Regulating your serotonin levels during pregnancy can protect your child’s brain development and reduce their risk for ADHD!
Serotonin is a neurotransmitter that is associated with mood regulation, gut motility, sleep, appetite, and pain modulation.
What do low serotonin levels look like? A person who is deficient in the neurotransmitter serotonin may experience depression, inner rage or paranoia, feel easily overwhelmed, lose joy in hobbies or favorite foods, and be unable to fall into a deep and restful sleep.
A breakdown of serotonin synthesis:
- Serotonin is synthesized from the amino acid tryptophan.
- Two enzymes, tryptophan hydroxylase (TPH) and amino acid decarboxylase (AAAD), help to carry out this conversion. TPH exists in two forms, TPH1 and TPH2.
- Once tryptophan is actively transported across the blood-brain barrier, TPH converts it into 5-HTP. The essential cofactor ferrous iron is critical for this to take place.
- 5-HTP is then converted to serotonin with the help of the other enzyme we mentioned, AAAD.
Meats, such as turkey, beef, liver, and lamb, provide a rich source of tryptophan. Spirulina has incredibly high levels of tryptophan. Spirulina can be difficult to digest. In order for the gastrointestinal tract to absorb all its valuable nutrients, the best spirulina is fermented.
Body Ecology offers a product called Potent Proteins, which is 50% fermented spirulina. Outside of food-sourced tryptophan, it has been found that supplementing with the amino acid tryptophan to correct a serotonin deficiency is usually not as effective as supplementing with its precursor, 5-HTP.
Other important nutritional cofactors that are essential for serotonin production are vitamin B3 (niacinamide), vitamin B12 (methylcobalamin), folic acid, magnesium, and iron. Iron anemic individuals typically have low levels of serotonin – in this case, 5-HTP supplementation has a limited response.
Serotonin deficiency can seriously alter the pleasure one experiences in life. Not only that, but serotonin deficiency is also at the root of other chronic degenerative diseases and can even affect your child if you are pregnant.
A new study revealed that if a mother is deficient in serotonin due to a genetic variance, it is likely that her child will present symptoms of attention-deficit/hyperactivity disorder (ADHD).
The genetic variance that researchers looked at was the inability to produce tryptophan hydroxylase 1 (TPH1), the enzyme that is used to convert the amino acid tryptophan into serotonin. Without this peripheral enzyme, serotonin levels are significantly lower, and genetic variances of both TPH1 and TPH2 enzyme subtypes have been linked to several disorders involving anxiety and depression.
Researchers concluded that, “maternal serotonin production may have long-term consequences for brain development and increase the risk of ADHD-related symptoms and behavior in offspring”. The study looked at the children of both mothers and fathers with this genetic variance and found that ADHD was largely only present in the children whose mothers were unable to produce sufficient amounts of serotonin.
Scientists have an identifiable and genetic link between serotonin deficiency and its effects in utero that permanently alter the development of a child’s brain. The study concludes that it is plausible that when a woman is pregnant, serotonin deficiency, with or without a genetic basis, will effect the brain development of the fetus. (1)
Neurodegenerative disease has been associated with an alternate tryptophan pathway.
When tryptophan breaks down, it can produce serotonin. It can also take another pathway, known as the kyurenine metabolic pathway, and produce quinolinic acid.
The kyurenine pathway leads to the production of NAD+, nicotinamide adenine dinucleotide. This is a coenzyme found in all living cells and is involved in the production of ATP – or energetic fuel for each cell in the body. When this pathway is compromised, the metabolism of the cell is altered and ultimately leads to the neuron’s death. This sets off a cascade of neuronal death.
Quinolinic acid has been linked to neurodegenerative conditions such as dementia, Alzheimer’s disease, Huntington’s disease, multiple sclerosis, and Parkinson’s disease.
Niacin, or vitamin B3, is a supplement that has been found to inhibit the conversion of tryptophan into quinolinic acid. Interestingly enough, it has also recently been found to inhibit Candida as well. (2) Fermented spirulina is a great absorbable source of B-vitamins.
Elevated levels of cortisol and an excited immune response can also increase the conversion of tryptophan into quinolinic acid.
Elevated levels of cortisol increase inflammatory cytokines. Think of inflammation as fire – cells are driven to destruction, and the immune response activates. Like fire, this activation easily spreads through a local area or throughout the entire body. Within the brain, inflammatory triggers will then tell the glial cells to produce more inflammatory triggers and neurotoxic agents that cause cell death.
This glial cell inflammatory response in the brain is like throwing a Ping-Pong ball in a room full of set mousetraps. One Ping-Pong ball sets off one trap, then this sets off three more, then those set off twelve, and so on.
Adaptogenic herbs, like Holy Basil, regulate levels of cortisol in the body and are an effective way to cool the body down and prevent neurodegeneration. Holy Basil is also called Tulsi. In India, women eat the leaves and drink the tea. It is safe for children after the age of two.
It is important to note that 90% of the serotonin in the body is produced in the gut.
Most of us know that the brain is full of neurotransmitters, neurons, and glial cells. Well, guess what? The gut is comprised of these same components; this is known as the enteric nervous system. When you hear about the gut-brain axis, it is important to understand the similarities between the gut and the brain, which goes right down into the tissues. (3)
Proper maintenance and care of serotonin levels also involves making sure that the gastrointestinal tract is healthy.
This means healing and maintaining a strong gut mucosal barrier by eating fermented foods, which are easy to make with a culture starter, drinking probiotic beverages, and supplementing with enzymes if necessary. When the gut is inflamed, it may be necessary to work with digestive aids until balance is restored. Sometimes, especially when any kind of neurodegeneration is present, it is necessary to support the digestive process with foods rich in beneficial microflora and enzymes.
Too many sugars lead to serotonin dysregulation.
The release of insulin, which takes place after a meal that has many carbohydrates and sugars, promotes the transport of tryptophan to the brain for serotonin production.
When there are abnormal surges of insulin, this leads to abnormal surges in serotonin production. Drowsiness and fatigue after meals is an indicator that this has taken place.
WHAT TO REMEMBER MOST ABOUT THIS ARTICLE:
- You can help the production of serotonin along by eating tryptophan-dense foods like fermented spirulina and by supplementing with 5-HTP.
- Supplementing your diet with B vitamins, especially B3 and B12, assists in the smooth transition from tryptophan to serotonin. Fermented spirulina is a great source of absorbable B-vitamins.
- Taking adaptogenic herbs, such as Holy Basil, cools the body and helps to stop the inflammatory cascade that can lead to serious neurodegenerative disease.
- Always include fermented foods, probiotic beverages, and enzymes in your diet. One reason is that it helps regulate serotonin levels by nourishing the integrity of the digestive tract, which produces 90% of the serotonin in your body.
- Sugars and excessive carbohydrates can stimulate an insulin surge. In the process of regulating serotonin levels, this leads to imbalance.
REFERENCES:
- Arch Gen Psychiat. 2010;67:1033-1043.
- William Shaw “Overview of organic acid testing“. Townsend Letter. FindArticles.com. 07 Mar, 2011. http://findarticles.com/p/articles/mi_7396/is_330/ai_n56632303/
- “Glial cells in the Gut.” Neurogastroenterol Motil. 2005 Dec;17(6):777-90.
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