One group’s diet included choline while the other did not.  Examining their brain cells researchers found the group that did not receive choline had epigenetic changes on the proteins that wrap genes in cells responsible for the creation of new brain cells.  The  two proteins  (G9a and Calb1) responsible for new neuronal cell creation and maturation in the hippocampus were altered in the group that did not receive choline.

Gerald Weissmann, MD Editor-in Chief of the FASEB Journal said.  “This is yet another example showing that good prenatal nutrition is vitally important throughout a child’s entire lifetime.”

Choline is found in meat, nuts and eggs.

http://www.sciencedaily.com/releases/2010/01/10010410113.htm

One explanation is that the hormone prolactin may play a role, in that the prolactin stimulates both the onset of maternal behavior as well as new neurons.  The other explanation is that the stimulation from the young themselves plays a crucial role in increasing neurons in the maternal rats.

http://www.sciencedaily.com/releases/2009/12/091217115832.htm

Lead author Shanna H. Swan Ph.D professor of Obstetricts and Gynecology, director of the URMC Center for Reproductive Epidemiology, and expert in phthalates said, “Because testosterone produces the masculine brain, researchers are concerned that fetal exposure to anti-androgens such as phthalates – which are pervasive in the environment – has the potential to alter masculine brain development”.

Previous findings also showed that phthalates altered male genital development.

Food packaged, stored or cooked in plastic is a major source of exposure for humans.  Phthalates are used to soften plastic, soaps, shampoos, lotions, vinyl and many other household products.   You can find more information on phthalates at Wikipedia

Another study published in February 2008 also found “Babies Recently Treated With Lotion, Shampoo, And Powder More Likely To Have Phthalates Chemicals In Urine“.

And the recent study can be found here http://www.sciencedaily.com/releases/2009/11/091116085040.htm

Researchers have already treated cancer and cardiovascular disease by developing drugs that increase or decrease growth factors.  Growth factors are proteins that stimulate growth and typically act as signaling molecules between cells.

Abnormalities in the number and shape of dendritic spines, the protrusions that allow communication between brain neurons have been implicated in some developmental disorders.  Previous studies have found that the growth factor, BDNF (brain derived neurotrophic factor) regulates the number and shape of dendritic spines required for spatial learning and memory.

When researchers from Georgetown University Medical Centre halted the transport of BDNF to dendritic spines, it caused dendritic spine abnormalities in mice that resembled those in humans with certain developmental disorders, they also had impaired learning and memory.

BDNF plays a key role in the regulation, survival, growth and maintenance of neurons.  A study in 2006 found that BDNF is released from the brain and is inhibited by high blood glucose levels, but interestingly not by high insulin levels.

We know that brain function is better when blood glucose is stable and can argue that this relationship of regulation between blood glucose and BDNF could be one of the reasons.  It also strengthens the case for maintaining stable blood glucose during pregnancy whether you have gestational diabetes or not.

Researchers hope to develop drugs that will increase the transport of BDNF to treat developmental disorders.

http://www.sciencedaily.com/releases/2009/10/091020161950.htm

http://docs.google.com/gview?a=v&q=cache:4oMaH5CK75IJ:inflammation-metabolism.dk/misc/download.php%3Furl%3D../files/reprints/PMID%252017151862.pdf%26type%3Dtxt+BDNF+insulin&hl=en&gl=au&pid=bl&srcid=ADGEESgn8a2FCxdG11aifqoZC6gU-Gwh4G8sLvmP8oLjCwCZJrJTHamb3tCI2dlfLmUnQ6r5pLR30wIw_wOl4nm7f8MD0fbmmXtw80iaIWgwd8ksCLWURg0GvTV0inU2-iae-wmEM2y0&sig=AFQjCNEVSfHhXbKHY0k6LbMKHN-nZRWs8w

A surprise discovery in an Alzheimer’s disease study found that a high protein, low carbohydrate diet may lead to a smaller brain with a less developed hippocampus.

Researchers compared the following diets;

a regular diet

a high fat/low carbohydrate custom diet

a high protein/low carb diet

a high carbohydrate/low fat diet

Looking for triggers in brain plaque formation associated with Alzheimer’s, the researchers made the unexpected discovery that compared to the other three diets the brains of mice fed a high protein/low carb diet had brains that weighed 5% less, with the hippocampus also less developed.

Researchers will now undertake further studies on mice not engineered to develop Alzheimers disease to test the result.

http://www.sciencedaily.com/releases/2009/10/091020192206.htm

“It is commonly agreed that the precise placement and strength of each person’s trillions of synaptic connections closely maps with that person’s cognitive, emotional and behavioral makeup.”

A key molecular player in guiding the formation of synapses have been identified by researchers at the Stanford University School of Medicine and this discovery has raised concern about the use of the antiseizure drug Gabepentin during pregnancy.

Gabepentin originally developed for epilepsy is also used as pain reliever, especially for people suffering from chronic pain.

Professor and chair of neurobiology Ben Barres MD, PhD said “We have solved the longstanding mystery of how this blockbuster drug acts.”

In 2005 Professor Barres and colleagues discovered that the protein thrombospondin, secreted by astrocytes, are essential for synapses formation.  In this most recent study they demonstrated how thrombospondin binds to a receptor named alpha2delta-1, found on neurons outer membranes.  Neurons lacking alpha2delta-1 were unable to form synapses.

They also grew neurons bioengineered to overexpresss alpha2delta-1 in a dish, neurons grew twice as many synapses when stimulated with thrombospondin than unmodified neurons.

Barres and colleagues found that the drug Gabepentin prevented the formation of new synapses by binding to alpha2delta-1, preventing thrombospondin from binding to this receptor.     Because adult brains don’t form many synapses, produces very little thrombospondin  and Gabepentin did not dissolve pre-existing synapses, it does not pose an enormous risk to adults.  However, because the majority of synapses are formed during development and the early years, Gabepentin poses a serious threat for a developing baby.

Professor Barres said “It’s a bit scary that a drug that can so powerfully block synapse formation is being used in pregnant women… there is no question that pregnant women with epilepsy who have been advised by their neurologists to continue their anticonvulsant treatment with Gabapentin during their pregnancy should definitely remain on this drug until instructed otherwise.  But there is no long term registry being kept to track Gabapentin-exposed babies.  Our findings are saying that we need to be following up on these newborns so that their cognitive performance can be studied as they grow older.”

http://www.sciencedaily.com/releases/2009/10/091008123226.htm

“There is a large body of scientific literature in humans that points the finger at PCB’s, linking them to neurodevelopmental problems we see in kids,” said Pamela Lein, lead author.

The first showed that low level exposure in utero and neonatal exposure alter the development of brain cells.  In fact low level exposure had more pronounced effects than a higher dosage.

“We think that one of the major reasons we have not seen effects in previous studies is that at higher doses PCB’s become toxic to cells and the brain has defense mechanisms to deal with disposing of these damaged cells,” said Pessah.  “Future studies of PCB’s and related compounds should be examined at lower doses more relevant to human exposures” he continued.

The second study showed that PCB’s affected brain-cell circuits in the hippocampus, an area in the brain known to be impaired in many neurodevelopmental disorders and behavioral disorders like autism, ADHD, learning disabilities, sensory deficits, developmental delays and mental retardation.

The third study describes the effect of PCB’s in detail on a molecular level.  They found that PCB’s lock the calcium channels in the brain in the open position, resulting in over-excitations on neural circuits.

Calcium channels are responsible for generating the signals needed for the extension and branching of dendrites.

PCB exposure, in utero and neonatal, alters dendritic plasticity.  Dendrites receive signals from other cells in the body, and changes shape in response to the signals they receive.  The study showed how this alteration in plasticity negatively affected learning.

Pamela Lein said, “Dendritic plasticity is important to how we process information and, when you perturb that, you interfere with complex behaviors like learning and memory.”

Examining the hippocampus, Pessah said he believes PCB’s lead to overgrowth of dendrites and inhibition of neonatal pruning that takes place during gestational development.  Brain cells exposed to PCB’s cannot respond to proper learning.

Explaining why some children go on to develop autism while others don’t, Pessah said, “We think that in autism, for example, at-risk children have deficient inhibitory circuits.  So, if you have a PCB that promotes the excitatory side of the circuit, they would be much more at risk of developing the disorder.”

The question for me now is why “at risk children” have deficient inhibitory circuits? Are there some other chemicals out there that can cause deficient inhibitory circuits, like for example cigarette smoke, and is it possible that certain nutrients, a hormone like vitamin D or overall a good nutrient rich diet can protect against this predisposition?

You can find more information on PCB’s here

http://www.sciencedaily.com/releases/2009/04/090413204546.htm

The latest finding in animal studies, “A Diet High In Fructose Impairs Memory”. There is mounting evidence that insulin levels and function in the brain is vital to learning and memory. Also explaining the link between diabetes, Alzheimer’s and impaired cognition.

Research shows that levels of brain insulin and its related receptors are disrupted in people that suffer from Diabetes, and in people suffering from Alzheimer they found diminished insulin receptor signaling. Scientists found that disruption of insulin signaling with receptors leads to loss of synapses functioning, vital for connectivity between brain cells.

A landmark study in June 2008 on tadpoles found that Insulin receptors in the brain regulate the maintenance of synapses, contributes to the processing of sensory information and is involved in adjusting the plasticity
of brain circuits.
Two remarkable facts came from this study ;

The insulin receptor correlates with the
density of the synapses (neuron to neuron connections) in brain circuits. Synaptic density is maintained by the insulin receptors and when the receptors are dysfunctional the synaptic density decreased.
Insulin receptor signaling regulate the formation and function of brain circuits in
response to experience or learning.
And they just keep rolling in, a study in June this year headlined “Brains Plasticity Changes And Resets In Homeostasis”.

What does this mean for your baby?

Your brain use more glucose than any other organ in your body, and during pregnancy your baby’s brain needs a constant supply of glucose to develop. However whilst keeping up this flow of glucose to your baby, you need to stick to low GI carbohydrates to make sure you do not elevate insulin levels. Make each one count, keep it as nutritious as you possibly can.

Don’t eat for your body, eat for your baby’s brain, the knock on effect will have a better outcome for both you and your baby, physically and mentally.

http://www.sciencedaily.com/releases/2009/07/090716113247.htm

http://www.cshl.edu/public/releases/08_insulin_receptor.html

Researchers found 229 genes that are active at the beginning of neurogenesis, involved in forming the initial scaffolding for assembling cortical circuits. Surprisingly the genes include a substantial network related to the sex hormone estrogen .

Mary E. Hatten, Frederick P. Rose Professor and head of the Laboratory of Developmental Neurobiology said, “That these sex pathways are involved from the get-go is a particular surprise. The research provides a new starting point for people to say, “What exactly, are all of these new pathways doing?””

A question I would like to see answered sooner rather than later is, if estrogen is involved in early brain development, how does oestrogen mimics in the many products pregnant women are exposed to on a daily
basis influence early brain development?

http://www.sciencedaily.com/releases/2009/05/090530173757.htm

Dio3 is a gene that control thyroid hormone levels in the fetal brain. Laura Sittig a student from Northwestern University Feinberg School of Medicine said, “Specific concentrations of thyroid hormones must be available in the fetal brain to support normal neurological development.”

The researchers hypothesized that alcohol exposure in the womb cause epigenetic changes to developmental genes like Dio3 in the fetal brain. They tested their theory by studying the gene Dio3 in rats.
Dio3 normally originate from the father’s gene, while the maternal gene is silenced by epigenetic control.
The study author’s found that alcohol changes the paternal-maternal dosage of Dio3 and this increases the amount of the gene present in certain brain regions of the fetus.

This increase reduces the availability of thyroid hormones in the parts of the brain that control learning, memory and emotional behaviors. Sittig said, “In light of our current finding we can begin testing specific dietary supplements that could reverse the epigenetic alterations that disrupt the regulation of Dio3. When given to the mother or newborn, this might correct the imprinting deficits induced by alcohol.”

http://www.sciencedaily.com/releases/2009/06/090610124426.htm