Depression is a ruthless disorder that makes people feel sluggish, disinterested, and overwhelmed by sadness. Many choose to treat this disease with prescription medication. For some, however, this is not an option. There are many reasons to choose a natural antidepressant.
All prescription depression medications have certain side effects. These are often not pleasant and can even be dangerous for some people. Sexual side effects are common, causing people to lose interest in sex or be physically unable to engage in sexual activity. This can have serious consequences in relationships. It is also well documented that many children and adolescents commit suicide or have thoughts of suicide while taking prescription antidepressants.
Some people simply cannot afford prescription drugs. Medications are very expensive without insurance coverage. Underinsured people have similar problems paying for their medication.
Others prefer a natural and holistic lifestyle. There are ways to treat depression naturally. These methods have been around for thousands of years and have helped many people find relief.
The best tested natural antidepressant is called St. John's wort. It is a flowering plant native to Europe. It is a herbal remedy for depression that comes in capsule and liquid form. In some countries like Germany, it is often prescribed for children and adolescents. In clinical trials, the herb has achieved results similar to common prescription drugs.
The side effects are very mild and rarely stop taking them. This includes dizziness, fatigue and sensitivity to light. One of the reasons why many people choose St. John's wort is the low frequency of side effects. There are also few drug interactions. Women who use hormonal contraception should avoid St. John's wort, as this can affect its effectiveness. It can also interfere with certain immunosuppressants. Always consult a doctor or other healthcare professional before starting treatment. This can prevent potentially harmful drug interactions.
Another natural antidepressant is exercise. When the body is working, the brain releases "wellness" chemicals called endorphins. These relieve stress and relieve physical pain. People with severe depression may not be able to take advantage of exercise. However, people with mild depression can feel much better after training. This can be done independently or in a group. Working in class or with friends can help motivate them.
Prescription drugs are not always the answer. There are many people who choose a natural way to cure depression. Since it is a serious illness, it is important to consult a doctor or psychologist.
Worms, flies and antidepressants
You may think that scientists know everything about antidepressants like Prozac or Fluoxetine (its generic name). After all, these drugs have been around for a while. Fluoxetine-type antidepressants are known for their selective inhibition of proteins called serotonin transporters that bind neurochemically active serotonin in cells (hence the term SSRI or selective serotonin reuptake inhibitor). Surprisingly, one can still wonder whether this molecular activity of SSRIs alone is responsible for their therapeutic effects. Therefore, molecular research, generally performed in a petri dish or on laboratory animals, particularly worms (C. elegans) and fruit flies (Drosophila melanogaster), sought alternative explanations.
Worms and fruit flies have proven to be useful models of whole organisms for genetic research. More recently, these tiny animals have started to provide clues to the genetic mechanisms of human brain disease and are increasingly useful in the search for new molecular targets in drug discovery.
A decade ago, a group of geneticists came up with the idea that Prozac forces worms to fold their noses. These scientists tried to find the molecular reason for this unexpected effect of the drug. It turned out to be a family of genes that, when mutated, reduced the muscle contractions of the nose caused by Prozac. They called the nasal gene family resistant to fluoxetine or NRF. By identifying the proteins produced by the NRF worm genes, the scientists hoped to be able to find a corresponding human protein that they could study as a new target for the effects of Prozac, a target other than the transporter. already known serotonin. Unfortunately, no human counterpart was known.
Dr. Svetlana Dzitoyeva of the University of Illinois at Chicago found similarities between the DNA sequence of the NRF genes and a sequence in the DNA of fruit flies. She and her colleagues hypothesized that this fruit fly DNA sequence could be an NRF-like gene. If they could identify this fruit fly gene, they could potentially locate its human counterpart and discover a new target for its antidepressant effects.
Active genes produce gene-specific messenger RNAs; These mRNAs lead to the production of corresponding proteins. Dzitoyeva and his colleagues have developed a method to identify new active genes into which they inject fruit flies anesthetized with molecules called dsRNA. These dsRNA molecules can be designed to destroy a particular mRNA. As a result, the injected fly loses its targeted endogenous mRNA. For all practical purposes, this treated fly would behave as if the corresponding gene was inactivated. By examining the cellular or behavioral consequences of such gene silencing, scientists can determine what the gene would do.
Dzitoyeva and his colleagues designed a dsRNA against the fruit fly sequence similar to the nose of the fluoxetine-resistant worm and were able to find a new functional gene for the fruit fly. They saw its activity in various tissues, including the fly brain. The silencing of this gene in fly embryos has led to the loss of developmental markers known as belts. So they called the new gene without a belt.
Unfortunately, fruit flies differed from worms in that they did not show any obvious behavioral reactions when given Prozac. There was no fly behavior that corresponded to Prozac's nasal contractions in worms. Since Dzitoyeva and his colleagues could not have examined how the silence of the strapless belt would affect the effects of fluoxetine on fruit flies, their project lost momentum and was abandoned.
These old studies can be revitalized by recent developments seeking the human homologue of the beltless gene and its possible role as a target for fluoxetine drugs. Improved annotation and recent characterization of the fruit fly genome have shown that the beltless gene sequence corresponds to a gene previously predicted based on mutation studies and termed drop-dead. Therefore, the strapless and the drooping strap appear to be the same unit and are related to the fluoxetine-resistant snail nose.
The dead mutant flies are normal at first, but show flight deficits after a few days, develop brain damage and die quickly. The main deficit caused by the dead mutation occurs in the white blood cells of the brain (glia). It has been suspected that this gene normally produces proteins that are necessary for the maintenance of the adult brain. This maintenance is often referred to as neuroplasticity. Neuroplasticity is generally impaired during aging and can lead to neurodegeneration. It is known that fluoxetine drugs can support neuroplasticity. Therefore, the fluoxetine-resistant nose can indicate a new target for the action of antidepressants; Neuroplasticity due to dead gout.
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