Friday, April 24, 2009

Biological clock ticks for men as well

Biological clock ticks for men as well
By Jenifer Goodwin (Contact) Union-Tribune Staff Writer
8:00 a.m. April 24, 2009
Ever since women began putting off childbearing to go to college and build careers, they've had to face a cold, hard truth. A growing body of research is showing that men have a biological clock, too. - JupiterimagesEver since women began putting off childbearing, they've had to face the harsh truth that there are only so many years they can have babies.
If a woman dares wait until age 35, she's declared “advanced maternal age” and told about the increased risk of having a baby with certain genetic conditions.
As it turns out, a growing body of research is showing that men have a biological clock, too.
The children of older fathers scored lower than the offspring of younger fathers on IQ tests and other cognitive measures at 8 months old, 4 years old and 7 years old, according to results of a study released in March.
Men who becomes fathers in their 40s or older are more than 1.5 times more likely to father children who are autistic, according to a 2006 study.
Other research has shown increased risk of schizophrenia and bipolar disorder in the children of older fathers, and that the risk of miscarriage rises with the father's age.
“Men are in denial,” said Dr. Harry Fisch, an expert on male infertility and author of the 2005 book “The Male Biological Clock.” “Men think as they age, they get better or more distinguished. As men get older, they get older.”
Scientists knew for years before the highly publicized autism and IQ studies that the children of older fathers were at higher risk of certain rare genetic conditions, such as dwarfism, Fisch said.
Yet outside of the science realm, few paid much attention.
Men were operating under the mistaken belief that since they generated new sperm every day, they could have children well into old age with no added risk.
What was missing from the equation was that even new sperm made by an older man is more prone to genetic defects. “As the body ages, there is no reason to think why these sperm cells wouldn't age too,” Fisch said.
So what should men do with the information?
Plenty of older dads father healthy, intelligent children. Still, men should consider the potential consequences of putting off childbearing, Fisch said.
The older both spouses are, the greater the chance they will have fertility problems, he said. “People need to know this information for family planning.”

Jenifer Goodwin: (760) 476-8210; (Contact)


Wednesday, April 22, 2009

For Whom The Clock Ticks

For Whom The Clock Ticks
A growing body of research supports the idea that there are biological disadvantages to late-in-life fatherhood. But will society's view of male fertility ever change?

By Daniel Heimpel | Newsweek Web Exclusive
Apr 22, 2009

In season two of Bravo's wildly popular television series "Millionaire Matchmaker," host Patti Stanger rants against older men who perpetually search for 20-somethings to date. What Stanger knows intuitively and what researchers are illustrating empirically, is that men 50 and older, no matter their financial stability, aren't always the greatest catch.

Even if they can theoretically father children till the day they die, a growing compendium of knowledge points to a male "biological clock" largely driven by the replication of sperm with damaged DNA. According to a number of recent studies, offspring of older men have increased chances of a wide range of problems from autism to psychiatric disorders such as schizophrenia. Unlike women, who are equipped with their life's supply of eggs at birth, men replicate sperm from their bar mitzvah to their funeral. It's like a Xerox copy of a Xerox copy millions of times over. The damage can be caused by glitches in the process of replicating DNA millions of times over, reduced efficiency of the DNA repair mechanism, or attributed to environmental factors like stress, smoking or heavy drinking.

But the bottom line is: as men age, the percentage of damaged sperm they carry in their testes tends to increase. "Men are making millions of sperm all the time, and the chance for a copy error is much higher," says Dr. Ethylin Jabs, director of the Center for Craniofacial Development and Disorders at Johns Hopkins, who has conducted extensive research on paternal age and mutations within sperm. Where older women may be concerned about the viability of their remaining eggs, the problem for men, says Jabs, is "quantity not quality."

Semen samples of men over 45 showed impairment to sperm in three categories: their motility (swimming capability), vitality and DNA integrity, according to Dr. Sergey Moskovtsev of Mount Sinai Hospital's Department of Pathology and Laboratory Medicine in New York. Moskovtsev's research shows that men older than 45 have twice as much damage to their sperm as men under 30. Researchers believe that an increase in the percentage of damaged sperm can have a number of consequences.

A report released in PLoS Medicine last month establishes a link between reduced intelligence and children who were fathered by older men. Using a sample of 33,000 children tested at the ages of 8 months, 4 years and 7 years, John McGrath of Australia's Queensland Centre for Mental Health Research and colleagues found that children of older fathers ranked consistently lower in cognitive ability tests than the offspring of younger fathers. For example, 7-year-old children born to 50-year-old dads performed two IQ points lower than peers born to 20-year-old fathers. This difference in IQ is of course subtle, and McGrath says that the results of his study shouldn't be cause for individual men to stop having children.

But he cautions that the mounting studies pointing to a male biological clock are worth considering on a macro level. "As a researcher, I am concerned that we have neglected the issue of paternal age," McGrath says. "Worryingly, the mutations associated with advanced paternal age can be passed on to the next generation. As the population delays parenthood, these mutations could, theoretically, accumulate. Other researchers—not me—have called this process a 'mutational time-bomb'."



Wednesday, April 08, 2009

Sharing the Biological Clock by Eric Steinman

I am pushing forty, and when I say pushing forty–I mean pushing forty. I have one child, and would like to have another one in the near future. Up until last Sunday, when Lisa Belkin, columnist for the New York Times, published a piece exploring new data that indicates that men my age, and younger even, may not have all the time in world to procreate, I lived in a state of false confidence.

This false confidence consisted of the faith that, while my wife was held by the constraints of her biological clock, I (and other men of similar advancing age) were free to inseminate and breed well into our golden years. Now it would be disingenuous for me to say that I had no knowledge of these stats or these claims prior to reading this report (I did), but there is something about reading it in plain black and white that helps you identify the unmistakable tick of your own biological clock.

A friend of mine who is over forty, unmarried, and toying with the idea of getting married and having children, periodically will call me to get a window into the loving bounty and rampant frustrations of parenthood. When he contends with the idea of putting off parenthood for a few more years, he will usually say something like, “Well, I don’t want to be too old to kick around a ball with my child.” According to a report sited in the aforementioned article, he may have larger issues of concern than being able to play ball. Researchers at the University of Queensland found that children born to older fathers have, on average, lower scores on tests of intelligence than those born to younger dads. In addition, other studies have indicated there is an increased risk of schizophrenia, bipolar disorder, and autism, and that the chances of successfully conceiving a child begins to diminish once the man is older than thirty-five and falls sharply if he is older than forty.

Now you should take what you will from this data, as the results certainly shouldn’t dissuade anyone from attempting to have children. If anything it might motivate prospective parents to speed the plough (so to speak). Data is data, and as we all know everything is subject to dispute, as well as exception. The more interesting aspect of this report (as noted by author Lisa Belkin) is how this impacts traditional gender dynamics around the subject of having children. Typically (and I am generalizing here) it is thought that women, due to a limited window of opportunity, hold much more awareness, as well as enthusiasm, about the prospect of having children, and that men tend to hold off the inevitable procreation until a desired comfort level is reached (financial stability, etc). While these new findings don’t exactly reverse that paradigm, they do sort of even the playing field.

If prospective fathers are serious about becoming actualized fathers of healthy and hearty children, they best adopt a little bit of urgency on the matter and drop the “all the time in the world” attitude.

So scare tactics aside, how do you think these new findings will potentially impact the existing gender clash around if and when to have children? Does it change anything? Will men change their tune and start charting their partner’s basal body temperature as they sleep? Or are we in for more of the same?

Eric Steinman is a freelance writer based in Rhinebeck, N.Y. He regularly writes about food, music, art, architecture and culture and is a regular contributor to Bon Appétit among other publications.


Monday, April 06, 2009

The Coming of the Daddy Wars

The Coming of the Daddy Wars
My favorite item from this week's Sunday papers was Lisa Belkin's Times Magazine piece on men's biological clocks. Belkin looks at new research showing that as men age beyond about 30, their chance of fathering a child with an autism-spectrum disorder or schizophrenia increases. Simultaneously, men's overall fertility decreases after age 35. Put simply, in the words of NYU psychiatry researcher Dr. Dolores Malaspina: “It turns out the optimal age for being a mother is the same as the optimal age for being a father.”

If these preliminary findings are upheld over time, their cultural significance -- especially for college-educated, type A, planner types -- could be huge. It isn't surprising that it has taken science this long to seriously question men's biological role in producing healthy children; we are all conditioned to see women as the folks primarily responsible for children, from conception through pregnancy, childbirth, and child-rearing. Young women know they are facing menopause down the road, and have often been warned by mothers and other older women about the difficulties of conception. As a consequence, it isn't uncommon to talk to women in their twenties who are aware of the latest trends on prenatal testing or fertility, but whose male partners have never bothered to inform themselves on such issues, even though they fully intend on having children "someday." As Belkin writes:

The push and pull between timetables and dreams, between our bodies and our babies, is at the core of many women’s worldview, which also means it is at the core of relationships between the sexes. This tension feeds the stereotype of woman as eager to settle down and men as reluctant, and it’s the crux of why we see women as “old” and men as “distinguished.”

Imagine a world in which the stereotype of women rushing men to the alter, biological clocks on overdrive, simply disappeared, as men took full 50 percent ownership over the reproductive process. Or in which wealthy 50- year old divorced men ceased to be such catches for 30-year old women, because of weakened sperm. I wouldn't want to return to a society in which both men and women are pressured into settling down and having babies at an unduly young age. But I do like the idea of rejiggering our notions about the intersection of gender and aging. It isn't just women who have a lot to fit into their lives in terms of career, romance, and parenthood. Science is beginning to tell us that men are facing the same pressures.

cross-posted at TAPPED

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MSNBC Lisa Belkin, Nancy Snyderman, Matt Lauer Male Biological Clock

Saturday, April 04, 2009

Schizophrenia Risk and the Paternal Germ Line

Schizophrenia Risk and the Paternal Germ Line
By Dolores Malaspina

Paternal age at conception is a robust risk factor for schizophrenia. Possible mechanisms include de novo point mutations or defective epigenetic regulation of paternal genes. The predisposing genetic events appear to occur probabilistically (stochastically) in proportion to advancing paternal age, but might also be induced by toxic exposures, nutritional deficiencies, suboptimal DNA repair enzymes, or other factors that influence the

fidelity of genetic information in the constantly replicating male germ line. We propose that de novo genetic alterations in the paternal germ line cause an independent and common variant of schizophrenia.

Seminal findings
We initially examined the relationship between paternal age and the risk for schizophrenia because it is well established that paternal age is the major source of de novo mutations in the human population, and most schizophrenia cases have no family history of psychosis. In 2001, we demonstrated a monotonic increase in the risk of schizophrenia as paternal age advanced in the rich database of the Jerusalem Perinatal Cohort. Compared with the offspring of fathers aged 20-24 years, in well-controlled analyses, each decade of paternal age multiplied the risk for schizophrenia by 1.4 (95 percent confidence interval: 1.2-1.7), so that the relative risk (RR) for offspring of fathers aged 45+ was 3.0 (1.6-5.5), with 1/46 of these offspring developing schizophrenia. There were no comparable maternal age effects (Malaspina et al., 2001).

Epidemiological evidence
This finding has now been replicated in numerous cohorts from diverse populations (Sipos et al., 2004; El-Saadi et al., 2004; Zammit et al., 2003; Byrne et al., 2003; Dalman and Allenbeck, 2002; Brown et al., 2002; Tsuchiya et al., 2005). By and large, each study shows a tripling of the risk for schizophrenia for the offspring of the oldest group of fathers, in comparison to the risk in a reference group of younger fathers. There is also a "dosage effect" of increasing paternal age; risk is roughly doubled for the offspring of men in their forties and is tripled for paternal age >50 years. These studies are methodologically sound, and most of them have employed prospective exposure data and validated psychiatric diagnoses. Together they demonstrate that the paternal age effect is not explained by other factors, including family history, maternal age, parental education and social ability, family social integration, social class, birth order, birth weight, and birth complications. Furthermore, the paternal age effect is specific for schizophrenia versus other adult onset psychiatric disorders. This is not the case for any other known schizophrenia risk factor, including many of the putative susceptibility genes (Craddock et al., 2006).

There have been no failures to replicate the paternal age effect, nor its approximate magnitude, in any adequately powered study. The data support the hypothesis that paternal age increases schizophrenia risk through a de novo genetic mechanism. The remarkable uniformity of the results across different cultures lends further coherence to the conclusion that this robust relationship is likely to reflect an innate human biological phenomenon that progresses over aging in the male germ line, which is independent of regional environmental, infectious, or other routes.

Indeed, the consistency of these data is unparalleled in schizophrenia research, with the exception of the increase in risk to the relatives of schizophrenia probands (i.e., 10 percent for a sibling). Yet, while having an affected first-degree relative confers a relatively higher risk for illness than having a father >50 years (~10 percent versus ~2 percent), paternal age explains a far greater portion of the population attributable risk for schizophrenia. This is because a family history is infrequent among schizophrenia cases, whereas paternal age explained 26.6 percent of the schizophrenia cases in our Jerusalem cohort. If we had only considered the risk in the cases with paternal age >30 years, our risk would be equivalent to that reported by Sipos et al. (2004) in the Swedish study (15.5 percent). When paternal ages >25 years are considered, the calculated risk is much higher. Although the increment in risk for fathers age 26 through 30 years is small (~14 percent), this group is very large, which accounts for the magnitude of their contribution to the overall risk. The actual percentage of cases with paternal germ line-derived schizophrenia in a given population will depend on the demographics of paternal childbearing age, among other factors. With an upswing in paternal age, these cases would be expected to become more prevalent.

Biological plausibility
We used several approaches to examine the biological plausibility of paternal age as a risk factor for schizophrenia. First, we established a translational animal model using inbred mice. Previously it had been reported that the offspring of aged male rodents had less spontaneous activity and worse learning capacity than those of mature rodents, despite having no noticeable physical anomalies (Auroux et al., 1983). Our model carefully compared behavioral performance between the progeny of 18-24-month-old sires with that of 4-month-old sires. We replicated Auroux's findings, demonstrating significantly decreased learning in an active avoidance test, less exploration in the open field, and a number of other behavioral decrements in the offspring of older sires (Bradley-Moore et al., 2002).

Next, we examined if parental age was related to intelligence in healthy adolescents. We reasoned that if de novo genetic changes can cause schizophrenia, there might be effects of later paternal age on cognitive function, since cognitive problems are intertwined with core aspects of schizophrenia. For this study, we cross-linked data from the Jerusalem birth cohort with the neuropsychological data from the Israeli draft board (Malaspina et al., 2005a). We found that maternal and paternal age had independent effects on IQ scores, each accounting for ~2 percent of the total variance. Older paternal age was exclusively associated with a decrement in nonverbal (performance) intelligence IQ, without effects on verbal ability, suggestive of a specific effect on cognitive processing. In controlled analyses, maternal age showed an inverted U-shaped association with both verbal and performance IQ, suggestive of a generalized effect.

Finally, we examined if paternal age was related to the risk for autism in our cohort. We found very strong effects of advancing paternal age on the risk for autism and related pervasive developmental disorders (Reichenberg et al., in press). Compared to the offspring of fathers aged 30 years or younger, the risk was tripled for offspring of fathers in their forties and was increased fivefold when paternal age was >50 years. Together, these studies provide strong and convergent support for the hypothesis that later paternal age can influence neural functioning. The translational animal model offers the opportunity to identify candidate genes and epigenetic mechanisms that may explain the association of cognitive functioning with advancing paternal age.

A variant of schizophrenia
A persistent question is whether the association of paternal age and schizophrenia could be explained by psychiatric problems in the parents that could both hinder their childbearing and be inherited by their offspring. If this were so, then cases with affected parents would have older paternal ages. This has not been demonstrated. To the contrary, we found that paternal age was 4.7 years older for sporadic than familial cases from our research unit at New York State Psychiatric Institute (Malaspina et al., 2002). In addition, epidemiological studies show that advancing paternal age is unrelated to the risk for familial schizophrenia (Byrne et al., 2003; Sipos et al., 2004). For example, Sipos found that each subsequent decade of paternal age increased the RR for sporadic schizophrenia by 1.60 (1.32 to 1.92), with no significant effect for familial cases (RR = 0.91, 0.44 to 1.89). The effect of late paternal age in sporadic cases was impressive. The offspring of the oldest fathers had a 5.85-fold risk for sporadic schizophrenia (Sipos et al., 2004); relative risks over 5.0 are very likely to reflect a true causal relationship (Breslow and Day, 1980).

It is possible that the genetic events that occur in the paternal germ line are affecting the same genes that influence the risk in familial cases. However, there is evidence that this is not the case. First, a number of the loci linked to familial schizophrenia are also associated with bipolar disorder (Craddock et al., 2006), whereas advancing paternal age is specific for schizophrenia (Malaspina et al., 2001). Next, a few genetic studies that separately examined familial and sporadic cases found that the "at-risk haplotypes" linked to familial schizophrenia were unassociated with sporadic cases, including dystrobrevin-binding protein (Van Den Bogaert et al., 2003) and neuregulin (Williams et al., 2003). Segregating sporadic cases from the analyses actually strengthened the magnitude of the genetic association in the familial cases, consistent with etiological heterogeneity between familial and sporadic groups.

Finally, the phenotype of cases with no family history and later paternal age are distinct from familial cases in many studies. For example, only sporadic cases showed a significant improvement in negative symptoms between a "medication-free" and an "antipsychotic treatment" condition (Malaspina et al., 2000), and sporadic cases have significantly more disruptions in their smooth pursuit eye movement quality than familial cases (Malaspina et al., 1998). A recent study also showed differences between the groups in resting regional cerebral blood flow (rCBF) patterns, in comparison with healthy subjects. The sporadic group of cases had greater hypofrontality, with increased medial temporal lobe activity (frontotemporal imbalance), while the familial group evidenced left lateralized temperoparietal hypoperfusion along with widespread rCBF changes in cortico-striato-thalamo-cortical regions (Malaspina et al., 2005b). Other data linking paternal age with frontal pathology in schizophrenia include a proton magnetic resonance spectroscopy study that demonstrated a significant association between prefrontal cortex neuronal integrity (NAA) and paternal age in sporadic cases only, with no significant NAA decrement in the familial schizophrenia group (Kegeles et al., 2005). These findings support the hypothesis that schizophrenia subgroups may have distinct neural underpinnings and that the important changes in some sporadic (paternal germ line) cases may particularly impact on prefrontal cortical functioning.

Genetic mechanism
Several genetic mechanisms might explain the relationship between paternal age and the risk for schizophrenia (see Malaspina, 2001). It could be due to de novo point mutations arising in one or several schizophrenia susceptibility loci. Paternal age is known to be the principal source of new mutations in mammals, likely explained by the constant cell replication cycles that occur in spermatogenesis (James Crow, 2000). Following puberty, spermatogonia undergo some 23 divisions per year. At ages 20 and 40, a man's germ cell precursors will have undergone about 200 and 660 such divisions, respectively. During a man's life, the spermatogonia are vulnerable to DNA damage, and mutations may accumulate in clones of spermatogonia as men age. In contrast, the numbers of such divisions in female germ cells is usually 24, all but the last occurring during fetal life.

Trinucleotide repeat expansions could also underlie the paternal age effect. Repeat expansions have been demonstrated in several neuropsychiatric disorders, including myotonic dystrophy, fragile X syndrome, spinocerebellar ataxias, and Huntington disease. The sex of the transmitting parent is frequently a major factor influencing anticipation, with many disorders showing greater trinucleotide repeat expansion with paternal inheritance (Lindblad and Schalling, 1999; Schols et al., 2004; Duyao et al., 1993). Larger numbers of repeat expansions could be related to chance molecular events during the many cell divisions that occur during spermatogenesis.

Later paternal age might confer a risk for schizophrenia if it was associated with errors in the "imprinting" patterns of paternally inherited alleles. Imprinting is a form of gene regulation in which gene expression in the offspring depends on whether the allele was inherited from the male or female parent. Imprinted genes that are only expressed if paternally inherited alleles are reciprocally silenced at the maternal allele, and vice versa. Imprinting occurs during gametogenesis after the methylation patterns from the previous generation are "erased" and new parent of origin specific methylation patterns are established. Errors in erasure or reestablishment of these imprint patterns may lead to defective gene expression profiles in the offspring. The enzymes responsible for methylating DNA are the DNA methyltransferases, or DNMTs. These enzymes methylate cytosine residues in CpG dinucleotides, usually in the promoter region of genes, typically to reduce the expression of the mRNA. The methylation may become inefficient for a variety of reasons; one possibility is reduced DNA methylation activity in spermatogenesis, since DNMT levels diminish as paternal age increases (Benoit and Trasler, 1994; La Salle et al., 2004). Another possible mechanism is that this declining DNMT activity could be epigenetically transmitted to the offspring of older fathers. There are a number of different DNMTs that differ in whether they initiate or sustain methylation, and which are active at different ages and in different tissues.

Human imprinted genes have a critical role in the growth of the placenta, fetus, and central nervous system, in behavioral development, and in adult body size. It is an appealing hypothesis that loss of normal imprinting of genes critical to neurodevelopment may play a role in schizophrenia. Indeed, one of the most consistently identified molecular abnormalities in schizophrenia has been theorized to result from abnormal epigenetic mechanisms (Veldic et al., 2004), that is, the reduced GABA and reelin expression in prefrontal GABAergic interneurons. An overexpression of DNMT in these GABAergic interneurons, hypermethylating the reelin and GAD67 promoter regions, might be responsible for reducing their mRNA transcripts and expression levels. These decrements could functionally impair the role of GABAergic interneurons in regulating the activity and firing of pyramidal neurons, thereby causing cognitive dysfunction. Later paternal age could be related to the abnormal regulation or expression of DNMT activity in specific cells.

These findings suggest exciting new directions for research into the etiology of schizophrenia. If there is a unitary etiopathology for paternal age-related schizophrenia, then it is likely to be the most common form of the condition in the population and in treatment settings, since genetic linkage and association studies indicate that familial cases are likely to demonstrate significant allelic heterogeneity and varying epistatic effects. Schizophrenia is commonly considered to result from the interplay between genetic susceptibility and environmental exposures, particularly those that occur during fetal development and in adolescence. The data linking paternal age to the risk for schizophrenia indicate that we should expand this event horizon to consider the effects of environmental exposures over the lifespan of the father. The mutational stigmata of an exposure may remain in a spermatogonial cell, and be manifest in the clones of spermatozoa that it will subsequently generate over a man's reproductive life.

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El-Saadi O, Pedersen CB, McNeil TF, Saha S, Welham J, O'Callaghan E, Cantor-Graae E, Chant D, Mortensen PB, McGrath J. Paternal and maternal age as risk factors for psychosis: findings from Denmark, Sweden and Australia.Schizophr Res. 2004 Apr 1;67(2-3):227-36. Abstract

Kegeles LS, Shungu DC, Mao X, Goetz R, Mikell CB, Abi-Dargham A, Laurelle M, Malaspina D. Relationship of age and paternal age to neuronal functional integrity in the prefrontal cortex in schizophrenia determined by proton magnetic resonance spectroscopy. Schizophrenia Bulletin, 31:443; 2005.

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Malaspina D, Corcoran C, Fahim C, Berman A, Harkavy-Friedman J, Yale S, Goetz D, Goetz R, Harlap S, Gorman J. Paternal age and sporadic schizophrenia: evidence for de novo mutations. Am J Med Genet. 2002 Apr 8;114(3):299-303. Abstract

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Malaspina D, Reichenberg A, Weiser M, Fennig S, Davidson M, Harlap S, Wolitzky R, Rabinowitz J, Susser E, Knobler HY. Paternal age and intelligence: implications for age-related genomic changes in male germ cells. Psychiatr Genet. 2005 (b) Jun;15(2):117-25. Abstract

Reichenberg A, Gross R, Weiser M, Bresnahan M, Silverman J, Harlap, Rabinowitz J, Shulman L, Malaspina D, Lubin G, Knobler HY, Davidson M, Susser E: Advancing paternal age and Autism. Archives of General Psychiatry.

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Wednesday, April 01, 2009

Audio of Lisa Belkin On the Truth of Male Genetic Biological Clock


Your Old Man

The Way We Live Now
Your Old Man
Published: April 1, 2009
Read between the lines of a recent study out of Australia and you can see hints of a coming shift in the gender conversation. Researchers at the University of Queensland found that children born to older fathers have, on average, lower scores on tests of intelligence than those born to younger dads. Data they analyzed from more than 33,000 American children showed that the older the man when a child is conceived, the lower a child’s score is likely to be on tests of concentration, memory, reasoning and reading skills, at least through age 7.

It was a small difference — just a few I.Q. points separated a child born to a 20-year-old and a child born to a 50-year-old. But it adds weight to a new consensus-in-the-making: there is no fountain of youth for sperm, no “get out of aging free” card. The little swimmers, scientists are finding, one study at a time, get older and less dependable along with every other cell in the male body.

And men don’t have to be all that old to be “too old.” French researchers reported last year that the chance of a couple’s conceiving begins to fall when the man is older than 35 and falls sharply if he is older than 40. British and Swedish researchers, in turn, have calculated that the risk of schizophrenia begins to rise for those whose fathers were over 30 when their babies were born. And another Swedish study has found that the risk of bipolar disorder in children begins to increase when fathers are older than 29 and is highest if they are older than 55. British and American researchers found that babies born to men over the age of 40 have significantly greater risk of autism than do those born to men under 30. (The age of the mother, in most of these studies, showed little or no correlation.)

Lay this latest I.Q. news atop the pile, and you find yourself reaching the same conclusion as Dr. Dolores Malaspina, a professor of psychiatry at New York University Medical Center, who has done some of the schizophrenia research: “It turns out the optimal age for being a mother is the same as the optimal age for being a father.”...