Sex-specific changes in cerebral blood flow begin at puberty, study finds

brain
White matter fiber architecture of the brain. Credit: Human Connectome Project.

Puberty is the defining process of adolescent development, beginning a cascade of changes throughout the body, including the brain. Penn Medicine researchers have discovered that cerebral blood flow (CBF) levels decreased similarly in males and females before puberty, but saw them diverge sharply in puberty, with levels increasing in females while decreasing further in males, which could give hints as to developing differences in behavior in men and women and sex-specific pre-dispositions to certain psychiatric disorders. Their findings are available in Proceedings of the National Academy of Science (PNAS).

"These findings help us understand normal neurodevelopment and could be a step towards creating normal 'growth charts' for brain development in kids. These results also show what every parent knows: boys and girls grow differently. This applies to the brain as well," says Theodore D. Satterthwaite, MD, MA, assistant professor in the Department of Psychiatry in the Perelman School of Medicine at the University of Pennsylvania. "Hopefully, one day such growth charts might allow us to identify much earlier before it leads to major mental illness."

Studies on structural have shown that is an important source of sex differences. Previous work has shown that CBF declines throughout childhood, but the effects of puberty on properties of brain physiology such as CBF, also known as cerebral perfusion, are not well known. "We know that adult women have higher blood flow than men, but it was not clear when that difference began, so we hypothesized that the gap between women and men would begin in adolescence and coincide with puberty," Satterthwaite says.

The Penn team imaged the brains of 922 youth ages 8 through 22 using arterial spin labeled (ASL) MRI. The youth were all members of the Philadelphia Neurodevelopmental Cohort, a National Institute of Mental Health-funded collaboration between the University of Pennsylvania Brain Behavior Laboratory and the Center for Applied Genomics at the Children's Hospital of Philadelphia.

They found support for their hypothesis.

Age related differences were observed in the amount and location of blood flow in males versus females, with declining at a similar rate before puberty and diverging markedly in mid-puberty. At around age 16, while male CBF values continue to decline with advanced age, females CBF values actually increased. This resulted in females having notably higher CBF than males by the end of adolescence. The difference between males and females was most notable in parts of the brain that are critical for social behaviors and emotion regulation such as the orbitofrontal cortex. The researchers speculate that such differences could be related to females' well-established superior performance on social cognition tasks. Potentially, these effects could also be related to the higher risk in women for depression and anxiety disorders, and higher risk of flat affect and schizophrenia in men.

More information: Impact of puberty on the evolution of cerebral perfusion during adolescence, PNAS, www.pnas.org/cgi/doi/10.1073/pnas.1400178111

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JVK
1 / 5 (1) May 26, 2014
Evolutionary theorists may not know that sex differences in the cell types of mammals are epigenetically effected by maternal nutrition and by the metabolism of nutrients to species-specific pheromones, which are associated with the epigenetic effects of food odors on the same central neuronal system.

The epigenetic effects of food odors and social odors complete the post-natal differentiation of cell types via conserved molecular mechanisms in species from microbes to man. In mammals, food odors and pheromones alter the secretion of GnRH, which modulates development of the central nervous system, neuroendocrine system, and reproductive system.

Evolutionary theorists typically attribute biodiversity and increasing organismal complexity to mutations, natural selection, and evolution. However, in mammals, epigenetic effects clearly are transmitted via the circulation of blood, which enables nutrients and pheromones to epigenetically effect sex differences in cell types.
JVK
1 / 5 (1) May 26, 2014
Molecular mechanisms for the inheritance of acquired characteristics—exosomes, microRNA shuttling, fear and stress: Lamarck resurrected? http://www.fronti...14.00133

Nutrient-dependent/pheromone-controlled adaptive evolution: a model
http://www.socioa...53/27989
anonymous_9001
5 / 5 (1) May 27, 2014
Intraorganismal differentiation and evolution are two separate things. Why you continue to insist that evolutionary theorists think they're the same is beyond me. Nobody claims that intraorganismal tissue differentiation is due to mutation. All the different cells in your body stem from the same genome, but the genome is not static over evolutionary time.
yvchawla
not rated yet May 27, 2014
The internal story of changes in CBF and so on is essentially represented in the form of 'feelings' in the front ground. When the 'feelings' (liked or disliked, pleasurable or non-pleasuarble) are experienced as they arise without labeling-one has a touch of the Original energy, the ground of all 'feelings', the ground of all changes.
JVK
1 / 5 (1) May 28, 2014
Sex specific changes in blood flow and odor perception that concurrently occur with puberty, link nutrient-dependent pheromone-controlled cell type differentiation in species from microbes to man via changes in the microRNA/messenger RNA balance, which result in amino acid substitutions that are fixed in the organized genome if the substitutions help to stabilize protein folding in all differentiated cell types. That's how ecological variation results in the ecological adaptations manifested in morphological and behavioral phenotypes that arise via ecological, social, neurogenic, and socio-cognitive niche construction with increasing organismal complexity that is not the result of mutations and natural selection.

http://medicalxpr...fts.html
Captain Stumpy
not rated yet May 29, 2014
ecological adaptations manifested in morphological and behavioral phenotypes that arise via ecological, social, neurogenic, and socio-cognitive niche construction with increasing organismal complexity that is not the result of mutations and natural selection
@jk
all fine and dandy and a nice word salad, but considering that, by your own admission, your own model creates MUTATIONS then what you are saying here is that your model is being ousted as a method for selection, right?
after all, since your model creates mutations, and you are arguing AGAINST mutations, then logically your model is being argued against, which means you are posting PSEUDOSCIENCE and known lies.

JVK
1 / 5 (1) May 29, 2014
"Sexual reproduction drives natural selection and adaptation of organisms by generating genetic diversity through recombination. This allows beneficial mutations to spread, and purges deleterious mutations in eukaryotic genomes [1,2]."
http://dx.doi.org....0080729

Claims like that have never been taken seriously by anyone who understands anything about biophysically constrained ecological adaptations, which are manifested in nutrient-dependent pheromone-controlled changes in morphology and behavior. Examples across species now include a moth-to-butterfly model. http://dx.doi.org...omms4957

I reported on this in my 2013 published review: "In Ostrinia moth species, substitution of a critical amino acid is sufficient to create a new pheromone blend (Lassance et al., 2013)."
http://www.ncbi.n...24693353

The substitution is nutrient-dependent; it does not result from any mutation. Mutation-driven evolution is pseudoscientific nonsense.
Captain Stumpy
not rated yet May 29, 2014
The substitution is nutrient-dependent; it does not result from any mutation. Mutation-driven evolution is pseudoscientific nonsense
@jk
you need to make up your mind, little guy
I asked
DOES your model make any changes to the nucleotide sequence of the genome of an organism, virus, or extrachromosomal genetic element?
This is a yes or no answer
to which jvk answered
YES!
--Thanks for asking...
IOW -YOUR model CAUSES MUTATIONS
http://phys.org/n...lts.html

So you are now saying that YOUR OWN MODEL IS PSEUDOSCIENCE NONSENSE
Mutation-driven evolution is pseudoscientific nonsense
so are you stupid or illiterate?
which one?

FFS,THIS is ONE reason why you are considered a pseudoscience hack: your ignorance of your field lexicon
your model is a part of evolution, and by arguing AGAINST mutations (and evolution), you argue AGAINST YOUR OWN MODEL, but USE your model as proof of argument
WTF?

JVK
1 / 5 (1) May 29, 2014
Two fixed differences among 597 amino acids drive a valine to alanine polymorphism that distinguishes morphological and behavioral phenotypes in white throated sparrows. In a clear indicator of what a single amino acid substitution can do, estrogen receptor 1 (ESR1), which is the gene that encodes estrogen receptor alpha (ERa), is most closely associated with what appears to be different nutrient-dependent hormone-organized and hormone-activated adult behavioral phenotypes.

A valine to alanine substitution also distinguishes a modern human population that arose during the past ~30K years from ancestral populations. The climate change, dietary change, and disappearance of the Neaderthals at the same time suggest nothing other than a nutrient-dependent pheromone-controlled ecological adaptation, which was modeled in the mouse.

Clearly, any idiot can claim that mutations cause something, but it is idiotic to say that my model causes mutations when it exemplifies ecological adaptations.
anonymous_9001
5 / 5 (1) May 30, 2014
Claims like that have never been taken seriously by anyone who understands anything about biophysically constrained ecological adaptations


You're the only one who wouldn't take that seriously. Isn't it funny how your own coauthors don't agree with you? Isn't it funny how when you point out somebody you consider a serious scientist (aka someone you think denies mutation and natural selection), I contact them and find out they don't agree with you?

How long is this going to go on? How long are you going to insist serious scientists have abandoned mutation and natural selection when, in fact, that's not true at all?

The substitution is nutrient-dependent; it does not result from any mutation.


If it were, it would be repeatable. You would be able to introduce the same nutrient to an organism without that substitution and watch it occur. Unfortunately, you can't, or else ALL of Lenski's populations would be Cit+ in aerobic environments.
JVK
1 / 5 (1) May 30, 2014
Former co-author, Bernhard Fink is co-editor of the journal "Evolutionary Psychology." This article appears and links moth predation by birds to predation in humans, which is somehow responsible for brain development. http://www.epjour...-humans/

Fink, and any of my co-authors who don't agree with me because they are uninformed and are committed to touting nonsense akin to the snake-centric theory of human evolution will continue to be among those cited in attempts to refute accurate representations of biologically based cause and effect by anonymous fools who also cite Lenski's works.

You can now discuss Fink's ridiculous views and compare them to established scientific facts while citing articles on snake-centric evolution in attempts to explain morphological and behavioral phenotypes. Go ahead, MAKE MY DAY! But watch out for snakes.

http://news.scien...te-brain
Captain Stumpy
not rated yet May 30, 2014
Clearly, any idiot can claim that mutations cause something, but it is idiotic to say that my model causes mutations when it exemplifies ecological adaptations
@jk
BUT YOU SAID IT!
YOU cannot understand/comprehend the lexicon of your field!
I give it to you again: your model DOES cause mutations, per the definition of the word used by biologists and geneticists in your field, remember? I asked
DOES your model make any changes to the nucleotide sequence of the genome of an organism, virus, or extrachromosomal genetic element?
This is a yes or no answer
to which you answered
YES!
--Thanks for asking
so, drawing from your own words AGAIN...
IF it is idiotic to say that your model causes mutations
it is idiotic to say that my model causes mutations
AND you say yourself that your model causes mutations
YES!
--Thanks for asking
THEN one can only conclude, per your own words and conclusions, that YOU are an IDIOT!
this is your own logic and in your own words, jk.
Captain Stumpy
not rated yet May 30, 2014
any of my co-authors who don't agree with me because they are uninformed and are committed to touting nonsense akin to the snake-centric theory of human evolution will continue to be among those cited in attempts to refute accurate representations of biologically based cause and effect by anonymous fools who also cite Lenski's works
@jk
so what you are saying here is: logic, science and empirical data be damned, I will not believe it because it does NOT conform to my faith/religion/personal delusion or what I think/feel the world SHOULD look like????
WOW!

THIS is ONE MAJOR DEFINING FACTOR of PSEUDOSCIENCE

you are saying that not only do you conform to the definition of a pseudoscience spamming troll, but that you are proud to admit it and ignore empirical data as well as modern science because you have a system of belief that promotes ignorance over intellect and rewards the dedicated acolyte!

thanks for pointing this out... but we already knew this about you
FFS
JVK
1 / 5 (1) May 30, 2014
This is pseudoscience, you idiot!

"[W]hat Haldane, Fisher, Sewell Wright, Hardy, Weinberg et al. did was invent.... The anglophone tradition was taught. I was taught, and so were my contemporaries, and so were the younger scientists. Evolution was defined as "changes in gene frequencies in natural populations." The accumulation of genetic mutations was touted to be enough to change one species to another.... No, it wasn't dishonesty. I think it was wish fulfillment and social momentum. Assumptions, made but not verified, were taught as fact."

"I would certainly go along with the view that gradual mutation followed by selection has not, as a matter of fact, been demonstrated to be necessarily a cause of speciation."

http://www.huffin...211.html

See for comparison: http://figshare.c...s/994281
JVK
1 / 5 (1) May 30, 2014
You would be able to introduce the same nutrient to an organism without that substitution and watch it occur.


The mouse model of nutrient-dependent pheromone-controlled ecological adaptation was extended to humans in experiments by Harvard researchers that showed how the same base pair change and single nutrient-dependent amino acid substitution was manifested in the morphological phenotype of a modern human population.

I have repeatedly cited the works of Kamberov et al (2013) and Grossman et al (2013) and everyone else, including Nicholas Wade in his latest book, ignores the mouse-to-human model and continues to discuss research that misrepresents what they showed, which was how ecological variation results in ecological adaptations -- no matter how it was reported (in terms of mutations, genetic variants, beneficial mutations, beneficial variants etc.)
JVK
1 / 5 (1) May 30, 2014
You would be able to introduce the same nutrient to an organism without that substitution and watch it occur.


"Consistently, TET1 regulates 5-hydroxymethylcytosine (5hmC) formation at loci critical for MET in a vitamin C–dependent fashion. Our findings suggest that vitamin C has a vital role in determining the biological outcome of TET1 function at the cellular level."

No need to cite the source, unless someone first looks at the model that includes the epigenetic effect (i.e., my model) of vitamin C.
anonymous_9001
5 / 5 (1) May 30, 2014
I can't believe I have to spell this out. I'm talking about GENETIC changes. Vitamin C in that example is inducing an epigenetic mark, not a codon change.
dollymop
not rated yet Jun 01, 2014
amusing. it really looks as if all the screaming and insults in the comments are from males.

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