The Genetic of Autism

August 28, 2015 by

July 17, 2015

By Medical Discovery News

The Genetics of Autism

In the past decade, autism has garnered a lot of media attention. Lately much of the focus has been on finding the cause. Much is still a mystery, despite confirming that vaccines and parenting are not responsible. Now a new study of twins has given us another clue, revealing that the influence of genetics on the development of autism may be between 56 and 95 percent.

According to the Centers for Disease Control, one in 68 children have autism, a neurodegenerative disorder that exists on a spectrum, meaning its symptoms and their severity varies tremendously. A hallmark feature of autism is impaired social interaction, noticeable even in babies. Those with autism find it difficult to interpret what others are thinking or feeling because they miss the social clues most take for granted. Other symptoms can include repetitive movements such as spinning or rocking, speech delays, and self-destructive behaviors. Children with autism can also have a variety of other conditions including epilepsy, Tourette’s syndrome, learning disabilities, and attention deficit disorder (ADD).

The cause of autism is probably rooted in genetics and environment. Comparing sets of twins is a well-established way of clarifying the extent of both these influences. Scientists in London studied over 6,400 pairs of twins in England and Wales between 1994 and 1996, all raised by their parents in the same environments. The data they collected revealed that the chance of identical twins having autism was 77-99 percent, whereas the chance of non-identical twins having autism was 22-65 percent. This suggests that additive genetic factors contribute to 56-95 percent of autism cases. This is far higher than previous estimates, which assumed environmental influences were more of a factor.

While no one gene has been attributed to autism, the majority of the genes that are associated seem to be linked to one specific symptom. For example, the gene EN2 is often studied for its role in autism because it is critical to midbrain and cerebellum development. Reelin, a protein found mainly in the brain, also plays an important role in autism development. In adults, reelin is important to learning and memory and is critical to inducing and maintaining long-term neuronal connections. Autistic individuals consistently show elevated levels of serotonin, otherwise known as the feel-good hormone. This has led researchers to examine the role of genes involved in serotonin regulation as potential causes of autism. Another hormone system called arginine-vasopressin affects social behavior, so one of the genes that regulates it is a candidate for autism as well. These are just a few of the many genes being studied.

As more people become aware of autism and more children are diagnosed, the pressure is building to further understand this disorder. Discovering the causes might translate to better diagnostics and treatment for autism.

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Microlesions in Epilepsy

June 26, 2015 by

June 26, 2015

By Medical Discovery News

Humans have been recording and diagnosing epilepsy for at least 4,000 years, but it only began to be understood a few hundred years ago. While doctors noticed some epileptic patients had brain lesions, others did not have any that were visible – until now. Using a combination of gene expression analysis, mathematical modeling, and microscopy, scientists have found microlesions in the brains of epilepsy patients, which may explain the cause of seizures in some people.

Epilepsy is characterized by unpredictable seizures that result from groups of neurons firing abnormally. Some people experience symptoms prior to a seizure that allows them to prepare. In some cases, seizures can include jerking, uncontrolled movements, and loss of consciousness. In others, the seizure may only cause confusion, muscle spasms, or a staring spell. Epilepsy patients experience repeated seizure episodes.

Epilepsy is a relatively common brain disorder affecting about 1 percent of people – 65 million worldwide, 3 million in the United States. Some causes of epilepsy are strokes, brain tumors or infections, traumatic brain injuries, lack of oxygen to the brain, genetic disorders such as Down syndrome, and neurological diseases such as Alzheimer’s. However, for two-thirds of people with epilepsy, there is no known cause. Not all seizures are related to epilepsy, as they can also be caused by low blood sugar, high fever, and withdrawal from drugs and alcohol.

Epilepsy can be treated using anti-seizure medications that control the spread of seizure in the brain, but about one-third of epileptic patients don’t respond to current medications. Some cases are treated by surgically removing or killing cells in the region of the brain that are responsible for the aberrant electrical signaling. If neither of those are options, a device can be implanted that stimulates the vagus nerve, which is part the autonomic nervous system that controls involuntary bodily functions such as heart rate and digestion.

In some people with epilepsy, the cause was traced to a visible abnormality in the brain. Now, scientists have identified millimeter-sized microlesions that could explain why a seemingly normal brain suffers seizures. Scientists compared the genes expressed in the microlesions of 15 people with epilepsy. Using mathematical modeling called cluster analysis, they discovered 11 groups of genes that were either expressed too much or too little in brain tissues experiencing the high electrical activity that causes seizures.

Based upon what these genes encoded, they predicted certain brain cells would be reduced and immune response or inflammation would increase in the microlesions. That’s exactly what they found when they stained those sections of the brain and examined them under a microscope. Brain cells lost communication with each other, limiting the brain’s communication network. This probably leads to the abnormal electrical signals that trigger seizures.

This conclusion still needs to be confirmed, but in the future it may guide the development of new treatments for epilepsy.

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Chocolate on My Mind

April 25, 2015 by

April 10, 2015

By Medical Discovery News

Chocolate

Peanuts creator Charles Schulz once said, “All you need is love. But a little chocolate now and then doesn’t hurt.” New research shows he might be right. In one study, certain compounds in cocoa called flavanols reversed age-related memory problems.

Flavanols, found in a variety of plants, are potent antioxidants that help cells in the body deal with free radicals. Free radicals arise from normal cellular processes as well as from exposure to environmental contaminants, especially cigarette smoke. Unless your body gets rid of free radicals, they can damage proteins, lipids, and even your genetic information. You can get flavanols from tea, red wine, berries, cocoa, and chocolate. Flavanols are what give cocoa that strong, bitter, and pungent taste. Cocoa is processed through fermentation, alkalization, and roasting among other methods, which can influence how much of the good flavanols are lost. Among the products made from cocoa, those with the highest levels of flavanol are cocoa powders not processed by the Dutch method, followed by unsweetened baking chocolate, dark chocolate and semi-sweet chips, then milk chocolate, and finally chocolate syrup contained the least.

In the latest study, a cocoa drink specially formulated by the Mars food company to retain flavanols was compared with another drink that contained very little flavanols. The study asked 37 randomly selected adults aged 50 to 69 to take one of the drinks. One group consumed 900 milligrams per day of flavanols and the others consumed only 10 milligrams per day for three months. Brain imaging and memory tests were administered before and after the trial.

Those who consumed the high levels of cocoa flavanols had better brain function and improved memories. Before the study, the subjects on average demonstrated the memory of a typical 60-year-old person. At the end, those who consumed more flavanols exhibited the memory capabilities more closely resembling a 30- to 40-year-old. Unfortunately, the average candy bar contains only about 40 milligrams of flavanol, so you would have to eat 23 of them a day to equal the amount of flavanol used in the study, which would lead to other health problems like obesity and diabetes.

Other studies have similarly revealed that high-flavanol cocoa beverages cause regional changes in the brain’s blood flow, suggesting that it could be used to treat vascular impairments within the brain. Flavanols have also been reported to reduce blood pressure and other factors that lead to cardiovascular disease, improve insulin sensitivity, modulate platelet activity thereby reducing the risk of blood clots, and improve the activities of the endothelial cells that line our blood vessels. The Kuna indians living on the San Blas Islands near Panama, who consume a type of cocoa rich in flavanol on a daily basis, have unusually low rates of hypertension, cardiovascular disease, cancer, and diabetes.

These studies need to be repeated with larger groups to confirm the benefits of consuming flavanols and to ensure that there are no negative effects. Still, if a cocoa beverage high in flavanols could be mass produced and marketed, we could improve human health in a very tasty way.

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Humanizing the Mouse

April 25, 2015 by

March 20, 2015

By Medical Discovery News

Humanizing the Mouse

In the 1986 horror movie “The Fly,” a scientist’s teleportation experiment goes awry when a fly lands in one of the teleportation pods and he undergoes a transformation into a part fly, part human monster. Today, science has given us the capability to create animal-human hybrids, although so far none of them has craved human flesh like they tend to do in the movies.

Neuroscientists at the Massachusetts Institute of Technology (MIT) have been introducing human genes into mice to study the effects on mouse brain function and capabilities. They are doing this in small steps, using genetic engineering techniques to introduce a specific, single human gene into a mouse. This will allow scientists to evaluate the impact of each human gene on the brain in another species. It’s not quite a monstrous Franken-mouse, but the results have definitely been revealing.

The human version of gene Fox2p is connected with language and speech development, a trait associated with the higher order brain function unique to humans. When this gene was introduced into mice in the experiment, they developed more complex neurons and more extensive circuits in their brains. Scientists wondered if this gene is responsible for the enhanced brain and cognitive abilities displayed in humans.

In the behavioral experiments at MIT, scientists placed mice in a maze and evaluated the reactions of mice harboring the Fox2p gene versus normal mice. The maze offered two modes of navigation to the mice: visual clues in the environment that were observable from within the maze and tactile clues in the pathways of the maze consisting of smooth or textured floor.

The hybrid mice learned to navigate the maze quickly, finishing it three times faster than normal mice. This cognitive enhancement or flexibility reflects the human capability of handling and processing information. The tactile information is handled by something called procedural or unconscious learning. However, the sight-derived clues represent declarative learning. It is the addition of the Fox2p gene that gave mice the ability to integrate both forms of learning.

Interestingly, if the visual clues or the tactile clues were removed, the hybrid mice did no better than the normal mice at navigating the maze. This might mean that the hybrid mice only performed better when they could utilize both forms of information. This ability to switch between and consider different forms of memory (procedural and declarative) is important and may explain in part why it is so important in human speech and language development.

Humanized animals are being used in a number of scientific fields to help us understand different elements of human physiology. Expect to see more of the humanization of animals in the future, but alas for you Sci-Fi fans – a Frankenmouse is not yet on the horizon.

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The Altitude Gene, A Denisovan Gift

January 27, 2015 by

Jan. 23, 2015

By Medical Discovery News

Altitude Gene, A Denisovan Gift

Those traveling to the Himalayas have a tough time adjusting to the harsh altitude. But for those native to Tibet, called the Roof of the World due its location 14,700 feet up, it’s not a problem. That’s because Tibetans have adapted to this harsh environment partly due to a gene they inherited from an extinct species of prehumans called the Denisovans.

Anyone traveling to high altitudes like those in Tibet can get altitude sickness and there is no way to predict who will get it. The severity of it varies according to genetics and the rate of ascent, but it is not influenced by age, gender, physical fitness, or previous altitude experience. Symptoms can include headaches, nausea, dizziness, fatigue, shortness of breath, loss of appetite, and disturbed sleep. Severe symptoms could indicate high altitude cerebral edema, which impairs brain function, progresses rapidly, and can become life-threatening in a matter of hours.

However, Tibetans live at these extreme altitudes without developing these problems. So how did they adapt to such a challenging environment?

Studies have linked the Tibetan’s adaptation to high altitude with several genes, including a unique form of the EXPAS1 gene. This gene responds to low oxygen levels to increase hemoglobin production. However, Tibetans with this gene do not have elevated levels of hemoglobin. This seems counterintuitive, since increasing hemoglobin could increase the amount of oxygen being transported in the blood. This would be advantageous at altitudes where the availability of oxygen is reduced, which then limits the uptake of oxygen in the lungs. On the other hand, increasing red blood cells would also thicken the blood, making it less efficient in distributing oxygen and increasing the risk of stroke. The Tibetan variant of EXPAS1 gene might then be protective, but we don’t know how exactly it works.

We know that the ancestors of Nepal’s Sherpa people carried the Tibetan EXPAS1 gene variant about 30,000 years ago. Today, only Tibetans carry this version of the gene, no other modern humans have it. New data suggests it may have come from an extinct population of prehuman called the Denisovans. So far they have only been found in a cave in the Altai Mountains in southern Siberia in East Central Asia. More proof is needed to eliminate another extinct species, the Neanderthals, who also have a version of EXPAS1 similar to the Tibetan one. This is another example of genes acquired by interbreeding between Homo sapiens and other ancient species. About 5 percent of the genetic information of Australasians is shared with Denisovans, while 2.5 percent of human DNA originates from Neanderthals. Modern humans have bits of DNA from these ancient species that have made important contributions to the success of our genome.

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More Bad News for Smokers

October 27, 2014 by

Oct. 24, 2014

By Medical Discovery News

Lung X-ray

Smoking isn’t the only thing that raises your risk of lung cancer. As it turns out, your DNA can have that effect too.

A scientific study scanned the genomes, the entire genetic code, of 11,000 people of European descent in an effort to identify if there was any correlation between gene sequences and a common form of lung cancer, non-small cell carcinoma. They discovered that variants of certain genes increase a person’s susceptibility to developing lung cancer, especially in smokers.

One of the three gene variants they identified, named BRCA2, can double a smoker’s chance for developing lung cancer. BRCA2 is a tumor suppressor gene. It encodes a protein involved in the repair of damaged DNA, which is critical to ensure the stability of cell’s genetic material. When cellular DNA is damaged, there are several ways for the body to detect and repair that damage. If the damage to DNA cannot be repaired, then the cell is programmed to die by a process called apoptosis in order to prevent the damage being passed on to its daughter cells.

Like other tumor suppressor genes, the BRCA2 protein helps to repair breaks in DNA. It also prevents damaged cells from growing and dividing too rapidly. Variants of BRCA2 associated with breast, ovarian, and now lung cancers produce proteins that do not repair DNA damage properly. This causes cells to accumulate additional mutations, which can lead to cells that grow and divide uncontrollably. Such mutations lead to an increased risk of developing cancer.

Scientists have discovered over 800 mutations of BRCA2 that cause disease, including breast, ovarian, lung, prostate, pancreatic, fallopian, and melanoma cancers. Most of the mutations result from the insertion or deletion of a few letters of genetic code into the part of the gene that code for a protein. This disrupts the production of the BRCA2 protein and results in a shortened and nonfunctional form of the BRCA2 protein.

Lung cancer is a leading killer of Americans. Nearly 160,000 Americans will die from lung cancer this year, representing 27 percent of all cancer deaths. Active smoking causes close to 90 percent of lung cancers.

The good news from this discovery is that since scientists first linked BRCA2 to an increased risk of breast cancer, new therapies have been developed. Current treatments for breast and ovarian cancers could be effective with BRCA2-associated lung cancers, such as PARP inhibition.  PARP1 is another protein involved in repairing DNA damage. When one of two strands of DNA are broken or nicked, PARP1 moves to the region and recruits other proteins to the site to repair the damage. Many chemotherapy agents kill cancer cells by inducing DNA damage in the tumor and inhibiting PARP1. This doesn’t allow cancer cells to repair damage and makes them more susceptible to chemotherapy and radiation therapy. Now that we know this gene is linked to lung cancer, such therapies may be more effective in treating lung cancer and saving lives.

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A One-Letter Blond

October 17, 2014 by

Oct. 10, 2014

By Medical Discovery News

Blond hair

Out of the 3 billion letters contained in the human genetic code, all it takes to be born a blond is a single change in a certain place from an A to a G. With the sheer complexity of the human genome, this new discovery shows how remarkably simple it is to be a natural blond. Especially when you consider the lengths people go to become one artificially.

This discovery actually came from research on the evolution of Sticklebacks, small fish that emerged from the oceans and colonized streams, rivers, and lakes at the end of the last Ice Age. Scientists at Stanford University have been studying how Sticklebacks have adapted to different habitats around the world, and particularly how different populations acquired their skin colors. They discovered that changes in a single gene determined the pigmentation of fish throughout the world. The gene responsible, the Kit ligand gene, is also in the human genome. Different versions of it have evolved around the world and are associated with differences in skin color.

The protein encoded in the Kit ligand gene aids in the development of pigment-producing cells, so its role in skin and hair color makes sense. However, the Kit ligand protein plays other important roles elsewhere in the body, such as developing stem cells into blood cells and producing sperm. Therefore, changes to this gene are not simple and could have detrimental consequences. This caused scientists to wonder how such an important gene could evolve while still preserving its essential roles. Both in fish and humans, the changes that lead to differences in pigmentation were not in the genetic region that encodes the Kit ligand protein, but rather at sites in the genome quite distant from here, where elements responsible for regulating that gene are located.

To find the regions that regulate the Kit ligand gene and therefore influence hair color, scientists cut out various regions at a time and linked them to a gene that produces a color when activated. Done in mice, only one of the regions activated in developing hair follicles. Comparing the DNA sequence of that region between brunettes and blonds, they then identified the single A to G change unique to blonds. This change reduced the amount of Kit ligand protein by 20 percent compared to brunettes. Even in mice, when scientists made this genetic alteration, their hair was lighter too. This means that changing a single letter only affects the utilization of the Kit ligand gene in one part of the body – the hair follicles. This region contributes to the diversity of hair color in humans while maintaining the same roles in other parts of the body. As it turns out, being blond is only skin deep.

This work further proves that large regions of our genetic information once thought of as “junk” DNA actually play critical roles. Subtle changes like this reveal how intricately genes are controlled and how even simple alterations are responsible for human diversity. This information can also help us understand how other gene variations may be associated with disease or resistance.

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Hope for Sickle Cell

September 20, 2014 by

Sept. 19, 2014

By Medical Discovery News

While sickle cell disease has long been studied, a recent discovery revealed that the disease significantly increases the levels of a molecule called sphingosine-1-phosphate (S1P), which is generated by an enzyme called sphingosine kinase 1 (SphK1). Inhibiting the enzyme SphK1 was found to reduce the severity of sickle cell disease in mice, which will hopefully lead to new drugs that target SphK1in order to treat sickle cell disease in humans.

Sickle cell disease is caused by a change in the gene that is responsible for a type of hemoglobin, the protein molecule in red blood cells that carries oxygen. This tiny change results in hemoglobin clumping together, changing the shape of red blood cells.

The name for sickle cell disease actually comes from misshapen red blood cells. Rather than being shaped like a disk, or a donut without a whole, sickle cells are shaped like a crescent, sort of bending over on themselves. The normal shape is critical to red blood cells’ ability to easily travel through blood vessels and deliver oxygen to cells and tissues. Sickle cells become inflexible and stick to each other, blocking the flow of blood through blood vessels.

Symptoms of the disease begin to appear at about four months of age. Normally, red blood cells live for about 120 days. Sickle cells only survive 10-20 days. Although the bone marrow tries to compensate for the rapid loss of red blood cells, it cannot keep up. The disease causes pain, anemia, organ damage, and possibly infections.

Although the symptoms and their severity vary, most people with sickle cell disease will have periodic crises lasting hours or days. Symptoms include fatigue, paleness, shortness of breath, increased heart rate, jaundice, and pain. Long-term damage can occur in the spleen, eyes, and other organs, and sickle cell disease increases the risk of stroke. People who only inherit one copy of the sickle cell hemoglobin gene have a milder case of the disease than those who inherit two copies, one from each parent.

Current treatments only reduce the number and the severity of crises using hydroxyrurea, blood transfusions, pain medications, and antibiotics. As the disease advances, dialysis, kidney transplants, eye surgeries, gall bladder removal, and other treatments may be necessary. The only cure for the disease is a bone marrow transplant, which is not an option for everyone.

So it’s pretty exciting that when scientists found that levels of S1P were elevated in mice with sickle cell disease, they inhibited the enzyme SphK1 to reduce the levels of S1P. As a result, red blood cells lived longer and had less sickling. The mice also had less inflammation and tissue damage, which would reduce damage to red blood cells and prevent symptoms of the disease. When they engineered sickle cell disease mice without the gene for the enzyme SphK1 that makes S1P, again the mice had less sickling and symptoms.

How does S1P influence sickling? Apparently, it binds directly to hemoglobin and reduces its ability to collect and carry oxygen, which causes the characteristic folding of cells. S1P has other roles in the body, so it is unknown whether inhibitors to SphK1 can safely and effectively be used in humans to treat sickle cell disease.

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A Risk-Free Test for Down’s

April 18, 2014 by

April 18, 2014

By Medical Discovery News

Keep Calm, It's Only An Extra Chromosome

When it comes to chromosomes, extra copies are not a good thing. Every cell in the human body carries the same genetic information in two copies of 23 chromosomes. Having an extra copy of a chromosome is called trisomy, and an extra copy of chromosome number 21 is what causes Down syndrome.

Physical signs of Down syndrome include upward slanting of the eyes, flattened facial features, small and unusually shaped ears, small heads, and broad hands with short fingers. Down syndrome can also cause more serious conditions such as varying degrees of mental retardation, poor muscle tone, an increased risk of early onset dementia, and heart, stomach, and eye problems. No two cases of Down syndrome are the same, and with therapy and support people with Down syndrome can live long, productive lives.

The risk of Down syndrome increases with the mother’s age during pregnancy. The risk of having a baby with Down syndrome increases from one in 1,300 to one in 25 at ages 25 to 49.

Women who are pregnant with a child who might have Down syndrome typically undergo an ultrasound test and blood tests for markers such as pregnancy-associated plasma protein-A and a hormone known as human chorionic gonadotropin. Abnormal levels of these markers may indicate a problem with the baby. These tests are generally done during weeks 11-13 of pregnancy. The American College of Obstetrics and Gynecology now recommends that all women undergo prenatal testing for chromosomal abnormalities.

Until recently, Down syndrome could only be confirmed by invasive tests that collect cells from the amniotic fluid surrounding the fetus, the placenta, or the fetus itself. These tests can be risky, with a one percent chance of miscarriage. However, a new, noninvasive screening test called circulating cell-free fetal DNA analysis may reduce the need for invasive prenatal tests. Circulating cell-free DNA from the fetus makes up three to 13 percent of the DNA fragments circulating in the mother’s bloodstream during pregnancy.

First, DNA is isolated from the mother’s plasma, the liquid component of blood. Then, there are two ways to determine if there are any chromosomal abnormalities. Massive parallel DNA genomic sequencing can be used to quantify millions of DNA fragments in just a few days and can accurately detect trisomies. Another approach is called Digital Analysis of Selected Regions, which analyzes only the chromosomes in question to evaluate them for any abnormalities.    

These tests are 99 percent accurate, can be done as early as the 10th week of pregnancy, and are more reliable. They can also diagnose other trisomies, like the ones that affect chromosome 18 (Edwards syndrome) and chromosome 13 (Patau syndrome). At this stage, invasive testing is still required to confirm the diagnosis of a trisomy. But in the near future this new technology will reduce or eliminate the need for additional invasive tests that put the fetus at risk. This is only the beginning of the development of safer and more accurate genetic tests.

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Do We Smell the Same Thing?

February 10, 2014 by

Feb. 7, 2014

By Medical Discovery News

Do We Smell the Same Thing?

Have you ever wondered if we all sense the world in the same way? Evidence suggests that the sense of smell is highly individualized, based on genetic differences. This could revolutionize scents and food flavors into custom-designed creations for individuals.

Humans have specialized neuronal cells within the lining the nasal cavities, part of what’s called the olfactory epithelium. The surface of these cells, like much of the nasal cavity, is covered with mucus. Odor molecules dissolve into this layer and are detected when they bind to receptors on the neurons. This sets off a string of biochemical events that produces a signal, which travels along the olfactory nerve to the olfactory bulb of the brain. Then that signal is transferred to different regions of the brain’s cerebrum. Here odors can be distinguished and characterized. These signals are stored in long-term memory, which is linked to emotional memory. That’s why particular smells can evoke memories. This process is quite complex due to the highly evolved sense of smell in humans.

The genes that are involved in olfactory or smell sensations are not well understood. People do perceive odors differently, but researchers have only identified genes for certain odors. For example, human perception of cilantro has been linked to the olfactory receptor OR6A2 and grassy odors have been linked to receptor OR2J3.

New Zealand scientist Dr. Richard Newcomb tested the ability of almost 200 people to smell 10 different chemicals associated with the key odors of things like apples and blue cheese. Then these individuals’ genomes were completely sequenced, and genetic variances that could account for these olfactory differences were determined. For four of the chemicals tested, clusters of genes were identified as being able to detect these odors. Interestingly, these genes were located on different chromosomes. Newcomb’s work almost doubled the number of genes known to be connected with the sense of smell. For beta-ionone, a chemical associated with the smell of violets, a single gene was shown to allow people to sense that fragrant flower’s scent. Overall, the result of this study was that people are capable of experiencing chemical smells in different ways.

This opens the door for scientists to define an individual’s olfactory profile. If it’s understood how an individual perceives smells, a chef could personalize food just for their senses. Imagine walking into a restaurant and handing your server a card with your olfactory profile based on your genes. And violá! A dinner prepared with the seasonings and flavors you find most pleasing. With continued research, our sense of smell may be able to experience this scenario and more. 

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