year.
It’s a far cry from what we were taught at uni in the seventies: that old ova stuck in meiosis for 40 years accumulated damage (leading to increased incidence of trisomy 21 or Down’s Syndrome), but because spermatogenesis was continuous, older males didn’t cause such problems.
This raises questions about how social policy affects societal health perhaps more serious than the "diabesity" epidemic, as obesity is more easily treated than something caused at the time of conception (even before).
The easy recommendation is for ladies: ignore the flattery and bank balances of older men!
For males, it’s worthwhile trying to settle down earlier, do the parenting bit with your career on hold.
For politicians, this means that education patterns and work/life balance policies need some attention - unless we want each generation of teenagers to be nuttier than than the previous one.
Someone in Canberra should be crunching the numbers between the census details on parental
age and epidemiology, taking into account greater diagnostic capabilities across the years.
I’m much relieved that at 48, my grandson is approaching 2, not only because of this research, but because I’ve got just enough energy to keep up with him for a couple of days (I stay with my daughter and grandson every second weekend on average). I’d be much less fun for him if my joints were any creakier!
Posted in Biology and Health, Politics, Society.

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Saturday, November 08, 2008

His advice? "If my son or daughter was to ask, I'd tell them to have kids early -- and that's before 30."

Harry Fisch, MD - His advice? "If my son or daughter was to ask, I'd tell them to have kids early -- and that's before 30."

Yo, dude, check your bio clock -- now
New studies warn that it isn't just women who become less fertile as they age
Sarah Treleaven , The Ottawa Citizen
Recently, I've had a lot of conversations about baby-making with my male friends.

"I worry that I might be too selfish to ever have children," said my friend Joe, 29, somewhat pensively over gin and cucumber cocktails. Ditto for Colin, who just broke up with a woman he loves because she wants to have kids in the next few years and, at 35, he just doesn't feel ready yet. Kids or no, they both feel like they have all the time in the world to decide.

I, on the other hand, just turned 30 and have been making a lot of jokes about needing an apartment with a second bedroom for my soon-to-be-frozen eggs.



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Font:****Lots of women wring their hands about having a baby. Not only do we have to worry about our plummeting fertility (which begins to tank in our mid-20s), but we also have to worry about job retention and advancement once those kids (come biology, adoption or surrogacy) eventually appear. And it's the physical limitations of the female ability to procreate that have placed such a heavy emphasis on the reproductive biological clock, shaping the way many women live, work and even date.

But evidence is increasingly emerging that men, too, have a reproductive biological clock -- and that it ticks much more loudly than most of us have thought. Even as stories occasionally emerge about septuagenarian and octogenarian men becoming proud papas -- author Saul Bellow, for example, fathered a child at 84 -- several recent studies are challenging the conventional wisdom that men have an invincible ability to procreate.

A French study released in July found that women's pregnancy rates drop and miscarriages increase when the mother is over 35 and the father is over 40. Another study suggests that a man's fertility begins to decrease as early as his 20s. Researchers from the University of California at Berkeley and the Lawrence Livermore National Laboratory tested men between the ages of 22 and 80, and found that semen volume and sperm motility were both significantly compromised by aging.

Additionally, the increased odds for older fathers producing genetic abnormalities have been well documented, and studies have demonstrated that fathers over 40 are six times more likely to produce an autistic child than fathers under 30.

The numbers related to schizophrenia are similarly compelling. A study utilizing health databases in Jerusalem found that fathers over 40 were twice as likely to produce schizophrenic children as fathers who were under 25; for fathers over 50, the odds tripled when compared to fathers who were under 25.

Dr. Harry Fisch, director of the Male Reproductive Center at New York-Presbyterian Hospital/Columbia University Medical Center and the author of The Male Biological Clock, says that he's been ringing the alarm bell for years.

"There's a female biological clock; we all agree on the decline in fertility, more genetic problems and a decline in estrogen.

"The same thing happens in men -- a little bit differently, but essentially the same," Fisch says. "Why is it important? Well, demographically more men and women are waiting until they're over 30 to have a baby."

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Friday, November 07, 2008

Beyond the Abstract - New Concepts in Klinefelter Syndrome Nov. 7, 2008

BERKELEY, CA (UroToday.com) - Klinefelter syndrome (47,XXY) is the most common numerical chromosomal aberration among men, with an estimated frequency of 1:500 – 1:1000 of live deliveries. Men with KS represent a broad spectrum of phenotypes, professions, incomes and socioeconomic status. Severe intellectual deficits are rare. Spermatogenic and steroidogenic dysfunction are cardinal and the most prevalent signs of Klinefelter syndrome.
The 47,XXY karyotype of Klinefelter syndrome arises spontaneously when paired X chromosomes fail to separate. Advanced maternal and paternal age have been linked to increased risk of Klinefelter syndrome. The X chromosome carries genes that regulate testis function, brain development and growth.
In the last decade, the combination of microsurgical testicular sperm extraction (TESE) and use of freshly retrieved sperm for in-vitro fertilization (IVF) resulted in life births of children from over 50% of patients with Klinefelter syndrome who attempted such a procedure . The fact that sperm can be found in the testes of men with Klinefelter syndrome has challenged the previous assumption that men with Klinefelter syndrome are always sterile. This has raised the hypothesis that children with Klinefelter syndrome are born with spermatogonia and later in life, most likely during early puberty, spermatogonia undergo massive apoptosis that results in depletion of spermatogonial population and subsequent azoospermia.
This hypothesis is based primarily on three observations: testicular sperm can be identified and recovered from at least half of adult men with Klinefelter syndrome; in rare cases, sperm can be found in ejaculates of men with Klinefelter syndrome; and data from boys with Klinefelter syndrome who were biopsied at different ages and development stages indicated that boys with Klinefelter syndrome have spermatogonia at birth but that damage to the germinal epithelium occurs early during puberty. Molecular mechanisms of spermatogonial loss are not known at this point. Sperm found in testes of men with Klinefelter syndrome have only a slightly increased frequency of sex chromosome polysomies, and most boys born from fathers with Klinefelter syndrome have a normal karyotype. These findings indicate that during early stem-cell proliferation or meiotic division, the checkpoint mechanisms are able to overcome X chromosome polysomy resulting in sperm with a single X (or Y) chromosome. We now have 3 boys when sperm was found in ejaculate early in puberty and subsequently lost, supporting that the damage to the testis occurs early during puberty.
The article we published in Current Opinions in Urology, summarizes our own experience in the fertility preservation program in adolescents with KS. It is based on often pioneering and out of the box thinking of our colleagues from around the world, who despite previous assumptions about sterility in men with KS, devoted time and resources to giving the hope and joy of fatherhood to thousands of men around the globe. KS brings tremendous opportunity to study how to best help our patients and potentially prevent progressive testicular failure. It also brings vast material for basic scientists to answer critical and broadly applicable questions about molecular mechanisms of how spermatogonia overcome presence of additional X chromosome-producing 23 X or 23 Y sperm, what are the underlying mechanisms of X chromosome inactivation in men with KS, and why despite high LH, a majority of men will become hypogonadal.
We hope this manuscript will result in renewed interest among clinicians and scientists in this common but under studied syndrome.
Written by: Darius A. Paduch, MD, as part of Beyond the Abstract on UroToday.com. This initiative offers a method of publishing for the professional urology community. Authors are given an opportunity to expand on the circumstances, limitations etc... of their research by referencing the published abstract.
New Concepts in Klinefelter Syndrome - Abstract

UroToday.com Male Infertility and Reproduction Section
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Increased Bipolar Risk Linked to Father's Age by Joan Arehart-Treichel



Psychiatr News November 7, 2008
Volume 43, Number 21, page 18
© 2008 American Psychiatric Association


























Articles by Arehart-Treichel, J.




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Clinical & Research News


Increased Bipolar Risk Linked to Father's Age
Joan Arehart-Treichel
Older men are more likely than younger men to father children with autism, schizophrenia, or early-onset bipolar disorder.

Fathering a child later in life seems to increase its risk of having autism or schizophrenia, research has shown. And now it seems to increase a child's risk of having bipolar disorder as well, a new study suggests.

The study was headed by Emma Frans, a doctoral student in epidemiology at the Karolinska Institute in Stockholm. Results were published in the September Archives of General Psychiatry.

Sweden's Multigeneration Register, as well as Sweden's National Hospital Discharge Register, made this new investigation possible. The former, which has been in existence since 1947, gives demographic information about all people living in Sweden as well as about their parents. The latter, which has been in existence since 1973, lists all people living in Sweden who have been hospitalized for various conditions.

Using the hospital discharge register, the researchers identified more than 13,000 persons who had been hospitalized for bipolar disorder at least twice since 1973 when the hospital discharge register was started. Using the Multigeneration Register, the researchers picked out five healthy individuals who matched each of the 13,000 persons on gender and date of birth. In other words, some 13,000 persons with bipolar disorder served as subjects, and 67,000 other individuals served as controls.

The researchers then used the Multigeneration Register to determine the age of each subject's father and of each control's father at the time of the subject's or control's birth. Finally, the researchers used this data to determine whether there was any link between paternal age at the time of birth and an offspring's chances of having bipolar disorder.

A link was found. Even when some possibly confounding factors such as socioeconomic status, family history of mental disorders, or maternal age at time of birth were considered, the offspring of men aged 55 or older were significantly more likely—1.37 times more likely—to have bipolar disorder than were the offspring of men aged 20 to 24. And for early-onset bipolar disorder (defined as occurring before age 20), the impact of paternal age was even more pronounced: the offspring of men aged 50 or older were 2.63 times more likely to have bipolar disorder than were the offspring of men aged 20 to 24.






Thus, paternal age seems to be "an independent risk factor for bipolar disorder," Frans and her colleagues concluded in their study report. "Furthermore, our results indicate that the paternal age effect might be most evident in patients with an early onset of the disorder."

Why older men are more at risk of fathering children with bipolar disorder, or autism or schizophrenia, than younger men are is not known. However, Frans and her team suspect that it is genetic, especially since they found a strong link between older paternal age and early-onset bipolar disorder, which has shown greater heritability than bipolar disorder that occurs later in life.

Furthermore, Frans and her group speculated in their report, older men's genetic proneness to father children with bipolar disorder may be due to the fact that "spermatogonial cells replicate every 16th day, resulting in approximately 200 divisions by the age of 20 years and 660 divisions by the age of 40 years [and even more divisions as a man grows older. Thus] disorders associated with advancing paternal age could partially result from de novo mutations."

Women, in contrast, they explained, "are born with their full supply of eggs that have gone through only 23 replications, a number that does not change as they age. Therefore DNA copy errors should not increase in number with maternal age."

The study had no outside funding.

An abstract of "Advancing Paternal Age and Bipolar Disorder" is posted at .

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Tuesday, November 04, 2008

HUMAN PAPILLOMA VIRUS VACCINE FRAUD

HUMAN PAPILLOMA VIRUS VACCINE FRAUD



By Dr. James Howenstine, MD.
November 3, 2008

NewsWithViews.com

For several years the pharmaceutical firm has made aggressive efforts to market the Gardasil human papilloma virus vaccine as a prevention for cervical cancer. The governor of the state of Texas made the administration of this vaccine to young girls mandatory.

What is the truth about this vaccine?

Natural News reporter Mike Adams has uncovered some interesting facts about this vaccine. The FDA has been aware since 2003 that Human Papillloma Virus [1] does not cause cervical cancer. The Gardasil vaccine is unable to eradicate HPV virus from women who have been exposed to HPV(nearly all sexually active women). This makes vaccinating all young women in Texas against HPV virus a very questionable decision.

To make matters even worse it has now been learned that vaccinating women with Gardasil may actually increase the risk that those women harboring a benign cervical HPV viral infection have a 44.6 percent increased risk of having their benign HPV infection converted into a precancerous state by the HPV vaccine administration. Thus women vaccinated with Gardasil not only receive no benefit those who were sexually active before the vaccine administration have become at increased risk for developing cervical cancer.

To summarize some of the facts about HPV and this vaccine:

• HPV vaccine increases the risk of developing a precancerous cervical lesion by 44.6% in women .previously infected with a HPV viral type found in the vaccine.
• HPV virus does not cause cervical cancer.
• HPV viral infections are self limiting and are not a health threat to healthy females.
• This valuable information about the etiology of HPV viral infections has been suppressed from public knowledge.
• Allowing untruths about Gardasil to be disseminated in public hearings and planting fear have been used to promote sales of this worthless vaccine.

The Evidence for the Gardasil Fraud

HiFi DNA Tech was involved in manufacturing a portable device for testing for HPV viral infection. This company, to improve sales, needed to have their product reclassified as Class II instead of Class III because Class III category products are not able to be sold to the public whereas Class II products can be sold to the public because they are deemed safe enough for public release.

For 20 years the FDA had classified the HPV test as a test for cervical cancer. In 2003 the FDA changed its position advising that HPV virus was not associated with cervical cancer. On Oct12, 2007 HiFi DNA Tech sued the FDA to get their testing device reclassified as Class II based on the knowledge that cervical cancer was not caused by HPV infection .and therefore did not need to be restricted from public sales. The fact that the FDA had already acknowledged in a policy statement on March 31, 2003 that “most infections by HPV are shortlived and not associated with cervical cancer. Most women who become infected with HPV are able to eradicate the virus and suffer no apparent long term consequences to their health.” It is not the HPV virus itself that causes cervical cancer but rather a persistent state of ill health on the part of the patient that makes her vulnerable to cervical cancer. Repeated transient HPV infections even when caused by high risk types of HPVs are characteristically not associated with an increased risk of developing squamous intraepithelial lesions, the precursor lesion of cervical cancer.

This was not revealed when the public hearings over the need for mandatory HPV vaccinations was pushed by manufacturer of Gardasil. The FDA had known for many years that HPV was unrelated to cervical cancer but to have this knowledge disseminated during the hearings would have instantly made the HPV vaccine worthless.

The main push from the drug company has been that we “must save these young girls from losing their lives to cervical cancers.” The FDA knew when these hearings were held that this argument was phony but said nothing.!!!

Does the HPV Vaccine Actually Increase the Risk of Cervical Cancer?

Gardasil vaccine actually increases the risk for a sexually active woman to develop cervical cancer (nearly all sexually active women have been exposed to HPV virus). Women who have already been exposed to HPV from sexual activity and have positive serologies for HPV viral types found in the HPV vaccine have a 44.6% increased risk [2] for developing high grade precancerous cervical lesions after they have received Gardasil vaccine injections. This means that young women carrying a harmless form of HPV viral infection often get converted after HPV vaccine, into a more dangerous precancerous cervical condition. that can lead to cervical cancer.

These patients were made worse by exposure to a vaccine that contained a virus that had already infected them. Thus this evidence reveals that Gardasil increases disease in 44.6 % of patients who already been exposed to the same serotype found in the vaccine. This strongly suggests that sexually active women can become more likely to develop cervical cancer after taking Gardasil vaccine.

This information puts the state of Texas in the position where theoretically the Gardasil should be given only to young females who are virgins (sexually active females have existing HPV infections that may become more dangerous if given the vaccine). Questioning these young women about sexual activity may lead to sexually active girls denying sexual activity in the presence of parents or physician thus leading to HPV viral administration to a female with previous HPV infection who does have an increased risk of developing pre-invasive cervical lesions because of exposure to the vaccine. Thus females denying sexual activity will have an increased risk of getting pre-cancerous cervical lesions which can lead to cervical cancer.

To make this situation even worse the health officials that will be involved in screening candidates for HPV vaccine are heavily involved in promoting vaccine administration (They almost certainly have no idea the vaccine is worthless and capable of causing precancerous cervical lesions). Therefore the truth about the danger of cervical cancer resulting from the vaccine given to sexually active girls will not be given to these young women. This will probably cause an unnecessary increase in cervical cancer.

The FDA Is A Badly Flawed Agency

The FDA is administered by 12 officials. Three of these 12 persons are automatic appointments given to the pharmaceutical industry. If there ever was a situation where the fox is in charge of the chicken house this is it. It is common knowledge among these 9 selected officials that if they play ball with the drug industry they will be moved up to high paying positions with drug companies for their final working years. Very few appointed officials will have the character, with these temptations placed in front of them, .to make honest decisions. One can be certain that no one who had a healthy skepticism about the pharmaceutical industry would ever get appointed to the FDA.


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It needs to be understood by the general public that the FDA is an effective arm of the pharmaceutical industry and has nothing at all to do with public health. Anyone who doubts this statement need only look at the record of scams condoned by the FDA:

1 - The original director of the FDA, Dr.Harvey W. Wiley, resigned in disgust when he realized in 1912 that pressure from the food and pharmaceutical industries was preventing him from abolishing nutritionally worthless white flour.

2 - Flouride was added to the water in both Germany under Adolf Hitler and Russia under Josef Stalin to keep the populace “dumbed down and easy to control.” There is scientific evidence that fluoride actually increases cavity formation [3] so the cover story about the virtue of fluoride decreasing cavity formation is fraud. Most US cities place fluoride in their water and this does increase the incidence of cancer by 10% when compared to cities not using fluoride in their water. The U.S. Environmental Protection Agency has classified fluoride as more toxic than lead but less toxic than arsenic. U.S. Congressmen placed spring water in their offices when faced with the danger they might be forced to drink fluoride containing water.

3 - Aspartame excites and kills neurons along with causing seizures.. This toxic substance is now found in most packaged foods and beverages. Aspartame causes neurologic symptoms that mimic Multiple Sclerosis and brain tumors. These symptoms disappear when aspartame intake ceases. FDA approval for this dangerous substance was obtained despite some serious health concerns. by responsible health oriented experts.

4 - Monosodium glutamate MSG (Accent) is an excitogen that increases the appetite leading to repeat food sales and weight gain. This substance is added to a multitude of foods with no labeling. MSG causes Chinese Restaurant Syndrome, mimics neurologic diseases (M.S.,. A,L.S., Parkinson’s Disease, headaches, and seizures), hypoglycemia, learning disorders, hyperactivity, and Attention Deficit Disorder

5 - Nitrogen, phosphorus, and potassium fertilizer has made North American soil the poorest of all the seven continents. Poor quality foods grown from these depleted soils obviously damage the health and mental capability of the unfortunate citizens living in North America. This fertilizer was approved over strenuous objections by knowledgeable academic agricultural experts. Much US soil no longer contains the critical element selenium(cancer risk increases, infections spread).

6 - Genetically modified food has never before been consumed by humans. World famous geneticist Dr. Mae-Wan Ho states that “insertion of foreign genes into the human gene pool has long been known to have many harmful effects including cancer in the recipient organism” The results of safety testing on GMO foods have never been released to authorities and the FDA does not require GMO foods to be labeled so the public is unable to avoid eating these dangerous foods..

7 - Salk polio vaccine was given to 10,000,000 persons even though FDA leaders knew that the vaccine contained Simian Virus 40 and other dangerous viruses which can cause leukemia, lymphoma, HIV and other significant health problems. Sloppy animal isolation techniques .were the probable cause for this problem. The whistle blower was admonished for discovering this important contamination because “it was beyond the scope of her job description.”

Read Dr. Howenstine's book, "The Physician's Guide to Natural Health Products, That Work"

8 - Federally mandated nitrogen, phosphorus and potassium fertilizer has resulted in making North American soil the most depleted soil of the 7 continents tested. The critical elements selenium and sulfur are now missing from large amounts of U.S. soil.

9 - Codex Alimentaris, now implemented in parts of Europe (Norway, Germany), will probably soon become law in the USA. This will change valuable nutrients like vitamin C, alpha lipoic acid, and CoQ 10 into drugs requiring prescriptions which will raise the cost of these valuable substances. This impending lack of less expensive supplements will damage the health of the American people. Supplement makers may be forced to sell .their companies to take it or leave it type pharmaceutical company offers.

10 - Vaccines cause major health problems(autism, 4000 deaths in children admitted in the first year of Hepatitis B vaccine{only 10 % of adverse reactions get reported. etc.}. Pharmaceutical firms have been exempted from lawsuits by Congress for vaccine damages which are common.



Health problems created by a malfunctioning FDA are wonderful for the pharmaceutical industry because they increase the sale of drugs.



The drug company involved in the sale of Gardasil is caught in a torrent of lawsuits caused by the failure to warn the public that a widely used arthritis drug they had marketed was known to commonly cause deaths from heart attacks. This company has a sordid history of price fixing, tax avoidance, biopiracy, collusion with the FDA on how to discredit critics, purchasing negative evidence for its drugs and other activities that could be considered criminal in nature. Their product Gardasil should obviously never be given to any woman.

© 2008 Dr. James Howenstine - All Rights Reserved

Footnotes:

1, FDA News Release March 31, 2003
2, FDA VRBPAC Background Document: Gardasil HPV Quadrivalent Vaccine May 18, 2006 VRBPAC Meeting
3, Howenstine, James A Physicians Guide To Natural Health Products That Work pg 76. 2008 Source www.mynaturalhealthteam.com Phone 1-800-416-2806

Related Article:

1 - Eighteen Deaths Linked to Gardasil Vaccine Report Claims



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Dr. James A. Howenstine is a board certified specialist in internal medicine. The Second Edition of his book A Physicians Guide To Natural Health Products That Work is available.

Dr. Howenstine can be reached by writing Dr. James Howenstine C/O Remarsa USA SB 37, P.O. Box 25292, Miami, Fl. 33102-5292.

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Advanced Parental Age Predicts Risk for Autism Spectrum Disorder in Children

Advanced Parental Age Predicts Risk for Autism Spectrum Disorder in Children CME/CE
News Author: Laurie Barclay, MD
CME Author: Hien T. Nghiem, MD
Disclosures

Release Date: April 5, 2007; Valid for credit through April 4, 2009 Credits Available

Physicians - maximum of 0.25 AMA PRA Category 1 Credit(s)™ for physicians;
Family Physicians - up to 0.25 AAFP Prescribed credit(s) for physicians;
Nurses - 0.25 nursing contact hours (None of these credits is in the area of pharmacology)

To participate in this internet activity: (1) review the target audience, learning objectives, and author disclosures; (2) study the education content; (3) take the post-test and/or complete the evaluation; (4) view/print certificate View details.



Learning Objectives
Upon completion of this activity, participants will be able to:

Report the outcomes associated with advanced paternal age.
Evaluate the association between maternal and paternal ages and risk for ASDs.
Authors and Disclosures
Laurie Barclay, MD
Disclosure: Laurie Barclay, MD, has disclosed no relevant financial relationships.



Hien T. Nghiem, MD
Disclosure: Hien T. Nghiem, MD, has disclosed no relevant financial relationships.


April 5, 2007 — Advanced maternal and paternal ages are independently linked with risk for autism spectrum disorder (ASD) in children, according to the results of a historical birth cohort study reported in the April issue of the Archives of Pediatrics & Adolescent Medicine.

Lisa A. Croen, PhD, from the Kaiser Permanente Medical Care Program in Oakland, California, and colleagues studied all singleton children born at Kaiser Permanente in Northern California from January 1, 1995, to December 31, 1999, and they identified 593 children who had ASD diagnoses (International Classification of Diseases, Ninth Revision, Clinical Modification, code 299.0 or 299.8) recorded twice or more in Kaiser Permanente outpatient databases before May 2005. These 593 children were compared with the remaining 132,251 singleton Kaiser Permanente births.

Primary endpoints were relative risks (RRs) for ASD, estimated from proportional hazards regression models evaluating maternal and paternal ages, adjusted for each other and for the sex, birth date, and birth order of the child; maternal and paternal educational levels; and maternal and paternal races/ethnicities.

The risk for ASDs increased significantly with each 10-year increase in maternal age (adjusted RR, 1.31; 95% confidence interval [CI], 1.07 - 1.62) and paternal age (RR, 1.28; 95% CI, 1.09 - 1.51). Children with autistic disorder had increased adjusted RRs for both maternal and paternal ages (maternal age: RR, 1.18; 95% CI, 0.87 - 1.60; paternal age: RR, 1.34; 95% CI, 1.06 - 1.69), as did children with Asperger disorder or pervasive developmental disorder not otherwise specified (maternal age: RR, 1.45; 95% CI, 1.09 - 0.93; paternal age: RR, 1.24; 95% CI, 0.99 - 0.55). Although sex differences were not statistically significant, associations with parental age were somewhat stronger for girls than for boys.

"We found that risk of ASD was independently associated with advanced maternal and paternal age in a contemporary cohort of California-born children," the authors write. "Major strengths of this study include a large population-based sample and prospective collection of autism diagnoses and covariates, thus avoiding biases due to differential reporting and recall by parents of affected and unaffected children."

Study limitations include possible underascertainment of ASDs, failure to control for pregnancy complications, and possible confounding by healthcare-seeking behavior measured in the first few years of life.

"If the relationship between parental age and ASD is causal, the fraction of autism in this sample attributable to having a mother or father older than 35 years is 4% to 13%," the authors conclude. "Future investigations focused on the identification of both genetic and environmental factors that correlate with advanced parental age are warranted."

The Centers for Disease Control and Prevention and the Kaiser Foundation Research Institute funded this study in part. The authors have disclosed no relevant financial relationships.

Arch Pediatr Adolesc Med. 2007;161:334-340.

Clinical Context
In the past few decades, the prevalence of ASDs has increased significantly. The cause of ASDs is unknown; however, there is evidence for a strong genetic contribution. Advanced maternal age has been associated with risk for autism in several studies, but the role of paternal age in autism has been examined less frequently. Currently, advanced paternal age has been associated with adverse reproductive outcomes, such as miscarriage, fetal death, childhood cancers, autoimmune disorders, schizophrenia, and other neuropsychiatric disorders. These outcomes may be explained by the age-associated increase in de novo mutations in male germ cells.

The aim of the current study was to explore the association between maternal and paternal ages and risk for ASDs in offspring.

Study Highlights
In this historical birth cohort study, all singleton children born at Kaiser Permanente in Northern California from January 1, 1995, to December 31, 1999, were included in the study.
593 children diagnosed with ASD (International Classification of Diseases, Ninth Revision, Clinical Modification, code 299.0 or 299.8) were identified. 277 (47%) were classified as cases of autistic disorder and 316 (53%) as cases of pervasive developmental disorder not otherwise specified or Asperger disorder.
These children were compared with all 132,251 remaining singleton Kaiser Permanente births.
The main outcomes measured included RRs estimated from proportional hazards regression models. In addition, the risk for ASDs was evaluated in relation to maternal and paternal ages, adjusted for each other, and for the sex, birth date, and birth order of the child; maternal and paternal educational levels; and maternal and paternal races/ethnicities.
The results of this study demonstrated that adjusted RRs for both maternal and paternal ages were elevated for children with autistic disorder (maternal age: RR, 1.18; 95% CI, 0.87 - 1.60; paternal age: RR, 1.34; 95% CI, 1.06 - 1.69) and children with Asperger disorder or pervasive developmental disorder not otherwise specified (maternal age: RR, 1.45; 95% CI, 1.09 - 1.93; paternal age: RR, 1.24; 95% CI, 0.99 - 1.55).
Specifically, the risk for ASDs increased significantly with each 10-year increase in maternal age (adjusted RR, 1.31; 95% CI, 1.07 - 1.62) and paternal age (RR, 1.28; 95% CI, 1.09 - 1.51).
Associations with parental age were stronger for girls than for boys; however, sex differences were not statistically significant.
The cumulative incidence of ASD by the age of 10 years increased nearly 2-fold from the youngest (< 20 years, 1 in 251) to the oldest mothers (≥ 40 years, 1 in 123) and more than 3-fold from the youngest (< 20 years, 1 in 387) to the oldest fathers (≥ 40 years, 1 in 116).
Compared with controls, children with ASDs were more likely to be boys and to have older, more highly educated, and white non-Hispanic parents.
Independent of parental age and all other covariates, the risk for ASDs was inversely correlated with birth order, positively correlated with birth date, and significantly elevated for boys and children whose mothers had a college or postgraduate education.
Pearls for Practice
The role of paternal age in autism has been studied less frequently than that of maternal age, but advanced paternal age has been associated with adverse reproductive outcomes, such as miscarriage, fetal death, childhood cancers, autoimmune disorders, schizophrenia, and other neuropsychiatric disorders.
Advanced maternal and paternal ages are independently associated with ASD risk.
CME/CE Test

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Why is autism, schizophrenia or bipolar caused by having an older father?

George Bartzokis,M.D.


Visiting Professor

Laboratory of Neuro Imaging,
Department of Neurology, UCLA School of Medicine
635 Charles Young Drive South, Suite 225
Los Angeles, CA 90095-7332



Education

1975-1979, BA Harvard University, Cambridge, MA
1979-1983, MD Yale Medical School, New Haven, CT
1983-1984, Internship, UCLA/WLA VA, Los Angeles, CA
1984-1987, Psychiatry Residency, UCLA NPI, Los Angeles, CA
1987-1990, Schizophrenia Research Fellow, UCLA Dept of Psychology, Los Angeles, CA


Research

Development of brain imaging biomarkers for use in diagnosis of neuropsychiatric disorders and medication development
Assessing brain maturation and degeneration trajectories over the life-span in normal populations and how neuropsychiatric disorders interact with these processes


Projects

Myelin breakdown in aging and Alzheimer's disease
In vivo quantification of age-related increases in brain iron levels
Evaluation of brain maturational trajectories in normal adults and patientss with neuropsychiatrc diseases


Skills

Quantification of brain iron levels
Quantification of limbic structures volumes
Quantification of brain myelination
Quantification of myelin integrity
Clinical trials
Administration of multidisciplinary teams


Honors

U.S. Patent, Method for Quantitatively Measuring Stored Iron in Tissue Using MRI










This quote is not from a published paper.
I had asked Dr. Bartzokis why risk of non-familial autism, schizophrenia, MS, and Alzheimer's risk increases with the age of the father at a person's birth.



"The issue is that the older man will have sperm that has undergone more divisions and therefore had more chances to have mutations.
The COMPLEXITY of the myelination process makes it more vulnerable to mutations. I am not talking of one specific mutation. Many things could MANIFEST in the myelination or myelin breakdown process because it is so vulnerable - something going slightly wrong will impact it while it will not impact bone growth or the heart. A good example is ApoE4 - whatever else it may affect, it manifests in the reduced capacity of myelin repair and earlier onset of AD."
Labels: I am not talking about a specific mutation, the complexity

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Monday, November 03, 2008

John McCain for President Endorsed by Ginger Taylor

Adventures in Autism: I Endorse John McCain for President. He is the Autism Candidate.

Sunday, November 02, 2008

Study links parental age to increased risk of autism

Study links parental age to increased risk of autism



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10:00 PM PST on Sunday, November 2, 2008

By JANET ZIMMERMAN
The Press-Enterprise

The first-born children of older parents are three times more likely to have autism than their siblings or those born to younger parents, according to a new federally funded study.

This is the largest study to look at the issue of parental age and its role in the developmental disability, said the author, Maureen Durkin, an epidemiologist at the University of Wisconsin School of Medicine and Public Health.

The study, funded by the U.S. Centers for Disease Control and Prevention, was published in last month's American Journal of Epidemiology. The age limits where Durkin found the increased risk were in women over 35 and men over 40.

But Durkin cautioned that many other factors could play a role in autism, including environmental causes, and would-be parents should not put off having children because of the findings.

"Even though we find this association statistically significant, I don't think it's a strong enough relationship to affect family planning decisions," Durkin said in a telephone interview. "Even with this strong increase in risk, the vast majority of children born to older parents -- more than 95 percent of these births -- are not going to have autism."

Durkin's research looked at 253,347 births from 10 states that participate in the CDC's Autism and Developmental Disabilities Monitoring Network. All births were in 1994 and included 1,251 children with autism.

The results echoed a smaller Kaiser Permanente study of California children that was published last year. That research traced an autism link when both parents were over 35.

Autism, which affects 1 in 150 American children, is characterized by impaired communication and social interaction and repetitive patterns of behavior such as hand flapping and spinning.

It is the fastest-growing developmental disability in the United States, and its prevalence worldwide has more than doubled in the past 20 years.

While Durkin's research doesn't fully answer questions about autism, it does provide clues for further research into the causes, she said.

Among them, factors associated with older parents, Durkin said.

Those factors that bear further investigation are: spontaneous mutations that occur in sperm as men age; fertility treatments that involve hormonal treatments and manipulations of genes during conception; and neurotoxins built up in the tissues of older, breastfeeding mothers, Durkin said.

Each 10-year increase in maternal age was associated with a 20 percent increase in autism risk and a decade added to the father's age kicked up the risk to 30 percent, according to the study.

The mean maternal age in the United States has increased steadily -- by 3.8 years -- between 1970 and 2004, especially for first-time mothers. Durkin questioned how much of a role advanced parental age and fewer children per family plays in the staggering growth in autism in recent decades.

"It might be playing some role, in particular if the families affected are better established and educated. They may be pushing more for better diagnoses and services, and may be more effective at that than younger and less well-educated parents," she said.

Beth Burt, president of the Inland Empire Autism Society, said she is pleased that money is being spent on studies into the cause of autism.

But she worried that Durkin's findings will prompt people to blame parents.

"I don't want society to go 'It's all the parents who are waiting to have kids that are causing the epidemic.' We have plenty of parents in their 20s where that isn't the case," she said.

Burt has a 15-year-old son with high-functioning autism. She was 28 when she gave birth.

Burt said she believes there are different types of autism and different triggers that require individualized and varied treatments. In addition to research studies, the government also needs to spend money on services for families, including employment and residential options.

"I'm glad they're funding studies, but I want to see something to help the families that are here now battling this," she said.

Reach Janet Zimmerman at 951-368-9586 or jzimmerman@PE.com.

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