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People often overlook how much their health is impacted by the kind of oil they use. Oils high in unsaturated fats can reduce the risk of heart disease, while those high in saturated or trans fats may increase heart disease risk. This article compares MCT oil vs coconut oil, both made from coconuts but with different health advantages. One provides rapid energy, while the other has several other health advantages. So which one should you be adding to your pantry?
Medium-chain triglyceride (MCT) oil is primarily derived from coconut and palm kernel oils but is also found naturally in dairy products such as cheese, yogurt, and milk.
Triglycerides are the primary type of dietary fat in our bloodstream. They consist of three fatty acids joined to a glycerol molecule.
Most dietary fats are long-chain triglycerides (LCTs) with more than 12 carbon atoms. MCTs are medium-chain fatty acids containing 6-12 carbon atoms.
This difference in chain length gives MCT oil unique properties compared to LCTs, found in foods like fish, avocados, nuts, seeds, and olive oil.
Unlike LCTs, MCTs are digested and absorbed quickly in the liver without requiring enzymes or bile acids.
This rapid metabolism sets MCTs apart – they are used immediately for energy or converted into ketones, energy sources derived from fat breakdown.
MCTs are classified into four types based on their carbon chain length:
These attributes make MCT oil a beneficial addition to the diet, especially for those seeking a quick energy source or following a ketogenic diet.
MCT oil is a favorite among those trying to get healthier overall and in terms of nutrition since it provides several health advantages.
MCT oil, which contains fatty acids like caprylic, capric, and lauric acids, may help reduce inflammation by fighting microbes.
Studies show that MCT-rich coconut oil can inhibit the growth of Candida albicans, which causes infections like thrush, and reduce Candida infections in premature babies.
Additionally, virgin coconut oil has been found to slow the growth of Staphylococcus aureus and enhance immune response, potentially helping control inflammation.
However, current evidence is primarily from lab and animal studies, which may not directly apply to humans. More clinical trials are needed to verify these effects in people.
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Coconut oil, extracted from copra (dried coconut kernel), is a natural leader in medium-chain triglyceride levels. Its fat composition contains an MCT concentration of approximately 54%.
This oil consists of lauric acid (42%), caprylic acid (7%), and capric acid (5%). However, coconut oil also contains long-chain triglycerides and unsaturated fats.
Even though lauric acid is technically considered a medium-chain fat, your body breaks it down and absorbs it more slowly, similar to how it handles LCTs.
This delayed processing has led some experts to argue that, despite its MCTs, the high amount of lauric acid keeps coconut oil from being classified as mainly MCT-rich.
While MCTs contribute significantly to coconut oil's health benefits, their unique composition includes other bioactive compounds that offer further advantages, such as:
The following table highlights the key differences between these two popular oils, focusing on their distinct characteristics and health impacts.
| MCT oil | Coconut oil | |
| Source | Extracted from refined coconut or palm oil to isolate MCTs | Derived from coconut flesh |
| Fatty acid | Primarily contains caprylic acid (50%-80%), and caproic acid (20%-50%) | Contains lauric acid (42%), caprylic acid (7%), and capric acid (5%) |
| Nutritional components | High concentration of MCTs | Natural source of MCTs along with other components |
| Uses | Added to coffee, smoothies, and sometimes used as butter substitute | Used in cooking, baking, and for skin and hair care |
| Benefits | Enhances energy levels Supports weight loss, especially for ketogenic diets | Hydrates skin Slows aging Promotes hair health Boosts metabolism |
| Risks | Weight gain High cholesterol Stomach issues ( cramping and bloating) Diarrhea Fat build-up in the liver Vomiting Bloating | Gastrointestinal discomfort Elevated heart disease or stroke risk |
| Digestive tolerance | Easier to digest and absorb | Requires more digestive effort |
| Allergies & sensitivities | MCT oil (refined) lowers coconut allergy risk, but reactions (like coconut allergy) are still possible. | Coconut allergies are relatively uncommon, but they do exist. Some symptoms are hives, rash, anaphylaxis (rare) |
When it comes to weight reduction, MCT oil might be more effective than coconut oil.
The body digests MCT oil and easily converts it into energy rather than storing it as fat.
This unique property can boost metabolism and energy consumption.
Various studies have indicated that MCT oil boosts feelings of fullness, potentially reducing overall calorie intake.
Coconut oil, on the other hand, includes both medium- and long-chain triglycerides.
Although it contains MCTs, a large component is lauric acid, which digests and absorbs like a long-chain fat.
This makes coconut oil less beneficial for weight reduction than pure MCT oil.
Coconut oil is a common pick for healthy skin due to its high concentration of lauric acid.
Lauric acid has powerful antibacterial qualities that are good for beauty and skin health.
Lauric acid can heal acne in human cells, and coconut oil has been proven to alleviate atopic dermatitis (eczema) symptoms such as redness and irritation.
Its fatty acids are excellent for preserving and moisturizing the skin, effectively treating xerosis, a common condition characterized by dry and itchy skin.
These characteristics also make it beneficial against skin diseases.
Even though MCT oil has its own advantages, it lacks some of the additional compounds present in coconut oil that contribute to skin health benefits.
It serves as an effective carrier oil for essential oils while providing moisturizing properties.
Therefore, coconut oil is typically recommended for topical skin care because of its wider range of benefits.
MCT oil and coconut oil both contain triglycerides, but their composition and metabolic effects differ.
MCT oil, with its higher concentration of MCTs, is less likely to raise triglyceride levels in the blood
Coconut oil, due to its LCT content, may cause a greater increase in triglycerides and take longer to digest.
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MCT oil is a flexible component that works well in various dishes and drinks. Here are some practical ways to use it:
Coconut oil, solid at room temperature unless processed, has a high smoke point, making it perfect for high-heat cooking. Here are some ways to use it:
MCT oil shines for those seeking a quick energy boost, weight management support, and potential benefits for neurological conditions. Its rapid conversion into fuel makes it ideal for ketogenic diets and enhancing cognitive function. However, be mindful of potential digestive side effects.
Coconut oil provides broader advantages, such as reducing stress and enhancing skin and hair health. While it boasts some MCTs for energy, its LCT content makes it less suitable for weight loss than MCT oil.
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The benefits of a warm cup of tea on a slow afternoon go further than just relaxation. Each heavenly sip is actively nourishing your gut and simultaneously boosting your metabolism. Teas have helped to combat digestive problems like nausea, constipation, bloating, and indigestion for millennia. This article will go over five of the best teas for your gut. Read on to know why, how, when, and when not to drink these five teas.
Ginger contains compounds known as gingerols and shogaols, which can stimulate stomach contractions and gut cleansing.
It's beneficial for nausea, bloating, and indigestion.
Ginger tea can also reduce the severity of morning sickness and nausea during pregnancy.
Ginger tea bags are readily available at grocery stores.
Making ginger tea at home with a few pieces of sliced ginger root can strengthen the brew's flavor.
Fennel is an herb rich in antioxidants, a set of molecules that control dangerous free radicals in the body.
As such, they are helpful in combatting gut ulcers and preventing their development.
Additionally, they can stimulate bowel movements.
The gas relief it provides can help manage the effects of Irritable Bowel Syndrome (IBS).
Fennel tea can be made by steeping the seeds or the freshly grated root of the herb in a cup of boiling water.
Black tea is jam-packed with healthy compounds like thearubigins and theaflavins.
These compounds help with indigestion and prevent stomach ulcers while promoting gut cleansing.
The polyphenols in black tea help moderate microbial activity in your gut. They effectively weed out harmful bacteria and promote the growth of beneficial bacteria.
Since black tea molecules are too large to be absorbed, they remain in the intestine and promote liver metabolism remotely, boosting endocrine health.
Black tea bags are widely available, although you could also use black tea leaves from the plant Camellia sinensis.
Peppermint tea is renowned for improving digestion by fighting indigestion and IBS.
One of the main compounds in peppermint tea is menthol, an essential oil with a host of digestive benefits against bloating and gas caused by IBS.
Since peppermint oil helps ease nausea in pregnant females, peppermint tea will likely have a similar effect.
Further research into the effects of peppermint tea on human digestion will yield more information.
Spearmint tea contains beneficial minerals and nutrients, including antioxidants, vitamin C, iron, and folate.
S-carvone is a compound that naturally occurs in spearmint tea at high concentrations.
It has a strong ability to inhibit muscle contractions in the gut, providing relief from digestive upsets.
Spearmint tea also stabilizes the gut during episodes of nausea.
Interestingly, spearmint tea is the drink of choice for people with PCOS since it reduces the body's oxidative stress and inflammation.
When drawing up a tea routine, you should be aware of the benefits of each kind of tea.
For instance, caffeinated teas can give you the energy boost you need to start the day.
Some examples of caffeinated teas include:
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Before a meal, a cup of tea can stimulate digestion.
The best teas to stimulate digestion are:
At the end of the day, caffeine-free teas can help you wind down.
These could include:
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Less than 2% of the global population carries the red hair gene, one of the most intriguing human traits. It may seem like common knowledge that red hair originated in the Viking lands of Scandinavia. However, research points to red hair originating in Central Asia as a mechanism against the harsh sun. Eventually, it spread to remote regions like Ireland, Scotland, and Scandinavia, where it is most abundant today. This article will help you learn more about the red hair gene: why some people have red hair, how the gene travels down generations, how red hair can affect your skin, and how to know if you could be a carrier of the gene.
Melanin, a coloring pigment produced by the melanocyte cells in the hair, determines hair color.
When melanocytes produce an excess of eumelanin, a dark-colored melanin pigment, people get black or brown hair.
Those who don’t produce enough of this pigment have blond hair.
In rare cases, the melanocytes produce another pigment called pheomelanin.
Pheomelanin is a yellow/reddish pigment responsible for the iconic red-colored hair.
The type of melanin pigment the melanocyte cells produce depends on a person’s genes.
Image: Types of Melanin Pigments
The MC1R gene is one of the strongest influencers of red hair.
Thus, it is also called the red hair gene.
It instructs your body to produce the melanocortin-1 receptor that decides which type of melanin the melanocytes produce.
When the receptor is active, it encourages the melanocytes to produce eumelanin, leading to darker hair color.
When the receptor is blocked or inactive due to mutations in the MC1R gene, it produces pheomelanin instead, leading to reddish hair color.
Pheomelanin production causes individuals to grow red hair.
Red hair is a recessive genetic trait.
This means that a person must inherit the genetic change associated with red-colored hair from both biological parents for it to be active.
Many people may be carriers of one copy of the mutated gene and still have darker hair color.
A study reports that up to 40% of people in Scotland carry at least one copy of the mutated gene despite only 13% having red hair.
In some families, a child could mysteriously be born with red hair despite generations of people having darker hair.
The darker hair implies that the previous generations were all silent carriers of the gene.
Genetic testing could predict an interesting turn of events like this.
Genetic testing can identify if the parents are carriers of the MC1R gene mutations and predict whether a child will have red hair.
The effects of carrying the MC1R gene don’t end with the hair alone.
A few conditions seen in such individuals include:
Genetic testing to know whether you carry the red hair gene is thus beneficial for you and your future generations.
The following scenarios will help you understand your likelihood of having a child with red hair.
Each scenario has a different genetic makeup of the biological parents involved.
Both parents have dark hair.
In this case, there is a practically 0% chance that your child will be red-haired.
Both parents have dark hair and carry one copy of the gene each.
In this case, there is a 25% chance that the child will have red hair and a 50% chance that the child may have dark hair but carry the red gene.
One parent has two copies of the gene, and the other has none.
In this case, the children may carry the red hair gene but will not have red hair.
In this case, there is a 50% chance the child will be red-haired and another 50% chance that the child will be dark-haired and a carrier of the red hair gene.
In this case, all the children will also have red hair.
Millions of Americans unwittingly endure glaucoma, an invisible cause of vision problems every year. The early symptoms of glaucoma can be hard to diagnose, so people don’t usually find out until it’s too late. Genetic mutations are one of the leading causes of glaucoma, and regular genetic and eye testing can help diagnose it in time, especially for those with a positive family history of the disease. Read on to learn about glaucoma, its genetic risk factors, its causes, and how to identify if you’re at risk.
Glaucoma is a hereditary condition that damages the optic nerve.
This nerve sends visual signals from the eye to the brain, helping you understand what you see.
Glaucoma progresses slowly. There are no clear early signs of this disease, and most people don’t seek medical attention until they notice a decline in their vision.
People with a genetic risk for the condition may need regular eye exams to monitor their optic nerve health and intraocular pressure (IOP).
High IOP is the main culprit of glaucoma.
A lubricant called aqueous humor circulates within the anterior chamber of the eye. In order to maintain a stable IOP, it is drained out of the eye regularly.
If this drainage system is blocked, the aqueous humor builds up in the eye, increasing the IOP.
Pressure builds on the optic nerve, gradually causing the death of optic nerve fibers, leading to blind spots and poor vision.
Research has shown that some forms of glaucoma are hereditary and can be passed down through generations.
Glaucoma is inherited in either an autosomal dominant or autosomal recessive manner.
In autosomal dominant inheritance, only one copy of the mutated gene from either parent is needed to express itself in both the parent and the offspring. Juvenile glaucoma is inherited in this manner.
In autosomal recessive inheritance, both parents must carry one copy of the mutated gene (in its recessive state), and the child must inherit both copies to be at risk for glaucoma. Congenital glaucoma is inherited in this manner.
Some variants of glaucoma may run in the family. The parents may be carriers of the mutated genes and not develop the condition themselves while passing it on to their children.
Sometimes, existing risk factors like hypertension, hypotension, diabetes, age, or eye injury in families could lead to the development of glaucoma.
A meta-analysis studied 46 published observational research papers to find gender-based risk factors for developing OAG.
The results found that men were 1.4 times more likely to develop glaucoma than women.
The myocilin (MYOC) gene produces the myocilin protein, which is essential for maintaining IOP.
Scientists have identified at least a hundred variations of the MYOC gene.
These variations may lead to the underproduction of myocilin, leading to increased intraocular pressure and glaucoma.
About 4% of all cases of primary OAG and more than 10% of all cases of juvenile OAG are due to MYOC mutations.
The Cytochrome P450 family 1 subfamily B member 1 (CYP1B1) gene produces the CYP1B1 enzyme.
Researchers have studied over 100 variations of this gene.
50% of all cases of primary congenital glaucoma are due to mutations in this gene at the GLC3A locus.
The Latent Transforming Growth Factor Beta Binding Protein 2 (LTBP2) gene produces the LTBP2 protein, which forms the anterior chambers of the eye.
A study found that null mutations in this gene could lead to an increased risk of developing PCG.
While these 3 are the most researched genes for glaucoma, other genes also play a minor role in causing the disease.
Changes in certain genes can increase your risk for many chronic health conditions, including glaucoma. Learn more:
Increased IOP slowly damages the optic nerve over time, leading to open-angle glaucoma (OAG)
Though it doesn’t show early symptoms, it could lead to blurry vision and the gradual loss of both peripheral and central vision.
A 2011 study reports that single-gene mutations cause 5% of all POAG.
For instance, mutations in the MYOC gene can cause juvenile open-angle glaucoma.
Multiple mutations and environmental risk factors can lead to the other 95% of cases.
Early-onset glaucoma is a type diagnosed before the age of 40 in adults.
This type is primarily hereditary and may occur even without related risk factors.
A majority of early-onset glaucoma cases turn out to be primary open-angle glaucoma.
Early-onset glaucoma is generally inherited in an autosomal recessive manner- meaning that while parents may carry one copy of the gene, the disease will not be inherited unless the child carries both copies.
Congenital glaucoma occurs in infants before the age of three, leading to optic nerve damage and vision loss.
Infants with congenital glaucoma generally exhibit red or cloudy eyes, an increased rate of blinking, light sensitivity, and tear production without crying.
Congenital glaucoma could be due to complications affecting the infant’s eye as a fetus.
Studies say that variations in the CYP1B1 or LTBP2 genes could lead to the development of primary congenital glaucoma in infants under the age of three.
Juvenile OAG (JOAG), diagnosed in childhood or early adulthood, is called juvenile open-angle glaucoma.
The cause and prognosis of the disease are the same.
Juvenile OAG is inherited in an autosomal dominant manner, meaning that if even one parent carries a MYOC gene with the specific mutation responsible for JOAG, the child will end up with JOAG.
Angle-closure glaucoma (ACG) occurs when the IOP suddenly increases, stopping the movement of the aqueous humor in the eye.
Since this is an acute attack, it presents with headaches, nausea, and eye pain. The vision turns blurry, and halos are visible around light sources.
ACG generally presents in one eye at a time. With timely medical aid, doctors could save the other eye.
Interestingly, normal-tension glaucoma damages the optic nerve without an increase in IOP.
Instead, normal-tension glaucoma could develop due to poor blood flow to the optic nerves or some other inherited trait.
Secondary glaucoma is the development of either open-angle or angle-closure glaucoma due to a separate condition, such as:
Analyzing your genes can also help you understand your risk of developing the disease.
Genetic testing is beneficial in identifying early-onset glaucoma if the condition begins manifesting itself in people under 40 years of age.
Suppose genetic testing reveals a higher risk of developing glaucoma. In that case, you may need regular eye exams done by an eye doctor to diagnose the condition before it worsens.
In fact, a comprehensive eye exam once every two years can be beneficial to anyone whose first-degree relatives are diagnosed with glaucoma.
Water helps lower IOP if consumed in moderation. Drinking too much water in a short time can lead to increased IOP.
Glaucoma is not a fatal condition. It will neither increase your mortality risk nor lead to fatal complications.
Stress does not directly lead to open-angle glaucoma. However, patients who are regularly overwhelmed may neglect their treatment courses, which could worsen their condition.
Tomatoes, a staple in everyone's pantry, and potatoes, a cult favorite, along with eggplants and peppers, belong to the nightshade family of vegetables. However, what's a delicious ingredient for many can be a source of discomfort for some. Experiencing symptoms like redness, itching, or digestive issues after a meal featuring these foods might point to a lesser-known but significant condition: a nightshade allergy. This comprehensive article covers everything you need to know about nightshade allergies, from the underlying causes and risk factors to the intricate genetics and effective management strategies.
Did You Know?
Genetic changes are the most common cause of food and other allergies. Using your existing DNA raw data file, you can find out which food, environmental, and drug allergies you're susceptible to. Learn more.
Nightshades are part of the Solanaceae family, consisting of 3000 flowering plants. Although some of these plants are beneficial, some can be dangerous if consumed.
For instance, belladonna, a deadly nightshade, increases heart rate and blood pressure.
Tobacco is a nightshade plant used to make cigarettes.
Yet, many nightshades, such as tomatoes, eggplants, potatoes, and bell peppers, are staple foods in various cuisines across the globe.
Nightshades are rich in potassium, iron, fiber, vitamin C, and antioxidants such as anthocyanins and lycopene.
They are beneficial for heart health and cancer prevention.
However, some people exhibit adverse effects after eating nightshades.
This condition is called nightshade allergy, intolerance, or sensitivity.
Nightshades possess certain chemical compounds that may be harmful to some people.
These chemicals, called phytochemicals, help plants fight against certain foreign substances.
A phytochemical called lectin may trigger an immune reaction if undigested, resulting in autoimmunity.
Genetic variants can be the root cause of the development of a nightshade allergy.
Mutations in the BCHE gene are associated with nightshade allergy.
The BCHE gene provides instructions for making butyrylcholinesterase (BChE). This cholinergic system enzyme plays a significant role in digestion, blood pressure, heart rate regulation, and spinal cord function.
BChE is a bio-scavenger, essential for:
Low levels of BChE in the body due to mutations may not be sufficient to fight against glycoalkaloids (BChE inhibitors) in nightshades.
Eventually, a nightshade allergy can develop.
Research studies suggest the involvement of specific genes in nightshade allergy.
While nightshade allergies aren't caused by a specific gene, a group of variations in certain genes can have a cumulative effect and increase the risk of allergic reactions.
For example, the BCHE gene plays a role in inactivating the alkaloids present in the nightshade plants.
Any variation in this gene that causes lower levels of poor functioning of the BChE enzyme may result in alkaloid build-up in the body, increasing the risk of a nightshade allergy.
Nightshade allergies are unusual, so you should also consider more common allergens, such as dairy, nuts, seafood, soy, and gluten. Additionally, two factors contribute to nightshade allergies.
Nightshade allergy is mainly caused by the toxic alkaloids in them that defend the plant against molds, pests, and other pathogens.
People develop allergies to alkaloids, which trigger the immune system.
It releases immunoglobulin E (IgE) antibodies to tackle the allergen by releasing histamine into the blood.
This results in nightshade allergy symptoms.
High concentrations of alkaloids like solanine, nicotine, and capsaicin can cause gut irritation and joint inflammation.
People with autoimmune disorders have a weakened immune system.
Weaker immune systems do not respond appropriately to the alkaloids in nightshades, allowing allergies to run rampant.
Rheumatoid arthritis, celiac disease, and inflammatory bowel disease (IBD) are some prevalent autoimmune disorders.
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You are more likely to develop nightshade allergy if you have certain risk factors:
Nightshade allergy is more severe than nightshade intolerance.
While intolerance causes loose stools, bloating, and nausea, which are uncomfortable rather than deadly, allergies can lead to severe symptoms like potentially fatal anaphylaxis.
Initial symptoms can take up to 72 hours to appear, and they can look like:
Similar to other allergies, a doctor can identify a nightshade allergy by performing some diagnostic tests, including:
A standard food allergy treatment involves deleting foods containing the allergen. As instructed by your doctor, keep a food log to track your symptoms and any possible triggers.
Drugs to prevent allergic reactions when exposed may also be part of the treatment approach. Typical prescription drugs include:
EpiPens: Epinephrine injections stop anaphylaxis, a severe allergic reaction that can be fatal.
The simplest method to prevent food allergy symptoms is to avoid the allergens. Here are some easy swaps to common nightshade foods:
| Allergens | Alternatives |
| Tomato sauce | Pesto or Alfredo sauce |
| Tomatoes, | Beetroots, carrots, or grapes |
| Blueberries | Raspberries, strawberries or cranberries |
| Eggplants | Mushrooms |
| Bell peppers | Carrots, onions, celery, or zucchini |
| White potatoes | Sweet potato, radish, or cauliflower |
| Paprika, cayenne, chili flakes | Basil, oregano, black/white pepper |
While onions aren't part of the nightshade family, it's best to stay away from them if you have IBS since they can exacerbate the symptoms.
Interestingly, black and white peppers come from a different family of plants, not from the nightshade family. They're safe to consume if you have a nightshade allergy or intolerance.
Though chocolate isn't a nightshade, it does contain some alkaloids. Fortunately, these are easier to digest than the alkaloids in nightshades, so they shouldn't cause an allergic reaction.
Did you know that Lewy body dementia is 1.5 times more likely to manifest in males rather than females? This condition affects 1.4 million people and their families across the US. If you're wondering what Lewy bodies are, they are clumps of alpha-synuclein protein. They accumulate in the brain, leading to an increasingly severe loss of brain function. Bringing awareness and understanding to this condition can help those affected by Lewy body dementia manage it better. This article will explore the 7 stages of Lewy body dementia and explain everything you need to know about the disease.
Parkinson's patients have Lewy bodies in their brains, too. That's why people who have been diagnosed with Parkinson's can end up with Lewy body dementia.
Read on to learn about the characteristic symptoms of this disease.
Lewy body dementia limits the capability to think and process information.
The main symptoms present in Lewy body dementia but not in Alzheimer's include:
Most patients experience episodes of delirium, with blank faces and slurred speech.
These phases can last hours or even days.
Patients with Lewy body dementia (LBD) often experience visual hallucinations featuring humans or even animals.
A few patients have even reported hearing and smelling things that aren't there.
Some even say their sense of smell got worse with time.
Difficulty in movement is a common symptom of Parkinson's disease, and this is seen in LBD as well.
They can include:
Subtle signs of the loss of motor function include:
LBD affects the regulation of other organs via the nervous system.
Dysregulated organs could cause:
Understanding how this condition progresses can help afflicted people and their families manage the condition better at each step of this challenging journey.
In this stage, no symptoms are noticeable to the patient or others.
They live life with no interruptions or inconveniences.
Unseen to anyone, proteins begin accumulating in the brain, eventually leading to the formation of Lewy bodies.
Minor instances of forgetfulness begin to take place.
There are rare instances of interruption in day-to-day life and activities.
Since mild lapses in reasoning are also symptoms of aging, it is hard to diagnose at this stage.
In the third stage of the condition, the symptoms become more apparent.
The memory loss worsens, and concentration becomes more difficult for the patient.
Maintaining a schedule becomes harder and harder.
By this time, those around the patient have noticed a decline in brain function and have begun to explore treatment and care options.
The loss of memory begins to take a toll on the patient's near and dear ones. Remembering recent events and even faces becomes a chore at this stage.
Performing day-to-day tasks becomes difficult.
It is at this stage that most patients seek medical intervention and are diagnosed with dementia.
The patient starts to depend on others for bathing and dressing.
Short-term memory loss becomes significant, leading to disorientation and frustration. For now, long-term memories remain preserved.
Significant memory loss accompanies a shift in personality.
At this stage, patients need constant aid to get through all parts of their day, including eating and bathing.
Swallowing and speaking become more difficult due to weaker throat muscles.
A large number of patients lose their ability to communicate verbally.
A handful of patients are no longer able to walk by this stage.
As their physical health worsens, their caregivers focus on comfort and quality of life. The last stage of LBD ends within 1.5 to 2.5 years.
A study published in Elsevier suggests that varied genetic components could lead to LBD.
These genes are related to the working of proteins in the central nervous system.
Mutations in the SNCA and SNCB genes affect neurotransmitter production in the brain, making it harder to think and recall information.
Eventually, misshapen proteins accumulate in the brain, forming Lewy bodies.
It can be hard to diagnose LBD against other neurodegenerative disorders.
The only reliable technique available right now is an autopsy.
Thus, doctors rely on other tests to study brain function.
The one-year rule helps differentiate LBD from other subtypes.
If dementia appears within one year of Parkinson's symptoms, the patient likely has LBD.
Further research into diagnosis through studying blood and cerebrospinal fluid is ongoing.
If successful, LBD could be diagnosed earlier with more accuracy.
There are several medications available to manage the different types of symptoms experienced:
It's important to remember to consult a physician about relevant medication or therapies for your condition.
Although the average life expectancy is 5-8 years after diagnosis, some people have lived up to 20 years with the condition.
Lewy body dementia weakens throat muscles. This deterioration can lead to food or water reaching the lungs, resulting in a fatal case of pneumonia. In most cases, patients succumb to pneumonia or heart failure.
Changes in lighting at dusk can lead to confusion, restlessness, agitation, and distress in patients suffering from Lewy body dementia.
Lewy body dementia - Symptoms and causes - Mayo Clinic
Diagnosing Lewy Body Dementia: For Professionals | National Institute on Aging (nih.gov)
Lewy Body Dementia: Symptoms, Stages, & Treatment (webmd.com)
Dementia with Lewy bodies - Treatment - NHS (www.nhs.uk)
Lewy body dementia - PubMed (nih.gov)
Risk factors for dementia with Lewy bodies - PMC (nih.gov)
