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Postpartum depression (PPD) is a condition that affects new mothers (or biological mothers) after childbirth.
About 10–15% of adult mothers yearly are affected by it every year.
Symptoms can include feelings of sadness, emptiness, hopelessness, and worthlessness and can last for weeks or months.
It can make it very difficult for new mothers to care for their babies and lead to sleep, appetite, and mood problems.
The effects on children may include behavioral, developmental, socioemotional, and cognitive delay and may last years beyond infancy.
Studies suggest that individual susceptibility to the development of PPD is related to the presence or absence of certain genetic changes associated with PPD risk.
Till now, hormones have been taught to be the biggest contributor to PPD. Estrogen and progesterone levels increase 10-fold during pregnancy.
The dramatic drop in these hormone levels after childbirth can contribute to the symptoms of PPD.
The levels of thyroid hormones seem to play a role in PPD.
They may also drop after giving birth, contributing to PPD.
Sleep deprivation and early-stage motherhood go hand-in-hand.
This accumulated fatigue can cause a dip in mood and energy.
The symptoms of sleep deprivation and PPD have a lot of overlap that sometimes, it can be difficult to each other apart.
The relationship between sleep and PPD is a two-way street; each can aggravate the other.
According to a study, the risk of depression in women with poor sleep quality was 3.34 times higher than in those with good sleep quality.
Compared to mothers with temporary sleep disturbances, those who consistently report very poor or drastically decreasing sleep quality are more likely to develop PPD.
Other risk factors for PPD are:
Studies show that 1 in 10 dads suffer from PPD.
Research describes certain hormonal changes in dads that promote their attachment to their newborns.
These may include decreased testosterone levels and increased estrogen, prolactin, and cortisol levels.
The hormonal changes may also increase the risk of PPD in men.
Other non-hormonal factors that are involved in PPD include:
Some signs of PPD in men are:
PPD was long thought to be due to the sudden drop in hormones following childbirth.
However, studies have reported nos significant differences in the hormone levels between depressed and non-depressed mothers.
But there’s a possibility that some may be more sensitive to hormonal fluctuations than others.
A group of researchers from Johns Hopkins studied the epigenetic changes introduced in the hippocampus by estrogen.
*epigenetic changes are DNA modifications that turn a gene “on” or “off.”
*hippocampus is a part of the brain governing moods.
They identified the involvement of two genes, TTC9B and HP1B3, in hippocampal activity.
They may regulate the brain’s ability to recognize and adapt to new situations - the two key elements of mood.
Estrogen seems to behave as an antidepressant, supporting the activity of these genes.
The researchers later replicated this experiment in 52 pregnant women with mood disorders.
They note that those with PPD had significant epigenetic changes in those genes that interact the most with estrogen.
This may make them more sensitive to the hormone’s effects.
TTC9B and HP1B3 genes, specifically, were highly correlated with PPD and predicted with 85% certainty about which women got PPD.
Depression is one of the most common mental disorders all over the world. According to experts, one in five people worldwide will experience a major depressive disorder at least once in their lifetime.
In 2020, 14.8 million U.S adults had at least one major depressive disorder that led to the inability to carry out everyday activities.
The brain uses various chemicals to send and receive information.
These chemical messengers are called neurotransmitters.
When there is an imbalance in brain chemical levels, it could lead to multiple mental health problems, including depression.
According to experts, imbalances in three primary monoamine neurotransmitters, dopamine, serotonin, and norepinephrine, can lead to depressive disorders.
Monoamine neurotransmitters are those chemicals with a single amino group.
These are mostly involved in processing emotions, memories, and arousals.
Here are the specific roles of these three neurotransmitters.
A study reported that depression is a combination of two events - loss of a favorable condition and the presence of an adverse situation.
Imbalances in these neurotransmitters can cause a combination of both these events, eventually leading to depression.
Several reasons can cause imbalances in neurotransmitters. Some common ones include:
Genetically, some people may have increased levels of Monoamine Oxidase A (MOA) in the body.
MOA is an enzyme controlled by the MAOA gene.
Higher levels of MOA break down the neurotransmitters and lead to deficient levels of dopamine, serotonin, and norepinephrine in the body.
There are many nutrients needed for producing and regulating neurotransmitters in the body.
Some of them include:
Nutritional deficiencies can hence reduce the levels of neurotransmitters in the body, leading to imbalances.
Lifestyle choices could be another common reason people have serotonin, dopamine, and norepinephrine imbalances.
For instance, chronic sleep deprivation may cause lower serotonin levels, leading to mental health conditions like depression.
Obesity and excessive consumption of sugar are both associated with dopamine deficiency.
Lack of physical activity is also associated with neurotransmitter imbalances.
Some studies suggest that drug abuse during early developmental periods or psychological stress can act as environmental factors, affecting neurotransmitter levels in the body.
Air pollutants may affect neurotransmitter levels in the body, especially serotonin and dopamine.
A study that analyzed suicidal trends in adolescents concluded that suicidal rates were highest when the pollen counts were high.
Image: Causes of Neurotransmitter Imbalance
Get your vitamin and mineral levels checked, and talk to your doctor about supplementing on nutrients that your body may need. Build your diet plan to include all the micro and macronutrients and choose fresher, healthier ingredients to cook with.
A 2015 study suggests that mind-body therapies like yoga and meditation may help handle neurotransmitter imbalances and, as a result, help combat issues like anxiety and depression.
Stress could cause neurotransmitter imbalances in the brain; mind-body therapies can reduce stress and relax the nervous system.
Studies claim that lack of sleep alters neurotransmitter functions in the brain and leads to changes in the production of chemicals like serotonin and dopamine.
Make sure you sleep at least 7-8 hours a day in a comfortable, dark space that allows the secretion of these chemicals.
If you have problems sleeping well, consult your doctor and get help.
Exercising helps release neurotransmitters like dopamine and endorphin.
Exercise also seems to help get better oxygen supply to the brain, allowing the neurons to transmit and receive signals better.
Exercise is a stress reliever, which may help handle norepinephrine imbalances.
Genetic testing may tell you if you are genetically prone to developing neurotransmitter imbalances, thereby having a higher risk for mental health conditions like depression.
Your doctor may be able to help with preventive therapies and solutions to handle the situation, if so.
If you think you show signs of depression, then the first thing to do is get professional help.
Depression or major depressive disorder is a mental health condition that affects an individual's behavior, mood, and overall health.
People with depression may experience prolonged feelings of sadness, hopelessness, and emptiness.
Depression usually begins in early adolescence or adulthood but can appear at any age.
Depression is one of the most common mental health conditions in the United States.
It is also more common in women and people assigned female at birth (AFAB) than men and people assigned male at birth (AMAB).
Common symptoms of depression are:
The symptoms of depression may vary slightly in the younger age group.
Common depression symptoms in adolescents and teens are:
Though the exact cause of depression is unclear, the disorder runs in families, hinting that genetic factors may increase one's risk of developing the condition.
Research is still underway to study the genetic variations that increase the risk for depression.
Other factors that may increase one’s risk for depression include:
Genetics plays a central role in the development of depression.
Scientists believe that nearly 40% of people with depression have a genetic link, while environmental and other factors make up for the remaining 60%.
Existing research states that a complex interplay of genes and other environmental (non-genetic) factors determine an individual’s risk of developing depression.
Few studies have reported that people having a first-degree relative with depression (a parent, sibling, or child) are three times more likely to develop the condition than the general population.
This shows that depression runs in families, and the disease has a significant hereditary component.
Some people can also develop the condition without a family history.
Though genetics influences the development of depression and anxiety, no single causative gene has been identified.
Research states that genetic variations on multiple genes contribute to the development of depression.
However, having a genetic variant does not confirm you will develop the condition.
Besides genetic variations, how genes are passed down to the next generation (mode of inheritance) may also affect an individual’s risk for depression.
A study published in The American Journal of Psychiatry reported that the research team isolated a gene prevalent in several families with a history of depression.
Chromosome 3p25-26 was found in over 800 families with recurrent depression.
Standard treatments used for depression are:
Most people require a combination of two or more treatments.
Did you know that your genes influence how well a treatment works for you? Several studies show that genes affect how your body absorbs, uses, and eliminates drugs like antidepressants.
Many genes influencing drug metabolism have been studied and are of specific interest to doctors and researchers.
If you have depression, it is essential to understand that treatment for this condition may take time.
You may have to undergo a couple of treatments to determine the most suitable one.
If you experience one or more symptoms of depression, it is important to seek medical care.
Before starting any antidepressant medications, informing your doctor about your medical history and current medication and supplements is essential.
This information will help your doctor determine the best treatment for you.
Learning about the genetic background of depression can help understand the condition better and provide optimal treatment options.
Caffeine is a psychoactive stimulant consumed worldwide mostly via two beverages, tea, and coffee. Pregnant women have always been advised to limit their caffeine intake since they may metabolize caffeine slowly. Studies also suggest that it can cross the placenta and enter the baby's bloodstream. A recent study published in the International Journal of Epidemiology reported that caffeine consumption alone might not contribute to adverse outcomes in pregnancy.
Pregnant women are often advised to cut off or limit their coffee consumption, owing to the reduced clearance of caffeine during pregnancy.
Pregnant women require a 1.5 to 3.5 times longer half-life to eliminate caffeine than non-pregnant women.
Caffeine, being a stimulant, increases the heart rate and blood pressure, because of which some people may experience jitters.
Further, since caffeine can cross the placenta to enter the baby's bloodstream, it is thought to endanger their health.
The safe upper limit for caffeine consumption in pregnancy is still a bit hazy.
According to the current WHO guidelines, pregnant women should restrict their caffeine intake to less than 300 mg/day (approximately 2-3 cups/day).
In comparison, the World Health Organization (WHO) allows up to 400 mg of caffeine per day for non-pregnant healthy adults.
On the other hand, the NIH advises pregnant women not to consume more than 200 mg of caffeine daily.
Studies on the effects of moderate caffeine consumption (≤200mg/day) report contradictory results.
Some find an increased risk for low body weight at birth and other poor outcomes, while others report no such risk.
Yet another study reported an average of 66 grams of lower birth weights in infants born to mothers who consumed about 50 milligrams of caffeine daily.
But it's important to note that such observational studies may not separate caffeine consumption from other risk factors such as alcohol consumption and smoking.
Thus, the unfavorable outcomes in pregnancies could also be attributed to other risk factors.
The CYP1A2 gene has the largest association with caffeine-related traits as the CYP1A2 enzyme is responsible for 95% of caffeine metabolism.
The CYP1A2 gene exists in different forms in different people.
Depending on the CYP1A2 gene variant one carries, they may metabolize caffeine slowly, at a normal rate, or fast.
This, in turn, impacts a person’s risk for caffeine-associated negative side effects.
Also Read Coffee And CYP1A2: 3 Ways High Caffeine Intake Can Affect You!
AHR is another gene that influences caffeine consumption.
This gene produces an enzyme that induces the activity of the CYP1A2 enzyme.
The more the AHR enzyme, the more the CYP1A2 enzyme, and the more the tendency for increased caffeine consumption.
The ADORA2A gene is associated with the wakefulness-promoting property of caffeine.
It also influences the effect of caffeine on sleep.
The A2A receptor produced by this gene is the main target for caffeine.
Typically, a molecule called adenosine binds to the A2A receptor and helps with sleep regulation.
Upon caffeine consumption, the caffeine molecules displace adenosine molecules from their receptors and sit in their place, promoting wakefulness.
Image: Interaction of Caffeine with A2A Receptors
Certain changes in this gene increase the risk for caffeine-induced insomnia.
The study, published in the International Journal of Epidemiology, investigated a potential causal relationship between caffeine consumption and adverse pregnancy outcomes.
While many previous studies have reported an increased risk of poor pregnancy outcomes with caffeine consumption, it’s been difficult to separate coffee drinking from other risk factors.
The researchers analyzed 8 genetic changes associated with caffeine consumption.
Additionally, they examined whether these changes were associated with birth outcomes (miscarriages, stillbirths, or pre-term birth).
Genome sequencing was performed in individuals who reported these outcomes, and the results were referenced against the controls.
The study reported that there was no greater risk of miscarriage, stillbirth or premature birth for women who drank coffee.
The study looked at the effects of caffeine only in terms of adverse outcomes.
Caffeine could still affect other aspects of fetal development.
So, Dr. Moen, one of the authors of the study, says, "we don't recommend a high intake during pregnancy, but a low or moderate consumption of coffee may be safe."
Certain genetic changes influence caffeine consumption in an individual.
These changes may be why one can consume 7 cups of coffee and still go to bed by 10, and another struggles to sleep even after a couple of cups.
They affect caffeine consumption in both the general population and pregnant women.
The current recommendations for caffeine consumption during pregnancy are based on observation studies where it's difficult to separate coffee drinking from other risk factors like smoking, alcohol, or poor diet.
But caffeine alone doesn't seem to increase the risk for pregnancy-related adverse outcomes.
https://academic.oup.com/ije/advance-article/doi/10.1093/ije/dyac121/6605011#358171758
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4507998/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7209255/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6947650/
Vitamins are essential micronutrients and form an integral component of a balanced diet.
They are organic substances that are not produced by the body.
So, they are derived from the food we eat.
Vitamins are classified as:
Though several diseases are studied in association with vitamin deficiency, few people know the impact vitamins have on mental health.
Mental health illnesses are any condition or disorder that affects an individual’s mood, behavior, or thinking.
While several treatment modalities are available for treating mental health illnesses, nutrition therapy may be effective in some.
Depression is one of the most common mental health conditions and affects nearly 8% of Americans.
Deficiency of one or more B vitamins may contribute to symptoms of depression and anxiety.
Several vitamin deficiencies have been associated with anxiety and other mental health symptoms. These include:
Thiamine or vitamin B1 belongs to the B complex vitamins.
This vitamin participates in energy metabolism, cell function, development, and growth.
A study published in the International Journal of Clinical Medicine in 2011 stated that 100 mg of vitamin B1 daily in the participants improved their Hamilton Anxiety Rating Scale (HARS) scores.
The study also reported that these patients showed improved appetite and energy levels and reduced fatigue.
Vitamin B6 is also called pyridoxine and is essential for the metabolism and health of the central nervous system.
A study published in the International Journal for Vitamin and Nutrition Research in 2019 stated that low intake of vitamin B6 was associated with increased risk for mental health conditions like depression and anxiety.
The study recommended adequate intake of nutritional status of the individual, including vitamin B6.
Vitamin B12, or cobalamin, is a vital B vitamin as it plays a role in red blood cell formation and acts as a co-factor in DNA synthesis.
A deficiency of vitamin B12 results in pernicious anemia, characterized by a problem in oxygen transport in the body.
Since vitamin B12 also acts as a co-factor in synthesizing neurotransmitters like serotonin and dopamine, vitamin B12 deficiency causes symptoms like mood swings, paranoia, irritability, and confusion.
Vitamin D is a fat-soluble vitamin produced by the body on exposure to sunlight.
You can also get this vitamin via diet and supplements.
People with anxiety and other psychiatric disorders tend to have lower vitamin D levels.
Since nearly 50% of the general population is at risk of vitamin D deficiency, the risk of developing associated anxiety is also relatively high.
Vitamin C plays an essential role in mental health.
People who are deficient in vitamin C experience depression and chronic fatigue.
Studies show vitamin C improves mood, lowers stress and anxiety symptoms, and boosts cognitive function.
Image: Vitamin deficiencies that play a role in anxiety
Besides vitamins, minerals are the other essential micronutrients that may contribute to mental health conditions, including anxiety.
Magnesium is the fourth most abundant mineral in the body.
Since magnesium plays a role in optimal neurotransmitter activity and proper nervous system functioning, it affects brain function and mental health.
Research states that low magnesium levels can contribute to and aggravate neuropsychiatric conditions, including anxiety, primarily due to changes in the composition of gut bacteria.
A study found that magnesium has a calming effect as it activates the GABA (A) receptors, so this mineral is often found in anti-anxiety medications.
Iron is a trace mineral found in every cell of the body.
It is an integral part of hemoglobin, the blood pigment responsible for carrying oxygen to all parts of the body.
Iron is also a co-factor in synthesizing the neurotransmitter serotonin ( a chemical found in the brain).
A deficiency of iron has been shown to increase the risk of developing anxiety, mood, and panic disorders.
Studies have shown that people with iron deficiency have increased anxiety and fearfulness.
Zinc is another mineral that is required as a co-factor for various enzymes in the body.
It is also essential for mental health as it participates in the production of neurotransmitters and is required for the normal functioning of the nervous system.
Studies have shown that people with lower levels of zinc have a higher tendency for anxiety.
Taking zinc supplements can help reduce anxiety symptoms.
Omega-3 fatty acids are called essential fatty acids as the body does not produce them and have to be obtained through diet.
These fatty acids are vital for the normal functioning of the brain and nervous system.
Some studies have shown low levels of omega-3 fatty acids in anxious individuals, and extremely low levels correlate to severe anxiety.
Nutritional therapy uses dietary recommendations to prevent and manage anxiety.
If you are struggling with anxiety, here are a few foods that you can include in your anti-anxiety diet:
Pharmacogenetics is the study of how certain changes in the genes influence drug responses.
This can be due to variations in the genes that produce proteins or enzymes involved in drug metabolism or interaction.
This field of research is increasingly important as it allows for personalized treatment based on an individual's genetic makeup.
Why personalized treatment?
We all are similar, but of course, we are also different.
And the idea of a "one size fits all" approach to diagnostics and treatment is very flawed.
Different people respond to the same drug differently.
Because of the aforementioned genetic variants, some people may be at increased risk for adverse drug reactions (ADRs) for certain medications.
Others may not experience the desired effect of the drug because they clear it from their body too quickly.
Pharmacogenetic information can help identify medications best suited for a particular person.
It can also factor in when clinicians choose the appropriate dosage for individual patients.
In clinical trials, pharmacogenomics can help identify new targets for drug development.
The benefits of knowing how you'll respond to a medication or which drug will work best for you before you even consume it are not hard to imagine.
One of the popular choices of mental health providers for treating anxiety is psychiatric medications.
Implementing pharmacogenomics here lowers the room for trial and error.
It can also help discover what drugs could potentially cause ADRs in an individual.
The pharmacogenomic approach also helps lower the economic burden as less, or no money will be wasted on drugs that aren't effective for an individual.
Some key players in anxiety medications fall into the following categories:
Serotonin Reuptake Inhibitors (SSRIs): SSRIs, originally designed to treat depression, have revolutionized the treatment of anxiety. They work by blocking serotonin (happy hormone) reuptake, thereby increasing its availability for nerve signaling.
Changes in the CYP2C19 gene link to differences in the metabolism of SSRIs.
People who are ultrarapid metabolizers may not experience the therapeutic effects of the drugs due to their quick elimination from the body.
In contrast, poor metabolizers may have a build-up of the medication in the body and experience side effects, some of which may be adverse.
Tricyclic Antidepressants (TCAs): Physicians use TCAs to treat panic disorder, PTSD, anxiety, and depression that occurs with anxiety. They act on 5 brain chemicals (or neurotransmitters). They block the reuptake of serotonin and norepinephrine.
Changes in the CYP2D6 and CYP2C19 genes affect TCAs' exposure time, effectiveness, and safety.
Other medicines used to treat anxiety, like benzodiazepines and serotonin norepinephrine reuptake inhibitors (SNRIs), also have a pharmacogenomic aspect.
Having this information in hand provides many benefits.
Genetic testing for psychiatric medications is a pretty straightforward procedure.
The DNA raw data (the particulars of your DNA in text format) is obtained through a saliva or cheek swab sample.
The raw data is then matched against a database that contains information about the gene changes influencing drug metabolism.
For each drug, the sample DNA data is referenced against the database, and depending on the genetic changes, the metabolizer classification (slow, moderate, normal. Rapid, ultrarapid) is entered.
This report can then be interpreted with the guidance of a qualified medical practitioner and used to understand which drug may work the best for you.
The overall efficacy of genetic testing has improved by leaps and bounds over the years.
However, no genetic test for psychiatric medications has a 100% effectiveness rate.
Genetic testing for medication can be quite expensive.
Studies have found that people would be more inclined to have the test done if the costs were lower or covered by insurance.
A 2017 survey conducted in Singapore reported cost as the biggest concern for pharmacogenomic testing, with over 94% of respondents concerned about cost.
The main concern for mental health practitioners about implementing genetic testing for psychiatric medications is the lack of pharmacogenomic knowledge.
In a survey conducted on psychiatric pharmacists in the US (2015), half of them reported being completely or partially unaware of pharmacogenomics.
Another main concern in employing pharmacogenomics in clinical practice seems to be a lack of clear guidelines about using genetic test results in prescribing psychiatric medications.
Currently, most reports adopt a “traffic light” style for displaying the results.
This leads to a wrong interpretation of ‘green meaning the drug will work’ and ‘red, the drug won't.’
Both clinicians and patients may misinterpret the results.
