Future dads of the world relax! Stressing now could affect the health of your future kids

Parents pass on a unique genetic makeup to their children. Little Johnny is a blonde-haired, blue-eyed boy with a one-of-a-kind thumbprint all because it is encoded in the DNA provided by his parents. But did you know that the quality of the DNA you pass on to your children can be impacted by stressful events in your life such as disease, malnutrition, and old age, ultimately influencing the way your children’s bodies respond to stress? That is what a new study  looking at the impact of paternal stress on sperm genetics suggests.

First let’s take a look at how the body reacts to a stressful situation. The hypothalamic-pituitary-adrenal axis, or HPA-axis, is a major component of the neuroendocrine system, a system in our body that allows our brain to communicate with hormone producing glands, such as the adrenal gland. During a stressful event, for example happening upon a giant, hungry-looking bear during a hike in the woods, the HPA-axis is activated resulting in the brain telling the adrenal gland to release cortisol, a major stress hormone that tells your body to fight the bear (poorer option) or get the heck out of there as fast as humanly possible (better option).  Actually, trying to outrun a bear is probably a terrible idea because they’re wicked fast. Check back for future posts on bear encounter etiquette. Anyway back to the HPA-axis…

The HPA-axis is remarkably susceptible to environmental stressors and improper management of the HPA-axis has been linked to a number of psychiatric disorders including autism, schizophrenia, and depression.

Ali B. Rodgers et al. (2013). Paternal Stress Exposure Alters Sperm MicroRNA Content and Reprograms Offspring HPA Stress Axis Regulation. The Journal of Neuroscience33(21): 9003-9012

So can the stresses of life, occurring years prior to conception, really impact how your future kid’s HPA-axis handles stress? Rodgers and colleagues exposed both adolescent and adult male mice to prolonged stresses before breeding, such as leaving the lights on all night, creating funny odors, or introducing novel objects into their home. Researchers stressed male mice instead of female mice to limit the number of variables that could potentially influence their findings. Male mice only contribute their DNA to the pups, whereas in addition to changes in DNA female mice can also affect pups through life events during pregnancy or rearing.

When evaluating the pups from stressed fathers, HPA-axis response was significantly reduced compared to pups of unstressed fathers. Decreased HPA-axis responsiveness is bad news for pups because it means they’re unable to respond appropriately to changes in their environment. Consistent with HPA-axis dysregulation, transcription, which is the first step of gene expression, was altered in brain regions responsible for regulating the body’s response to stress.

But how exactly were these changes passed on? Did the father’s DNA change? Not exactly.

Epigenetics is the study of changes in gene expression by modifying DNA without changing the actual nucleic acid sequence often by adding small molecules to the DNA nucleotides or altering the accessibility of the sequence. Several studies suggest that stress can lead to epigenetic modifications in sperm germ cells. Rodgers et al. found considerable changes in 9 sperm microRNA, molecules responsible for epigenetic alterations, within the group of fathers exposed to environmental stressors. Thus when the fathers were stressed over a prolonged period of time, it caused changes in the how the DNA they would eventually pass on to their offspring would be expressed.

What’s the bottom line? Relax, eat well, and stay healthy to keep your sperm and subsequently all your future children happy and healthy! Oh, and stay away from bears.

ResearchBlogging.orgRodgers A.B., Morgan C.P., Bronson S.L., Revello S. & Bale T.L. (2013). Paternal Stress Exposure Alters Sperm MicroRNA Content and Reprograms Offspring HPA Stress Axis Regulation, Journal of Neuroscience, 33 (21) 9003-9012. DOI:

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In the quest to slow aging, have researchers found the Holy Grail?

What if I told you that it may be possible to live longer than ever while remaining sharp as a tack? Now what if I told you that you’re NOT going to like the key to achieving this immortality?

Ready? To live longer and prosper all you have to do is restrict your calorie intake by at least 30%. That’s it. So kiss that dessert and all future indulgences good-bye! According to several studies conducted in rodents, caloric restriction can increase lifespan by slowing the aging process, preserving brain structure and cognition, and even reducing the occurrence of Alzheimer’s disease pathology. But just as you sink into a deep dark depression over never sampling another Ben & Jerry’s flavor, there may be a light at the end of the tunnel.

Johannes Gräff et al. (2013). A Dietary Regimen of Caloric Restriction or Pharmacological Activation of SIRT1 to Delay the Onset of Neurodegeneration. The Journal of Neuroscience, 33(21): 8951-8960

Adding to the mounting pile of evidence in support of caloric restriction, a recent study conducted by Gräff et al. demonstrated that expression of SIRT1, a protein critically involved in cellular metabolism, stress, and survival mechanisms, reduces neurodegeneration, which is the breakdown of brain cells, caused by aging.

Using a transgenic mouse that experiences neurodegeneration, brain atrophy, and memory loss the authors of the study reduced mouse food intake by 30% and saw protection against synapse loss in the hippocampus, the brain region responsible for memory.

This neurodegeneration is visualized in the image below. Neurons in the hippocampus shown in green and their synapses shown in red are significantly reduced in the transgenic animals without caloric restriction (left) compared to animals undergoing caloric restriction (right).

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Prognosis for the caloric restriction group looks good, showing a significantly greater number of synapses, but how are their brains functioning? Do the increased number of synapses even work properly? Memory task performances of the calorie-restricted mice were also unimpaired compared to mice that that were free to eat as much as they liked. Importantly, SIRT1 activation was also increased in the calorically restricted group of animals.

Great! So calorie restriction seems to be saving the minds of these otherwise doomed mice from dementia through SIRT1 activation, but how does this impact your Rita’s Italian Ice gelato habit?

Well, if SIRT1 is directly involved in keeping our neurons in tip-top shape following caloric restriction, then maybe it’s possible to take caloric restriction out of the equation and deal with SIRT1 directly. And that’s exactly what Gräff and colleagues did.

Instead of undergoing caloric restriction, neurodegenerative mice ingested a SIRT1-activating compound (STAC) and still reaped the aging benefits of caloric restriction without the severe reduction in calorie consumption. Both synapse density and memory scores were improved in the STAC supplement group compared to the control group that did not receive STAC. Bring on the feasts!

While other factors in addition to caloric restriction likely impact longevity, such as diet and exercise, I’ll play the odds and ask for some STAC-laced sprinkles on my next ice cream sundae!

ResearchBlogging.orgGraff J., Kahn M., Samiei A., Gao J., Ota K.T., Rei D. & Tsai L.H. (2013). A Dietary Regimen of Caloric Restriction or Pharmacological Activation of SIRT1 to Delay the Onset of Neurodegeneration, Journal of Neuroscience, 33 (21) 8951-8960. DOI: