Free childbirth ebook from Connie

Dear Readers,

I am sharing my childbirth and women’s health ebook to all.

When Birthing Ways Healing Ways came out at amazon , sold my ebook to Amazon and so I did not get a penny. I was new to publishing and I love writing about my childbirth experience with Nurse Midwives in the bay area so I write for it is my passion.

So now, I am giving away my ebook in the hopes of getting referrals to my bay area senior caregiving , health coaching and health talks and soon an ecommerce site for

The link below contains my ebook, email me at for your feedback.

Once I massaged a pregnant woman while I provide childbirth tips to her. She followed my advice of walking one mile a day and other tips. Two weeks later she had her baby and only spent two hours in labor at the hospital. All natural birth happened so bonding with mother and baby went well.

During the three years that I was a full time mother to care for my two toddlers, I read medical, nursing and midwifery books which led me to my contract job as pharmacy technician instructor in the bay area which lasted for a year and  then I went back to the corporate world.

When pregnant, walk a mile a day for easy labor. When the baby is born, massage baby with calendula oil before each bath.

Happy birthing so they say. I also pray to parents who lost their babies via environmental toxins, miscarriage, forces of nature but seldom through childbirth in this century. May God and their community give them lots of love.




Birthing Ways Healing Ways connie of clubalthea 4088541883

Early synapse loss to Alzheimer’s disease

synapse loss.JPG


Structure of a typical chemical synapse

In the nervous system, a synapse[1] is a structure that permits a neuron (or nerve cell) to pass an electrical or chemical signal to another neuron or to the target efferent cell.

Santiago Ramón y Cajal proposed that neurons are not continuous throughout the body, yet still communicate with each other, an idea known as the neuron doctrine.[2] The word “synapse” – from the Greek synapsis (συνάψις), meaning “conjunction”, in turn from συνάπτεὶν (συν (“together”) and ἅπτειν (“to fasten”)) – was introduced in 1897 by the English neurophysiologist Charles Sherringtonin Michael Foster‘s Textbook of Physiology.[1] Sherrington struggled to find a good term that emphasized a union between two separate elements, and the actual term “synapse” was suggested by the English classical scholar Arthur Woollgar Verrall, a friend of Michael Foster.[3][4]Some authors generalize the concept of the synapse to include the communication from a neuron to any other cell type,[5] such as to a motor cell, although such non-neuronal contacts may be referred to as junctions (a historically older term).

Synapses are essential to neuronal function: neurons are cells that are specialized to pass signals to individual target cells, and synapses are the means by which they do so. At a synapse, the plasma membrane of the signal-passing neuron (the presynaptic neuron) comes into close apposition with the membrane of the target (postsynaptic) cell. Both the presynaptic and postsynaptic sites contain extensive arrays of a molecular machinery that link the two membranes together and carry out the signaling process. In many synapses, the presynaptic part is located on an axon and the postsynaptic part is located on a dendrite or somaAstrocytes also exchange information with the synaptic neurons, responding to synaptic activity and, in turn, regulating neurotransmission.[6] Synapses (at least chemical synapses) are stabilized in position by synaptic adhesion molecules (SAMs) projecting from both the pre- and post-synaptic neuron and sticking together where they overlap; SAMs may also assist in the generation and functioning of synapses.[7]

Chemical or electrical

An example of chemical synapse by the release of neurotransmitters like acetylcholine or glutamic acid.

There are two fundamentally different types of synapses:

  • In a chemical synapse, electrical activity in the presynaptic neuron is converted (via the activation of voltage-gated calcium channels) into the release of a chemical called a neurotransmitter that binds to receptors located in the plasma membrane of the postsynaptic cell. The neurotransmitter may initiate an electrical response or a secondary messenger pathway that may either excite or inhibit the postsynaptic neuron. Chemical synapses can be classified according to the neurotransmitter released: glutamatergic (often excitatory), GABAergic (often inhibitory), cholinergic (e.g. vertebrate neuromuscular junction), and adrenergic (releasing norepinephrine). Because of the complexity of receptor signal transduction, chemical synapses can have complex effects on the postsynaptic cell.
  • In an electrical synapse, the presynaptic and postsynaptic cell membranes are connected by special channels called gap junctions or synaptic cleft that are capable of passing an electric current, causing voltage changes in the presynaptic cell to induce voltage changes in the postsynaptic cell. The main advantage of an electrical synapse is the rapid transfer of signals from one cell to the next.[8]

Synaptic communication is distinct from an ephaptic coupling, in which communication between neurons occurs via indirect electric fields.

An autapse is a chemical or electrical synapse that forms when the axon of one neuron synapses onto dendrites of the same neuron.

Types of interfaces

Synapses can be classified by the type of cellular structures serving as the pre- and post-synaptic components. The vast majority of synapses in the mammalian nervous system are classical axo-dendritic synapses (axon synapsing upon a dendrite), however, a variety of other arrangements exist. These include but are not limited to axo-axonic, dendro-dendritic, axo-secretory, somato-dendritic, dendro-somatic, and somato-somatic synapses.

The axon can synapse onto a dendrite, onto a cell body, or onto another axon or axon terminal, as well as into the bloodstream or diffusely into the adjacent nervous tissue.

Different types of synapses

Role in memory

It is widely accepted that the synapse plays a role in the formation of memory. As neurotransmitters activate receptors across the synaptic cleft, the connection between the two neurons is strengthened when both neurons are active at the same time, as a result of the receptor’s signaling mechanisms. The strength of two connected neural pathways is thought to result in the storage of information, resulting in memory. This process of synaptic strengthening is known as long-term potentiation.[9]

By altering the release of neurotransmitters, the plasticity of synapses can be controlled in the presynaptic cell. The postsynaptic cell can be regulated by altering the function and number of its receptors. Changes in postsynaptic signaling are most commonly associated with a N-methyl-d-aspartic acid receptor (NMDAR)-dependent long-term potentiation (LTP) and long-term depression (LTD) due to the influx of calcium into the post-synaptic cell, which are the most analyzed forms of plasticity at excitatory synapses.[10]

Study models

For technical reasons, synaptic structure and function have been historically studied at unusually large model synapses, for example:

Synaptic polarization

The function of neurons depends upon cell polarity. The distinctive structure of nerve cells allows action potentials to travel directionally (from dendrites to cell body down the axon), and for these signals to then be received and carried on by post-synaptic neurons or received by effector cells. Nerve cells have long been used as models for cellular polarization, and of particular interest are the mechanisms underlying the polarized localization of synaptic molecules. PIP2 signaling regulated by IMPase plays an integral role in synaptic polarity.

Phosphoinositides (PIP, PIP2, and PIP3) are molecules that have been shown to affect neuronal polarity.[12] A gene (ttx-7) was identified in Caenorhabditis elegans that encodes myo-inositol monophosphatase (IMPase), an enzyme that produces inositol by dephosphorylating inositol phosphate. Organisms with mutant ttx-7 genes demonstrated behavioral and localization defects, which were rescued by expression of IMPase. This led to the conclusion that IMPase is required for the correct localization of synaptic protein components.[13][14] The egl-8 gene encodes a homolog of phospholipase Cβ (PLCβ), an enzyme that cleaves PIP2. When ttx-7 mutants also had a mutant egl-8 gene, the defects caused by the faulty ttx-7 gene were largely reversed. These results suggest that PIP2 signaling establishes polarized localization of synaptic components in living neurons.[13]

Toxic metals and BPA in babies and copper as culprit in Alzheimer’s brain

Image shows DNA strands.
The image shows the s1 of a mouse cerebral cortex.

Lending Late Neurons a Helping Hand

All kinds of positive and loving stimulation of the newborn using massage, breastfeeding, and other forms of communication help in growing neurons.



Lending Late Neurons a Helping Hand

Summary: Delayed neural migration in fetuses may cause behavioral disorders similar to autism, researchers report.

Source: University of Geneva.

During the foetal stage, millions of neurons are born in the walls of the ventricles of the brain before migrating to their final location in the cerebral cortex. If this migration is disrupted, the new-born baby may suffer serious consequences, including intellectual impairment. What happens, however, if the migration takes place but is delayed?

Researchers at the University of Geneva (UNIGE), Switzerland, have discovered that even a slight delay may lead to behavioural disorders that are similar to autistic characteristics in human. Furthermore, they found that these disorders are due to the abnormally low activity of the late neurons, which leads to permanent deficit of interneuronal connections.


The Geneva neuroscientists succeeded in correcting the activity of the relevant neurons, thereby restoring the missing connections and preventing the appearance of behavioural disorders.

The results, which are published in the journal Nature Communications, will open up new avenues for preventing neurodevelopmental disorders linked to the cerebral cortex.

Neurons at the foetal stage are generated in the walls of the brain’s ventricles before migrating to their final destination in the cerebral cortex between the sixth and sixteenth week of pregnancy in women. This migration is governed by numerous molecular signals that control the tempo of this movement so that neurons arrive at the right place at the right time. If this migration is permanently disrupted, the new-born infant could suffer mental deficiencies or epileptic seizures, for example. But what happens if neurons arrive at the right place but are delayed?

The importance of punctuality for creating neural connections

“To find an answer, we manipulated in utero the Wnt signalling pathways which regulates the pace of migration in a few thousand rat neurons, begins Jozsef Kiss, professor in the Department of Basic Neuroscience at UNIGE’s Faculty of Medicine, so that the neurons are positioned appropriately but late. We then checked that they were in the right place and conducted various behaviour tests on the rats once they became adult”. The neuroscientists made two discoveries: not only did the rats exhibit sociability problems but they also developed repeated compulsive behaviours – both of which are symptoms related to autism in humans. But how can the late arrival of just a few thousand neurons out of millions disrupt brain function to such a degree?

“When we marked the late neurons,” continues professor Kiss, “we observed that they receive fewer fibres and, as a result, create fewer synaptic contacts with the other neurons compared to a ‘punctual’ neuron. This lack of connections leads to a decrease in neuronal activity, which ultimately has an impact on the interactions and connectivity between the left and right hemispheres of the brain”. The late neurons, since they are poorly connected at the outset, establish fewer contacts with their counterparts in the other hemisphere. During the post-natal period in rats, the neurons only have ten or so days to develop these connections between the two hemispheres: hence the impact of a delay of a few days on the development of the brain and the resulting behavioural consequences.

Making up for lost time!

The UNIGE researchers subsequently explored the possibility of catching up on the time lost by the neurons that did not migrate on schedule by stimulating their activity remotely. “We added a gene to the late neurons so that we could control the neuronal activity remotely. We stimulated them when we wanted to in order to try to make up for the delay and subsequent lack of activity. And it worked!” says Kiss. In fact, thanks to the remote activation ‘therapy’, the researchers found that the connections between the two hemispheres were formed correctly and that no behavioural disorders appeared in the adult rats. “But it has to be done during the critical period,” adds Kiss. “In other words, during the ten days postnatally; when the inter-hemispheric connections develop in the rats. The activation of neurons after this so-called “critical period” will not rescue normal connectivity and behaviour.”

The neuroscientists at UNIGE have demonstrated for the first time that, although a brain may be formed normally, it can malfunction due to delayed neuronal migration. This handful of badly integrated neurons appear sufficient to disrupt communication between the two hemispheres of the brain, inducing behavioural problems. More surprisingly, we now know that the effects of migration delay on the connectivity can be reversed if the neuronal activity is stimulated externally in a controlled manner during the critical period of axon development. As Professor Kiss concludes: “We can now think of ways of detecting a delay in interhemispheric connections and devise ‘activation therapies’ at clinical level to prevent the behavioural problems observed in neurodevelopmental disorders such as autism.”


Source: Jozsef Kiss – University of Geneva
Publisher: Organized by
Image Source: image is credited to Bocchi et al. Nature Communication 2017.
Original Research: Full open access research for “Perturbed Wnt signaling leads to neuronal migration delay, altered interhemispheric connections and impaired social behavior” by Riccardo Bocchi, Kristof Egervari, Laura Carol-Perdiguer, Beatrice Viale, Charles Quairiaux, Mathias De Roo, Michael Boitard, Suzanne Oskouie, Patrick Salmon & Jozsef Z. Kiss in Nature Communications. Published online October 27 2017 doi:10.1038/s41467-017-01046-w

University of Geneva “Lending Late Neurons a Helping Hand.” NeuroscienceNews. NeuroscienceNews, 7 November 2017.


Perturbed Wnt signaling leads to neuronal migration delay, altered interhemispheric connections and impaired social behavior

Perturbed neuronal migration and circuit development have been implicated in the pathogenesis of neurodevelopmental diseases; however, the direct steps linking these developmental errors to behavior alterations remain unknown. Here we demonstrate that Wnt/C-Kit signaling is a key regulator of glia-guided radial migration in rat somatosensory cortex. Transient downregulation of Wnt signaling in migrating, callosal projection neurons results in delayed positioning in layer 2/3. Delayed neurons display reduced neuronal activity with impaired afferent connectivity causing permanent deficit in callosal projections. Animals with these defects exhibit altered somatosensory function with reduced social interactions and repetitive movements. Restoring normal migration by overexpressing the Wnt-downstream effector C-Kit or selective chemogenetic activation of callosal projection neurons during a critical postnatal period prevents abnormal interhemispheric connections as well as behavioral alterations. Our findings identify a link between defective canonical Wnt signaling, delayed neuronal migration, deficient interhemispheric connectivity and abnormal social behavior analogous to autistic characteristics in humans.

“Perturbed Wnt signaling leads to neuronal migration delay, altered interhemispheric connections and impaired social behavior” by Riccardo Bocchi, Kristof Egervari, Laura Carol-Perdiguer, Beatrice Viale, Charles Quairiaux, Mathias De Roo, Michael Boitard, Suzanne Oskouie, Patrick Salmon & Jozsef Z. Kiss in Nature Communications. Published online October 27 2017 doi:10.1038/s41467-017-01046-w

Depression in Pregnancy and Low Birth Weight Tied to Biomarker

Summary: Researchers discover a link between low levels of BDNF protein, depression in pregnant women and low birth weight.

Source: Mediasource.

Depression is very common during pregnancy, with as many as one in seven women suffering from the illness and more than a half million women impacted by postpartum depression in the U.S. alone. The disorder not only affects the mother’s mood, but has also been linked to influencing the newborn’s development, according to recent research.

Lower blood levels of a biomarker called brain-derived neurotrophic factor (BDNF) have been associated with depression in multiple studies, mainly in non-pregnant adults.

Now, in a study published in the journal Psychoneuroendocrinology, research from The Ohio State University Wexner Medical Center found that BDNF levels change during pregnancy, and can cause depression in the mother and low birth weight in the baby.

“Our research shows BDNF levels change considerably across pregnancy and provide predictive value for depressive symptoms in women, as well as poor fetal growth. It’s notable that we observed a significant difference in BDNF in women of different races,” said Lisa M. Christian , an associate professor of psychiatry in the Institute for Behavioral Medicine Research at Ohio State’s Wexner Medical Center and principal investigator of the study.

Researchers took blood serum samples during and after pregnancy from 139 women and observed that BDNF levels dropped considerably from the first through the third trimesters, and subsequently increased at postpartum.

Image shows a pregnant woman.

Overall, black women exhibited significantly higher BDNF than white women during the perinatal period.

Controlling for race, lower BDNF levels at both the second and third trimesters predicted greater depressive symptoms in the third trimester. In addition, women delivering low versus healthy weight infants showed significantly lower BDNF in the third trimester, but didn’t differ in depressive symptoms at any point during pregnancy, which suggests separate effects.

“The good news is there are some good ways to address the issue,” Christian said. “Antidepressant medications have been shown to increase BDNF levels. This may be appropriate for some pregnant women, but is not without potential risks and side effects.”

“Luckily, another very effective way to increase BDNF levels is through exercise,” she said.” With approval from your physician, staying physically active during pregnancy can help maintain BDNF levels, which has benefits for a woman’s mood, as well as for her baby’s development.”

Other Ohio State researchers who participated in this study were Amanda M. Mitchell, Shannon L. Gillespie and Marilly Palettas.


Funding: Funding from the Eunice Kennedy Shriver National Institute for Child Health and Human Development supported this research.

Source: Drew Schaar – Mediasource
Image Source: image is credited to The Ohio State University Wexner Medical Center.
Video Source: Video credited to OSU Wexner Medical Center.
Original Research: Abstract for “Serum brain-derived neurotrophic factor (BDNF) across pregnancy and postpartum: Associations with race, depressive symptoms, and low birth weight” by Lisa M. Christian, Amanda M. Mitchell, Shannon L. Gillespie, and Marilly Palettas in Psychoneuroendocrinology. Published online August 27 2016 doi:10.1016/j.psyneuen.2016.08.025

Mediasource “Depression in Pregnancy and Low Birth Weight Tied to Biomarker.” NeuroscienceNews. NeuroscienceNews, 12 January 2017.


Serum brain-derived neurotrophic factor (BDNF) across pregnancy and postpartum: Associations with race, depressive symptoms, and low birth weight

Brain-derived neurotrophic factor (BDNF) is implicated as a causal factor in major depression and is critical to placental development during pregnancy. Longitudinal data on BDNF across the perinatal period are lacking. These data are of interest given the potential implications for maternal mood and fetal growth, particularly among Black women who show ∼2-fold greater risk for delivering low birth weight infants.

Serum BDNF, serum cortisol, and depressive symptoms (per CES-D) were assessed during each trimester and 4–11 weeks postpartum among 139 women (77 Black, 62 White). Low birth weight (<2500 g) was determined via medical record. Results Serum BDNF declined considerably from 1st through 3rd trimesters (ps ≤ 0.008) and subsequently increased at postpartum (p < 0.001). Black women exhibited significantly higher serum BDNF during the 1st trimester, 2nd trimester, and postpartum (ps ≤ 0.032) as well as lower serum cortisol during the 2nd and 3rd trimester (ps ≤ 0.01). Higher serum cortisol was concurrently associated with lower serum BDNF in the 2nd trimester only (p < 0.05). Controlling for race, serum BDNF at both the 2nd and 3rd trimester was negatively associated with 3rd trimester depressive symptoms (ps ≤ 0.02). In addition, women delivering low versus healthy weight infants showed significantly lower serum BDNF in the 3rd trimester (p = 0.004). Women delivering low versus healthy weight infants did not differ in depressive symptoms at any time point during pregnancy (ps ≥ 0.34).

Serum BDNF declines considerably across pregnancy in Black and White women, with overall higher levels in Blacks. Lower serum BDNF in late pregnancy corresponds with higher depressive symptoms and risk for low birth weight in Black and White women. However, the predictive value of serum BDNF in pregnancy is specific to within-race comparisons. Potential links between racial differences in serum BDNF and differential pregnancy-related cortisol adaptation require further investigation.

“Serum brain-derived neurotrophic factor (BDNF) across pregnancy and postpartum: Associations with race, depressive symptoms, and low birth weight” by Lisa M. Christian, Amanda M. Mitchell, Shannon L. Gillespie, and Marilly Palettas in Psychoneuroendocrinology. Published online August 27 2016 doi:10.1016/j.psyneuen.2016.08.025