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Epoch Health Article Gastroesophageal reflux disease (GERD) results from stomach acid repeatedly flowing back into the esophagus, the digestive tube that runs between the mouth and stomach, due to a dysfunction in the lower esophageal sphincter (LES). This can irritate the lining of the esophagus. Many people experience occasional gastroesophageal reflux (GER), more commonly known as acid reflux or heartburn. According to epidemiological data from the International Foundation for Gastrointestinal Disorder (IFFGD), up to 40 percent of people experience acid reflux at least once a month, with 20 percent experiencing it on a weekly basis. Occasional acid reflux is not a serious condition and can often be treated effectively at home. However, when acid reflux happens repeatedly and frequently, it can cause GERD—a condition in which the lining of the esophagus is damaged due to prolonged exposure to stomach acid. According to the National Institute of Health, 20 percent of Americans suffer from GERD. It can be a serious condition that should be treated in consultation with a physician. Acid Reflux Versus GERD Most people can manage the symptoms of GERD with lifestyle changes and/or medications. In rare cases, some may need surgery to address their symptoms. The differences between regular heartburn/acid reflux and GERD. GERD Versus LPR A lesser-known kind of acid reflux is laryngopharyngeal reflux (LPR)—sometimes called “silent reflux.” This is caused by the same dysfunction of the LES, but in LPR, stomach acid backs up all the way to the larynx (voice box) or the pharynx (back of the throat). It is called silent reflux because it is harder to diagnose in adults, though the condition is common in infants whose sphincter muscles have not yet fully developed. Only one or two of the symptoms listed below may be present in the case of LPR. GERD Symptoms Symptoms occur twice a week or more and may include: Difficulty swallowing Burning sensation in the chest Chest pain when lying horizontally Burning sensation in the throat Bad taste in the back of the throat Reflux that occurs at night and wakes you LPR Symptoms Symptoms may be chronic or rare and may include: Difficulty swallowing Chronic cough Hoarseness Sore throat Postnasal drip or mucus in the back of the throat Red, swollen, or sore voice box The feeling of a lump in the throat that doesn’t go away Difficulty breathing LPR is a serious condition that can result in a scarred throat and voice box. It can also increase the risk of cancer in these areas, impact the lungs, and aggravate conditions such as asthma, emphysema, or bronchitis. If you think you have either GERD or LPR, consult a physician as soon as possible. What Are the Symptoms and Early Signs of GERD? As described by the IFFGD, “The two most frequently reported symptoms of GERD are heartburn, which can be described as a burning discomfort that begins behind the breastbone and radiates to the neck and throat, and acid regurgitation, which is characterized as a bitter, sour tasting fluid.” Sometimes patients suffer from other symptoms, such as: Cough Laryngitis Asthma Difficulty swallowing Hoarseness in the morning The condition can also cause bad breath. Some GERD patients have no apparent symptoms. Acid Reflux...Gerd What Causes GERD? Acid reflux is caused by the failure of the sphincter muscle connecting the esophagus to the stomach to properly close after opening to admit food and drink. In GERD, the esophageal sphincter doesn't close properly, allowing stomach acid to creep into the esophagus. The Epoch Times Researchers have not isolated a single cause for this problem. Certain physical factors may cause GERD, including: Weak or injured LES Abdominal distention (as accompanies pregnancy or obesity) Delayed emptying of stomach content Presence of the bacteria Helicobacter pylori A single cause of GERD hasn't been determined, but several physical factors are typically at play. Who Is More Likely to Develop GERD? Research indicates that many factors can contribute to the development of the disease. Some are non-modifiable factors such as gender, age, or genetic factors. Among contributing modifiable factors are lifestyle, diet, and excessive body weight. Lifestyle risk factors include: Excess body weight, particularly obesity Moderate to high alcohol use Smoking Exercising immediately after a meal Lack of regular exercise Diet and eating habits In terms of diet, a number of foods likely to trigger acid reflux have been identified, including Fried and fatty foods Sour and spicy dishes Acidic foods such as citrus fruits and tomatoes Carbonated beverages Black tea Coffee (including decaf) Chocolate Alcohol Eating habits such as irregular mealtimes, overeating, and eating meals just before bedtime have also been correlated with the symptoms of GERD. How Is GERD Diagnosed? Your physician is likely to make an initial diagnosis based on your symptoms and eating habits. However, positive confirmation, including the ruling out of other conditions such as heart disease, requires testing. To confirm a diagnosis, your physician may order one or more of the following: Upper endoscopy:  This is a procedure in which a tube with a light and a camera is inserted down the throat, allowing your physician to see inside your esophagus and stomach. This is sometimes done simultaneously with a colonoscopy, though the procedures can be done separately. While this procedure will not always give a positive confirmation of the initial diagnosis, it will show whether any damage to the digestive system has occurred due to GERD. Transnasal esophagoscopy: This test looks for esophagus damage. A thin, flexible tube with a video camera is inserted through the nose, down your throat, and into the esophagus. The camera then sends photos to a video screen. This procedure requires no anesthesia and can be done in your doctor’s office. X-ray of the upper digestive system: X-rays are taken after you drink a chalky prep liquid that coats the lining of the digestive tract. The coating gives your doctor a clear silhouette of your esophagus and stomach. This is particularly helpful in evaluating people who are having trouble swallowing. This procedure may also involve swallowing a barium pill that can help diagnose a narrowing of the esophagus. Esophageal manometry:  This measures the rhythmic muscle contractions in the esophagus upon swallowing. Esophageal manometry also assesses the coordination and force of the working muscles of the esophagus. This test is typically only recommended for people who have difficulty swallowing. Ambulatory acid (pH) probe test: This test is the “gold standard” for GERD testing. A clip or small tube is placed in your esophagus to assess how often and how much stomach acid regurgitates. The monitor connects to a small computer that you wear over your shoulder or at belt level. The wide range of symptoms for GERD contributes significantly to the expense of tests needed to rule out other conditions. For example, the expense of excluding heart attacks and other cardiac problems can be quite costly. What Are the Complications of GERD? According to the American Gastroenterological Association, untreated GERD can lead to Esophagitis:  inflammation of the esophagus Stricture:  narrowing of the esophagus due to ulceration and scarring, making it hard to swallow and causing food to become lodged in the esophagus Breathing problems:  asthma or chronic cough, etcetera Barrett’s esophagus:  a change in the tissue lining your esophagus that elevates your risk for esophageal cancer GERD can also lead to complications beyond the esophagus, including inflammation of the pharynx and larynx. It may also affect the lungs, causing bronchitis, asthma, or pneumonia. What Are the Treatments for GERD? GERD is treated with diet and lifestyle adjustments, medication, and, in rare instances, surgical intervention. Diet and Lifestyle Diet and lifestyle are crucial first steps in treating GERD. Recommendations to relieve symptoms include: Achieving and maintaining a healthy weight. Stopping smoking, if you smoke. Eating frequent, smaller meals rather than fewer, large ones. Decreasing the amount of fat in your diet, including fatty meats, gravy, butter, oils, salad dressings, and full-fat dairy products (e.g., whole milk, cheese, and sour cream). Sitting upright while eating and remaining upright (standing or sitting) for an hour afterward (no slouching on the couch after a meal). Not eating for at least three hours before going to bed. Avoiding clothes that are tight in the belly area. By squeezing the stomach, they can push acid upward into the esophagus. Sleeping with the head of your bed raised 6 to 8 inches. You can elevate the bed by putting blocks under the bedposts. (Note: Extra pillows won’t work as this will squeeze the   stomach.) Cutting out possible trigger foods, including spicy or sour foods, and liquids such as coffee, alcohol, and vinegar-based products, which can affect the muscular movements of the digestive tract. Medications If your condition doesn’t respond to these lifestyle and diet changes, your doctor may prescribe medication. For GERD, these medications are either designed to decrease your levels of stomach acid or increase the peristalsis (muscular movement) of the upper digestive tract, forcing the acid back down into the stomach where it belongs. Antacids:  Over-the-counter antacids are best for relatively infrequent discomfort due to reflux. However, if taken too often, antacids can worsen the problem, as they can cause the stomach to produce more acid. Histamine blockers: Histamine 2 (H2) blockers are designed to lower acid secretion. H2 blockers help heal esophageal damage in about half of the patients who take them. Proton pump inhibitors: Proton pump inhibitors (PPIs) block the three primary acid production pathways. PPIs suppress acid production significantly more than H2 blockers. Many patients, even those with severe damage to the esophagus, have experienced healing of esophageal damage when prescribed PPIs. Baseball Hall of Famer and sportscaster Jim Palmer has promoted their efficacy in treating his decades-long battle with GERD. Prokinetic agents:  Prokinetic agents are drugs that enhance the smooth muscle activity of your gastrointestinal tract. Your doctor may prescribe them in combination with an acid-suppressing drug. Surgery and Endoscopic Intervention Nissen fundoplication:  A surgical intervention may be recommended by your doctor if your treatment does not respond to lifestyle and medication changes. The goal of such surgery is to reinforce the anti-reflux barrier. In the procedure, the surgeon wraps a part of the upper stomach around the lower esophagus, enhancing the action of the LES. The procedure may also be done laparoscopically to reduce recovery time. Some patients choose this option over a lifetime of taking medication. Transoral incisionless fundoplication (TIF): A TIF is an alternative to surgery for some. It uses a device to create a passageway for an endoscope. In the procedure, the physician deploys preloaded tweezers and fasteners in the device to repair or reconstruct the lower esophageal sphincter. One form of therapy uses an endoscopic “sewing machine” to install stomach sutures that increase the anti-reflux barrier. LINX device:  Using minimally invasive surgery, a surgeon wraps a ring of magnetic beads around the LES. The magnetic attraction between the beads keeps the LES closed to refluxing acid but allows food to pass. The magnetic beads do not interfere with airport security systems or magnetic resonance imaging. How Does Mindset Affect GERD? Research has shown a link between GERD and psychological factors. In a seminal 2016 study of over 1,200 firefighters, researchers found a higher incidence of depression, stress, and low self-esteem among GERD sufferers than among those firefighters who were GERD-negative. The researchers concluded that “psychological and medical approaches should be combined in GERD assessment.” Some research has shown a connection between anxiety and GERD. If this is true in your case, you may want to speak with your doctor about medications to treat anxiety and/or depression. Activities that reduce anxiety, such as meditation, yoga, “forest bathing,” regular exercise, or breathing exercises, may also help address your symptoms. The Importance of Sleep Researchers have also found an association between GERD and poor sleep quality. The exact relationship is not understood, but researchers have suggested that improved sleep could also alleviate the symptoms of GERD. Discuss your sleep habits with your physician or health care provider. They may recommend supplementing melatonin or changes like using blackout blinds, white noise machines, removing or disabling electronics in your sleep space, and more. What Are the Natural Approaches to GERD? At least two studies have had promising results treating GERD symptoms with extracts obtained from Opuntia ficus-indica, commonly known as prickly pear cactus. According to Harvard Medical School, licorice, chamomile, and marshmallow root have been found to be effective in treating GERD in several studies. Slippery elm and d-limonene also have anecdotal evidence supporting their use.   How Can I Prevent GERD? While nothing you can do will be 100 percent effective in preventing GERD, losing weight if you are overweight and stopping smoking if you smoke are two lifestyle choices that can make a big difference. Reducing or stopping the usage of certain medications that can aggravate acid reflux/GERD may also be effective, though you should consult your physician before discontinuing or lessening your medications. Medications that aggravate GERD are: Benzodiazepines, a class of sedatives. Calcium channel blockers to treat high blood pressure. Certain asthma medications. Nonsteroidal anti-inflammatory drugs (NSAIDs). Tricyclic antidepressants. As indicated above, eating and sleeping well, in addition to lifestyle choices to manage stress and anxiety, can also help control acid reflux/GERD.

Epoch Health Article Lupus, short for lupus erythematosus, is an incurable chronic autoimmune disease capable of damaging any part of the body and manifesting with a wide range of symptoms affecting nearly any organ. The term “lupus” is Latin for “wolf” and was first used by a 13th-century physician to describe the disease’s facial lesions, which he believed resembled a wolf bite. The Lupus Foundation of America estimates that about 1.5 million Americans and 5 million people globally have some type of lupus. Lupus most often affects women of childbearing age. What Are the Types of Lupus? Lupus of America.... There are four main types of lupus. 1. Systemic Lupus Erythematosus (SLE) When people speak of lupus, they’re typically referring to systemic lupus erythematosus, the most common form of lupus, accounting for 70 percent of cases. SLE involves the immune system attacking the body’s own tissues, leading to widespread inflammation and tissue damage in various organs, including the skin, joints, brain, kidneys, lungs, and blood vessels. The severity of the condition can vary from mild to severe. Pediatric SLE, also known as juvenile lupus or childhood-onset SLE (cSLE), is when the clinical onset of lupus occurs in individuals under 18. It is rare, with a prevalence of 3.3 to 24 per 100,000 children. Approximately 10 percent to 20 percent of all SLE cases are diagnosed in childhood, and pediatric SLE often exhibits more severe symptoms than adult-onset cases. 2. Cutaneous Lupus Erythematosus (Skin Lupus) In cutaneous lupus, the immune system attacks skin cells, resulting in inflammation that produces red, thick, and typically scaly rashes and sores that can burn or itch. The rashes and sores may appear dark purple or dark brown on dark skin tones. There are three types of skin lupus Acute: Acute cases typically develop rapidly, often have a short duration, and usually don’t result in skin scarring. Almost all individuals with acute cutaneous lupus also have SLE. Acute cutaneous lupus can be localized and generalized (i.e., distributed diffusely over the skin). The butterfly rash, a red rash that can be flat or raised and covers the nose bridge and cheeks, is a localized presentation. Generalized acute cutaneous lupus manifests as raised red rashes across the entire body. Subacute: Subacute cutaneous lupus involves a rash of red, ring-shaped sores or scaly patches with well-defined borders. While it can be associated with SLE, it can also occur independently. Typically, these lesions are neither itchy nor painful and seldom result in scarring once they resolve. Chronic: There are many types of chronic cutaneous lupus. Chronic cutaneous lupus erythematosus lasts for a long time and may cause permanent scarring and, potentially, hair loss. Among the many kinds of chronic cutaneous lupus, discoid lupus, with its disk-shaped rashes, is the most common. These rashes often appear on the scalp and face and are typically red, scaly, and raised and can lead to scars, hair loss, or skin discoloration over time. When lupus results in rashes that resemble those seen in other conditions, they are categorized as nonspecific rashes associated with lupus. There are a vast number of these skin conditions, including hives, bruises, and vitiligo. 3. Neonatal Unlike its name implies, this rare acquired autoimmune disorder is not actually the infant form of lupus, nor is it genuine lupus. Newborns with neonatal lupus may experience temporary skin rashes, liver issues, or low blood cell counts, which generally resolve within six months without lasting consequences. 4. Drug-Induced This is a lupus-like disease caused by prescription drugs, including hydralazine (for hypertension), procainamide (for heart arrhythmias), valproate (an anti-epileptic), infliximab (for rheumatoid arthritis and Crohn’s disease), and isoniazid (for tuberculosis). What Are the Symptoms and Early Signs of Lupus? The earliest signs and symptoms of lupus may include Fatigue. Joint pain and stiffness. Photosensitivity: This is sun or light sensitivity, causing rashes, fever, fatigue, or joint pain upon light (i.e., UV radiation) exposure. Muscle pain. Gastrointestinal complaints. Fever. Butterfly-shaped rash on the face (in 30 percent of cases). Skin lesions. Chest pain. Headaches. Shortness of breath. Due to its potential impact on various body parts, lupus manifests with a wide array of symptoms. Not all individuals experience every symptom, which may fluctuate and evolve. Lupus symptoms typically follow a pattern of flares and remissions, meaning patients don’t experience them continuously. Lupus is characterized by periods of symptom exacerbation— flares—followed by intervals of symptom improvement or remission. Systemic Lupus Erythematosus (SLE) Common SLE signs and symptoms include Fever: Fevers often exceed 100 F (37.8 C), typically due to inflammation or infection. Some individuals may experience recurrent low-grade fevers below 101 F, which may signal impending illness or a forthcoming lupus flare. Rashes. Muscle and joint pain/stiffness/swelling: These symptoms often appear on the neck, thighs, shoulders, and upper arms. Photosensitivity. Mouth sores: These ulcers can appear inside the mouth or on the lips. Persistent tiredness: Patients may still feel extremely tired even with sufficient sleep. Weight fluctuations: This is due to heightened lupus activity or side effects of lupus medications. Chest pain: This results from inflammation in the lining of the lungs, leading to discomfort when breathing deeply. Abdominal pain. Anemia: Anemia is associated with fatigue due to a lack of red blood cells carrying oxygen throughout the body. Depression and anxiety: Almost one-third of all lupus patients experience these. Blood clotting: Elevated risk of blood clots, potentially leading to issues like leg or lung clots, stroke, heart attack, or recurrent miscarriages. Hair loss: Often presenting as patchy or bald spots, potentially triggered by medications or infection. Gastrointestinal issues: These may include heartburn from gastroesophageal reflux disease (GERD) and peptic ulcers linked to medications used in lupus treatment, such as NSAIDs and steroids. Memory problems: Some individuals may experience forgetfulness or confusion. Eye problems: Symptoms may include dry eyes, eye inflammation, and eyelid rashes. Sjogren’s syndrome: Up to 10 percent of lupus patients may develop this autoimmune disorder that affects tear and saliva gland function, as the immune system attacks these moisture-producing glands. This leads to dryness in the eyes, mouth, and vagina, often causing a gritty feeling in the eyes. Autoimmune thyroid disease. Arthritis. Discoloration of fingers and toes. Swelling in the legs or around the eyes. Children with SLE have distinct symptoms, generally more severe disease, and a poorer outlook than adults with SLE. Specifically, more cases of kidney inflammation, blood problems, photosensitivity, brain-related issues, and skin and mouth troubles are observed among patients with childhood-onset SLE. In severe cases, patients may experience psychosis and/or seizures. Pediatric SLE is also linked to more damage than SLE in adults. Neonatal Signs and symptoms of neonatal lupus include Skin symptoms such as rashes. Heart symptoms, including congenital heart block. Liver disease. In rare cases, macrocephaly, meaning an unusually large head. Low platelet count. Low white blood cell count. Anemia. Drug-Induced Drug-induced lupus shares some characteristics with SLE. It may also include serositis, or inflammation around the lungs or heart. Fortunately, drug-induced lupus rarely affects major organs. What Causes Lupus? The cause of lupus is unknown, but the disease is believed to result from a complex interplay of genetic, environmental, and hormonal factors. Because most people with lupus are women, researchers have theorized that estrogen may have a role to play in developing the disease, at least in terms of its severity. Individuals with a genetic predisposition to lupus, like those with the gene families MHC classes 1 and 2 (which code for proteins involved in immune response), may develop the condition when exposed to environmental triggers. Typical triggers include: UV light exposure. Cigarette smoke. Infections. Certain medications. Stress. Severe fatigue. Vitamin D deficiency, though vitamin D’s relationship to lupus may be bidirectional. Exposure to toxins. Major surgeries or significant injuries. Lupus Illustration The cause of lupus is unknown, but it is believed to be related to a combination of genetic, hormonal, and environmental factors. Illustrations by Shutterstock, The Epoch Times Systemic Lupus Erythematosus (SLE) Normal gene variations, often involving multiple genes related to the immune system, can impact the risk of SLE. In rare instances, specific gene mutations can directly cause the condition. In individuals with SLE, cells that have self-destructed due to damage or obsolescence are not effectively removed. The exact connection between this malfunction and the origins or characteristics of SLE remains uncertain. Some researchers propose that these deceased cells might release substances that trigger an abnormal immune response, leading to the body’s own tissues being mistakenly attacked and causing the manifestations of SLE. Neonatal Neonatal lupus is not actually lupus. It gets its name from the similarity of the rash to lupus, but the baby does not have lupus. Most often, the mother does not have lupus either. It arises in a newborn due to antibodies received from the baby’s mother rather than from inherited genes. These antibodies, produced by the mother’s immune system, typically protect against harmful substances. A mother naturally passes antibodies to her child during pregnancy, as babies cannot make their own. Even if she has lupus herself, it is very uncommon for a mother to transmit the antibodies that can cause neonatal lupus to her baby, which is why the condition is rare. Who Is at Risk of Lupus? The people with a higher risk of developing lupus include Women: Although lupus can affect anyone, it predominantly impacts women, with approximately 90 percent of adults diagnosed with the disease being female. Female hormonal factors play a substantial role in the risk of developing SLE. Estrogen, for example, triggers the activation of various immune cells, such as B cells, macrophages, and thymocytes, and the release of certain cytokines. Also, the use of contraceptives containing estrogen and hormone replacement therapy after menopause has been linked to an increased occurrence of SLE. Younger people: Although lupus can develop at any age, it is most commonly diagnosed in people between 15 and 44. About 20 percent of SLE cases are in patients over 50. Nonwhite racial groups: In the United States, blacks, Hispanics, Asians, and Native Indians are more likely to develop lupus than whites. Residents of industrialized Western countries: The incidence of SLE has inexplicably increased by 10 percent in Western nations over the past five decades, while Africa and Asia exhibit notably lower SLE prevalence. Researchers propose that factors like ethnic diversity, tobacco use in industrialized countries, and regional variations in infectious diseases may contribute to these distinctions. People with specific genes: Researchers have identified over 100 gene variants linked to lupus; these variants may impact the body’s immune system. When one of two twins has lupus, there is an elevated likelihood that the other twin will also develop the disease (approximately 30 percent for identical twins and 5 percent to 10 percent for fraternal twins). People taking certain drugs: Over 100 medications have been linked to lupus due to their capacity to induce DNA demethylation and modify self-antigens, with procainamide and hydralazine being those with the highest incidence of drug-induced lupus. People with particular infections: Epstein-Barr virus (EBV) has been shown to increase the risk of lupus. People living with high stress: People going through a divorce, illness, or losing a loved one have a higher risk of developing lupus. People with vitamin D deficiency: Evidence indicates that vitamin D plays a significant role in SLE development and progression. People exposed to toxins: Researchers have identified links between lupus and various toxins, including silica, mercury, and cigarette smoke. How Is Lupus Diagnosed? Diagnosing lupus can be challenging, as its symptoms may resemble those of many other conditions. Your doctor/rheumatologist will first examine your medical history and conduct a physical checkup. Then, you may need to undergo multiple tests, as lupus cannot be definitively diagnosed with one single test and may require several months or even years to confirm a diagnosis. Blood Tests Although a blood test alone cannot diagnose lupus, specific proteins in the blood provide valuable information to your doctor so he or she can make an accurate diagnosis. The following tests may be performed: Complete blood count (CBC): This test measures the levels of white blood cells, red blood cells, and platelets in the blood. The results are then compared to reference ranges. Antinuclear antibody (ANA) test: The ANA test is commonly used to detect autoantibodies that can trigger autoimmune disorders by attacking components within the cell nucleus. While around 95 percent of people with lupus test positive for ANA, those with drug-induced lupus linked to quinidine often test negative for ANAs. However, a positive ANA test doesn’t conclusively indicate lupus. Conversely, a negative ANA test significantly lowers suspicion. Therefore, additional tests are typically conducted for those with a positive ANA to confirm the diagnosis. Known as an ANA panel, this assesses various antibodies. The antibodies tested may vary among laboratories. Complement test: This test measures the concentration of complement, a group of proteins in the bloodstream responsible for eliminating foreign substances. Reduced levels of complement in the blood are frequently linked to lupus. Erythrocyte sedimentation rate (ESR or sed rate): This test measures the rate at which red blood cells settle at the bottom of a test tube. In the presence of swelling and inflammation, blood proteins aggregate and become denser, causing them to settle more rapidly. Typically, the faster the descent of blood cells, the more pronounced the inflammation. C-reactive protein (CRP) test: This blood test identifies inflammation in the body. While both ESR and CRP indicate comparable levels of inflammation, there are instances where one may be elevated while the other is not. Tissue Biopsies Skin: A small sample of skin tissue is removed for examination under a microscope. Skin biopsies can help determine the cause of skin abnormalities, such as symptoms caused by lupus, assess the extent of a skin condition, and guide treatment decisions. Kidney: A small tissue sample is removed from the kidneys for examination. Other Tests Urinalysis: Urine samples may reveal elevated levels of blood or protein in the urine, suggesting potential kidney involvement in lupus. X-rays and scans: If your doctor suspects some of your organs might have been affected by lupus, X-rays and scans will be employed. Echocardiogram: This noninvasive procedure evaluates the heart’s function and structures, aiding in the diagnosis of various heart issues in adults with SLE, including congenital heart blocks due to neonatal lupus. What Are the Complications of Lupus? Lupus has various complications, including the following major ones, sorted by type of lupus: Systemic Lupus Erythematosus (SLE) Complications in SLE patients can arise from either disease-related organ damage or medication side effects. Specifically, disease-related complications include: Lupus nephritis: This is a severe complication of SLE. In lupus nephritis, the immune system mistakenly attacks the kidneys, leading to inflammation and damage to the kidney tissue, potentially causing kidney dysfunction and, in severe cases, kidney failure. Accelerated atherosclerosis and coronary heart disease. Neurological deficits. Lupus vasculitis (LV): Vasculitis is the inflammation of blood vessels, which develops in about 50 percent of SLE patients. It primarily affects small, sometimes medium-sized, and rarely large vessels. It can manifest across various organ systems, displaying symptoms based on the size and location of the affected blood vessels. Unfortunately, it is often associated with an unfavorable prognosis. Abnormal blood clotting: This is a common complication, leading to either excessive clotting or insufficient clotting, as the body produces too many antibodies. This condition can persist even when a person’s lupus is well-managed. Anxiety and depression. Lung issues: Approximately half of SLE patients will eventually encounter lung complications in their disease course. There are five primary lung issues associated with lupus: pleuritis, acute lupus pneumonitis, chronic (fibrotic) lupus pneumonitis, pulmonary hypertension, and “shrinking lung” syndrome (where a patient experiences breathing difficulties, chest pain, and a gradual reduction in lung capacity). Pregnancy-related complications: A high-risk pregnancy is not a direct complication of lupus itself, but active lupus during pregnancy can lead to complications such as miscarriage, stillbirth, or serious health issues for both mother and baby. In fact, all pregnancies in women with lupus are classified as high-risk. To maximize safety, it’s essential for the mother to have her disease well-controlled or in remission for at least six months before conceiving. Infections: SLE patients are often immunocompromised due to the disease itself and the use of immunosuppressive treatments. Secondary infections are a common and significant source of health issues, with bacterial infections accounting for 60 percent to 80 percent of total cases. Cytomegalovirus is an opportunistic pathogen that can affect SLE patients. Urinary tract infections are also common, affecting nearly 40 percent of lupus patients. Macrophage activation syndrome (MAS): Although its causes are unknown, in MAS, the immune system becomes overactive, leading to the buildup of specific immune cells in organs. This can cause symptoms similar to a sudden disease flare, including fever and fatigue, with some variations in blood test results and physical findings. MAS is potentially fatal and less often detected in adult SLE cases. Fibromyalgia. Complications due to long-term corticosteroid use in SLE patients include: Osteoporosis. Avascular necrosis. Glaucoma. Cataracts. Weight gain. Worsened diabetes. Acute psychosis. Cyclophosphamide use is linked with a high risk of interstitial cystitis, also known as painful bladder syndrome, and bladder cancer. Cutaneous Lupus Erythematosus Common complications of CLE include: Advancement to SLE. Skin discoloration. Scarring, permanent hair loss, and the development of cutaneous squamous cell carcinoma in discoid lupus erythematosus (DLE) cases. Neonatal Complications of neonatal lupus include: Congenital heart block, which results in a slow heartbeat and is potentially life-threatening. Endocardial fibroelastosis: This rare heart condition involves the thickening of the muscular lining of the heart chambers resulting from an increase in the amount of supportive connective tissues. This can affect the heart’s ability to pump blood effectively, leading to various heart problems. Dilated cardiomyopathy: This heart condition is characterized by the initial enlargement (dilation) of the heart’s left ventricle, the main pumping chamber responsible for pumping blood throughout the body. In this condition, the heart muscle becomes weakened and cannot contract effectively, decreasing the ability to pump blood. Congestive heart failure, typically due to the factors above. Drug-Induced Most individuals with drug-induced lupus do not face severe complications. There are rare cases of pericarditis, neuropsychiatric disorders, and glomerulonephritis (inflammation and damage to the filtering part of the kidneys). The occurrence of lasting kidney damage in glomerulonephritis is uncommon. What Are the Treatments for Lupus? While there is currently no cure for lupus, treatments can alleviate symptoms and improve a patient’s well-being. The treatment plan will be tailored to address the specific symptoms and requirements, thus preventing flares and minimizing adverse outcomes. Systemic Lupus Erythematosus (SLE) Common lupus medications include: Nonsteroidal anti-inflammatory drugs (NSAIDs): Non-prescription NSAIDs, such as ibuprofen and naproxen, can ease mild joint and muscle pain and reduce swelling. Corticosteroids: Also called steroids for short, these drugs reduce swelling, tenderness, and pain, and in higher doses, they can control the immune system. Lupus symptoms typically respond rapidly to these potent medications. However, doctors aim for the lowest effective dose due to their side effects. Antimalarial drugs: Drugs used to treat malaria, including hydroxychloroquine and chloroquine phosphate, effectively treat joint pain, skin rashes, fatigue, and lung inflammation in lupus. Hydroxychloroquine is a first-line treatment for childhood-onset SLE. Research has shown that these medications can prevent lupus flares and potentially extend the lifespan of individuals with lupus. BLyS-specific inhibitors: These inhibitors, such as belimumab, reduce the number of abnormal B cells, which are immune system cells that produce antibodies and are considered an issue in lupus. Immunosuppressive agents: In severe and treatment-resistant cases of lupus affecting major organs, immunosuppressive agents may be prescribed. However, they can also lead to severe side effects, as they weaken the body’s immune system. Systemic glucocorticoids are an important treatment for pediatric SLE. Anifrolumab-fnia: This is a first-of-its-kind type 1 interferon receptor antagonist used for adults with moderate to severe SLE. Voclosporin: This is the only oral medication approved by the U.S. Food and Drug Administration (FDA) for treating lupus nephritis. Biologic agents: The monoclonal antibody rituximab may benefit some lupus patients, but more studies are needed to determine its long-term effects and efficacy. Disease-modifying anti-rheumatic drugs (DMARDs): These reduce joint pain, swelling, and long-term joint damage by calming the immune system. Cutaneous Lupus Erythematosus When treating CLE, dermatologists aim to clear skin rashes, sores, and other issues, relieve itching and pain, prevent scarring, and address hair loss in discoid lupus. Typically, patients visit their dermatologist every three to six months. Treatment options include: Sun protection: This prevents new flare-ups and worsening of lupus. Medications used for treating SLE. Tacrolimus ointment: This is used when corticosteroids are unsuitable for the affected skin. It may also promote hair regrowth. Laser therapy: Laser therapy can treat persistent thick discoid lupus patches, dark patches, and scarring. How Does Mindset Affect Lupus? A positive attitude and overall mental well-being can positively impact an individual living with lupus. Although a positive attitude may not directly improve the underlying condition, it can help individuals cope with the challenges and stress associated with lupus. According to one study, almost 23 percent of the participants used a positive attitude as their coping strategy for lupus. In another small study, 56 people with SLE participated in six weekly psychosocial program sessions to enhance their self-confidence and develop a positive attitude toward the condition. The study revealed that in addition to increased self-esteem, participants in the program exhibited positive changes in anxiety, depression, coping, social functioning, and sleep disturbance. What Are the Natural Approaches to Lupus? Various natural treatments may help with symptom management. Dietary Although there is no special “lupus diet,” maintaining a healthy, unprocessed diet is crucial for managing lupus because it regulates inflammation and improves a patient’s overall health. According to the Lupus Foundation of America, people living with lupus should consume: Fruits and vegetables, including leafy greens. Whole grains, beans, and nuts. A combination of lean meats, poultry, tofu, seafood, and eggs. Foods with healthy fats, including olive oil, avocados, nuts, and fatty fish. Supplements Vitamin D: Vitamin D supplementation is essential, as people with lupus should avoid exposure to sunlight, which is needed for the body to produce vitamin D. In a study involving 177 SLE patients, about 82 percent of participants had low levels of vitamin D, which was linked to more severe disease activity and unfavorable blood test results. In another study, taking vitamin D supplements for five years, either alone or combined with omega-3 fatty acids, led to a 22 percent reduction in autoimmune diseases such as lupus. Vitamin D supplementation appears to positively impact inflammatory and hemostatic markers, potentially leading to improved clinical outcomes. Omega-3 fatty acids: Omega-3 polyunsaturated fatty acids have anti-inflammatory properties. In one study, participants taking omega-3 fish oil experienced a significant decline in lupus disease severity compared to placebo. N-acetylcysteine (NAC): NAC, a supplement containing a modified form of the amino acid cysteine, has antioxidant and anti-inflammatory properties. People with SLE have T-cell dysfunction. One pilot study indicates that NAC can safely reduce lupus disease activity by inhibiting a protein in T cells crucial in regulating various cellular processes. Herbs Several herbs can reduce lupus symptom severity, including Curcumin: Curcumin, a polyphenol found in turmeric, exhibits antioxidant, anti-cancer, and anti-inflammatory properties, and it may be an effective immunomodulator. Research found that lupus involves the immune system’s complement system going into overdrive, and curcumin can slow down this immune reaction. Additionally, curcumin prevented specific immune cells called B cells from becoming too active by reducing antibody production in mice models. Green tea: Green tea contains powerful antioxidants called catechins, especially epigallocatechin gallate (EGCG), which have potent anti-inflammatory and anti-cancer properties. In one study, drinking green tea extracts daily for 12 weeks reduced disease activity in SLE and enhanced patients’ quality of life. Ginger: Ginger, well-known for its anti-inflammatory and antioxidant properties, contains a key compound called 6-gingerol. One animal study revealed that 6-gingerol can reduce the release of neutrophil extracellular traps (NETs), which are relevant to lupus. This research highlights the protective potential of ginger-derived compounds in the context of lupus. Some herbs and supplements may interfere with other medicines, so consult your doctor before beginning any new therapies. Mind and Body Practices Exercise: Physical activity can help manage lupus symptoms, as it reduces inflammation by regulating key chemicals involved in the inflammatory process, helps reduce weight gain due to lupus medication side effects, enhances muscle flexibility, and improves mental well-being. Meditation: Stress is one of the triggers for lupus flares, so stress-reducing techniques such as meditation and yoga can help improve lupus patients’ overall health. In one study, 26 SLE patients received a mindfulness-based stress reduction (MBSR) group therapy. Compared to a waitlist group, the group practicing MBSR exhibited more significant enhancements in quality of life, reduced psychological rigidity concerning pain, and decreased lupus-related negative feelings. Acupuncture: Acupuncture is a traditional practice of using fine needles inserted into the skin for health treatment, dating back over 2,500 years. A meta-analysis of seven studies involving 514 SLE patients found that additional acupuncture treatment, when combined with conventional drug therapy, improved the overall response rate, regulated immunological indicators, lowered SLE disease activity, and decreased the incidence of adverse events during treatment. How Can I Prevent Lupus? Since the cause of lupus is unknown, there’s no way to prevent the disease. However, you can minimize your exposure to environmental triggers to reduce the risk of a lupus flare by practicing the following behaviors: Using UV radiation protection: Wearing protective clothing and sunscreen when necessary, avoiding excessive sun exposure, and avoiding tanning equipment can minimize the UV radiation that can trigger lupus flares. Minimizing exposure to toxins: These include silica, mercury, and cigarette smoke. Avoiding smoking. Leading a healthy lifestyle: Maintaining a balanced diet, staying physically active, and managing stress effectively can support one’s immune system and overall health. Managing medications: Learn about the risk of developing drug-induced lupus from the intake of your medications and monitor your health condition.

Epoch Health Article Peripheral Neuropathy (PN) is a severe and complex neurological disorder affecting 20 million to 30 million people in the United States. PN damages nerves outside the brain and spinal cord, primarily in the feet and hands. Symptoms such as numbness, tingling, burning pain, and muscle weakness can drastically reduce quality of life, making even simple tasks challenging. Identifying and treating the root cause of PN is vital to prevent further nerve damage and preserve mobility. If left unaddressed, PN can lead to severe complications, including the risk of limb amputation. What Are the Symptoms and Early Signs of Peripheral Neuropathy Definition? Recognizing the Peripheral Neuropathy Definition and symptoms is necessary for early diagnosis and treatment to prevent irreversible damage. Common early warning signs include numbness that may feel like “walking on pillows” and pain or burning sensations in the feet or hands. PN can manifest differently depending on the cause and the type of nerves affected. Symptoms vary widely; some individuals experience severe pain, while others might have numbness with little discomfort. The onset can be gradual, as seen in diabetic peripheral neuropathy (DPN), or sudden, as in neuropathy from toxic exposure or Guillain-Barré syndrome. Typically, PN follows a “stocking and glove” pattern, starting at the feet and progressing upward, eventually affecting the hands. This pattern occurs because the longest nerves are most susceptible to damage due to issues like reduced blood flow and metabolic disturbances. Peripheral nerves consist of sensory, motor, and autonomic nerves, with symptoms varying based on which type is affected. The severity and progression of symptoms also depend on whether the nerves are myelinated (with a protective sheath) or unmyelinated. Damage can be axonal or demyelinating, affecting the nerve fibers or the myelin sheath, respectively. Sensory Nerves These nerves transmit sensations like touch, temperature, and pain. Many sensory nerves, especially pain-sensing fibers, are unmyelinated and may be affected more gradually. Damage can cause: A tingling feeling, often described as “pins and needles” Numbness or a complete loss of feeling Increased sensitivity to touch or pain (hyperesthesia) and pain from things that usually do not hurt (allodynia) Problems with balance or walking due to loss of body awareness (sensory ataxia) Deep aching sensations Tiredness after activity Itching that feels different from regular itching (neuropathic itch) Motor Nerves These nerves control muscle movement. Most motor nerves are myelinated, allowing faster signal conduction and potentially quicker symptom onset when damaged. When affected, symptoms may include Muscle weakness Difficulty with fine motor skills, like buttoning a shirt Trouble walking or maintaining balance Autonomic Nerves These nerves regulate involuntary functions and may be myelinated or unmyelinated. Symptoms include Feeling dizzy when standing up Slow digestion (gastroparesis) Constipation or diarrhea Bladder problems Sexual dysfunction Blurry vision Dry eyes, mouth, or skin Burning and flushing of the skin What Causes Peripheral Neuropathy? PN is not a single condition but rather a group of related disorders that can have various causes and symptoms. PN occurs when the peripheral nerves, which connect the brain and spinal cord to the rest of the body, are damaged. This damage can occur through various metabolic and cellular pathways, affecting the nerves in different ways but ultimately leading to disruptions in nerve function. The development is often complex and likely involves multiple contributing factors. Peripheral neuropathy occurs when the peripheral nerves are damaged. Many factors can lead to the condition's development, including diabetes, hereditary disorders, infections, and toxic exposures. Healthy vs Damaged nerve  The following list of mechanisms and causes is not exhaustive, and ongoing research continues to uncover new insights, but some of the leading causes include the following: Metabolic factors: In conditions like Type 2 diabetes and metabolic syndrome, high blood sugar and lipid levels can disrupt nerve function and decrease blood flow to the nerves. In Type 1 diabetes, the deficiency of insulin and C-peptide, rather than excess glucose alone, may contribute to nerve damage. Ironically, rapid reductions in blood glucose levels during treatment can lead to treatment-induced neuropathy. Mitochondrial dysfunction:  The energy-producing structures within cells, called mitochondria, can malfunction, resulting in reduced energy production and increased harmful reactive oxygen species (ROS). While ROS play important roles in cellular signaling, an excess can harm nerve cells. Protein misfolding Misfolded proteins, such as amyloid, can impair blood supply, trigger inflammation, and cause toxicity to nerve cells. Circulatory problems:  Reduced blood flow from conditions like peripheral artery disease limits oxygen and nutrients to nerves. Immune-mediated and autoimmune causes Conditions like Guillain-Barré syndrome and lupus involve the immune system attacking nerves. Paraneoplastic neuropathy occurs when the immune response to cancer targets healthy nerves. Other autoimmune diseases, such as Sjogren’s syndrome, vasculitis, Crohn’s disease, ulcerative colitis, sarcoidosis, rheumatoid arthritis, and psoriatic arthritis, cause nerve damage indirectly. This can occur through chronic inflammation, nerve compression, nutrient malabsorption, blood vessel inflammation or damage, or granulomas that compress nerves or disrupt their blood supply. Gluten-related sensitivities:  Celiac disease and non-celiac gluten sensitivity may cause nerve damage through inflammation or malabsorption. Notably, one study found that 34 percent of people with idiopathic (unexplained) neuropathy had evidence of gluten sensitivity, and 9 percent had biopsy-confirmed celiac disease. Physical trauma:  Injuries or pressure on nerves occurring alongside conditions like carpal tunnel syndrome, tumors, and compression injuries can lead to damage. Infections and vaccine reactions:  Infections from certain viruses or bacteria, such as human immunodeficiency virus (HIV), hepatitis C, Lyme disease, shingles, COVID-19, and Campylobacter jejuni, can directly attack nerve tissue or trigger immune responses that damage nerves. PN has also been reported after vaccination for COVID-19, shingles, tetanus-diphtheria-pertussis (Tdap), and influenza. Toxic exposures:  Chemicals, medications, and environmental toxins can damage nerves. Many medications, including certain chemotherapy drugs, antibiotics, and cardiovascular and antiviral medications, can affect nerves. Other toxic exposures include heavy metals, solvents, pesticides, industrial chemicals, and chronic alcohol use. Hereditary disorders:  Genetic conditions, like Charcot-Marie-Tooth disease (CMT), affect nerve development and function. CMT often leads to muscle weakness and wasting in the lower legs and feet, causing high arches, hammer toes, and skin discoloration. In severe cases, hand muscles can also waste away, making the fingers curl into a “claw” shape. Nutritional deficiencies:  Deficiencies in vitamins D, B1 (thiamine), B12, and E, as well as copper and folate, can lead to PN. Malabsorption, chronic alcohol use, and bariatric surgery worsen these deficiencies. Conversely, excessive vitamin B6 intake can cause neuropathy. Chronic diseases:  Conditions such as kidney failure, gout, and thyroid disease can lead to nerve damage. Blood protein disorders and cancers : Multiple myeloma and other blood cancers can cause an abnormal buildup of proteins known as paraproteinemia that can damage nerves or the blood vessels that supply the nerves. What Are the Types of Peripheral Neuropathy? There are many different types of PN. It is classified in numerous ways, including by the nerves affected, underlying causes, and symptom characteristics. Some of the ways PN can be classified include the following Distribution Mononeuropathy: affects a single nerve Polyneuropathy: affects multiple nerves Multiple mononeuropathy: affects two or more nerves in different areas Nerve Fibers Affected Large fiber neuropathy: affects large, myelinated nerve fibers Small fiber neuropathy: affects small, unmyelinated nerve fibers Mixed fiber neuropathy: affects both large and small fibers Function Motor neuropathy: affects nerves controlling muscles Sensory neuropathy: affects nerves transmitting sensory information Autonomic neuropathy: affects nerves controlling involuntary functions Sensorimotor neuropathy: a combination of sensory and motor nerve involvement Cause Acquired neuropathy: caused by environmental factors, illnesses, infections, etc. Hereditary neuropathy: caused by genetics Idiopathic neuropathy: cause unknown Who Is at Risk of Peripheral Neuropathy? PN risk is influenced by various factors, some of which cannot be changed (unmodifiable) and others that can potentially be controlled through lifestyle choices (modifiable). Factors that increase the risk of developing PN include the following: Age: The risk of PN increases with age. In the general U.S. population, the prevalence is about 10.4 percent in those aged 40 to 69 and 26.8 percent to 39.2 percent for older adults. While some hereditary neuropathies, like CMT, may appear in childhood, other inherited neuropathies may develop in adulthood. Sex: Males have a much higher likelihood than females of developing PN, but females are more likely to experience pain. Race: PN is more common among black people than white. Height: Taller people are considerably more likely to develop PN, likely due to the longer length of their nerves. Genetics: Some sources of neuropathy, like CMT, familial amyloidosis, and Fabry disease, can be inherited. Diabetes and metabolic conditions: Prediabetes or diabetes substantially increases the risk of developing PN. The prevalence of PN is more than twice as high in adults aged 40 to 69 years with diabetes compared to those without diabetes. The risk increases with the duration of the disease, with more than half of diabetics likely to develop the condition. Body mass index (BMI): A higher BMI, calculated as weight (in kilograms) divided by height squared (in meters), is a risk factor for developing PN. Education: Research shows that those with less education may have higher odds of developing PN. Smoking: Many—but not all—studies indicate a higher risk of PN is associated with smoking. Circulatory diseases: Conditions affecting the heart, blood vessels, and circulation can increase the risk of PN. Cardiovascular disease affects the heart and blood vessels, influencing overall circulation. A family history of cardiovascular disease also increases the risk of developing PN. How Is Peripheral Neuropathy Diagnosed? Early diagnosis, identifying the cause, and ruling out other conditions is key to effective treatment. Diagnosing PN takes a stepwise approach. Step 1: Clinical Evaluation In the first step, symptoms are assessed, and a detailed history is taken to obtain information about alcohol use, family history of neuropathy, recent illnesses or vaccinations, and use of neurotoxic medications such as gout medications, antivirals, and chemotherapy. Additionally, information about blood transfusions, sexual history, and intravenous drug use is gathered to assess HIV and hepatitis C as potential causes. Clinical and neurological examinations follow, evaluating muscle strength, reflexes, and sensitivity to temperature, light touch, position, and vibration. The practitioner will consider the onset and progression of PN, whether symptoms are symmetrical or asymmetrical, their location, and the nerves involved, providing clues to the underlying causes and type of neuropathy. Urgent referral to a neurologist is warranted for individuals experiencing sudden, severe, or worsening symptoms to ensure prompt treatment. This is particularly critical for those showing nerve damage in multiple areas, unusual patterns, or having only motor or autonomic symptoms without sensory changes. Absent indications of referral necessity, this initial assessment may lead to a clinical diagnosis of PN. However, even in diabetics, additional testing is essential to eliminate other potential coexisting causes. Step 2: Laboratory Tests Laboratory tests help identify contributing factors and rule out other conditions. Depending on the individual’s clinical presentation and diagnostic findings, blood tests may include: Complete blood count (CBC) to evaluate overall health and detect a variety of disorders Erythrocyte sedimentation rate (ESR) to detect inflammation Comprehensive metabolic panel (CMP) to assess blood glucose, hemoglobin A1c, kidney function, and liver function Thyroid function tests to check for thyroid disorders Vitamin B12 with methylmalonic acid and homocysteine to identify vitamin B12 deficiency and its potential impact Vitamin B6 to check for deficiencies or excess that may affect nerve function Protein immunofixation to detect abnormal proteins in the blood Various autoantibody tests to identify autoimmune conditions Vasculitis tests to detect inflammation of the blood vessels Tests for specific viruses and bacteria to rule out suspected infections that can cause neuropathy Heavy metals to check for toxic exposure Genetic tests to identify hereditary neuropathies Some of these tests may be ordered by the primary care practitioner or a neurologist following referral.   Step 3: Electrodiagnostic and Medical Tests If initial tests are inconclusive, symptoms are complex, or other health conditions are present, further testing or a neurologist referral may be necessary. A specialist can then conduct advanced tests to provide valuable insights into the extent and nature of nerve damage. These additional assessments may include: Nerve conduction study (NCS): This test measures the speed and strength of nerve signals using sensors placed on the skin. It is considered the gold standard for diagnosing DPN. NCS can exclude other conditions, identify affected nerves, distinguish between axonal (nerve fiber) and demyelinating (nerve covering) damage, and determine damage severity. Electromyography (EMG): This test measures the electrical activity of muscles by inserting a small needle into the muscle. EMG helps confirm a PN diagnosis and provides additional information that can complement the findings of the NCS. Sweat testing: Sudoscan and Neuropad are noninvasive tests that diagnose small fiber neuropathy and early autonomic dysfunction by assessing sweat gland activity. Sudoscan uses electrochemical reactions to measure sweat gland function on the palms and soles, while Neuropad involves a color-changing patch on the foot to indicate sweat production. Imaging: Peripheral nerve ultrasound, magnetic resonance imaging (MRI), and magnetic resonance neurography (MRN) can reveal injured and compressed nerves not accessible by NCS or EMG. MRI provides detailed images of the overall anatomy, while MRN offers more specialized and specific imaging of peripheral nerves, but it is not as widely available. Biopsy: Nerve or skin biopsies may be obtained and analyzed. A nerve biopsy may help assess possible immune-mediated or infectious neuropathies, while a skin biopsy is used to determine nerve fiber density. Examination of cerebral spinal fluid (CSF): If the suspected cause is infectious, inflammatory, vasculitic (related to blood vessel inflammation), or paraneoplastic (related to cancer), the CSF may be analyzed. Other less common, newer, or not widely available tests include VibraTip, corneal confocal microscopy, laser-evoked potentials, and quantitative sensory testing. What Are the Possible Complications of Peripheral Neuropathy? While peripheral neuropathy is often a complication of other conditions, it can lead to its own set of complications due to nerve damage. These include: Injuries: Without sensations, sharp objects, heat, and extreme cold can cause unnoticed wounds. Falls: Nerve damage affects gait, coordination, and balance, increasing fall risk. Pain and hypersensitivity: Up to 24 percent of those with DPN experience pain affecting sleep and quality of life. Hypersensitivity, where unpainful stimuli cause pain, is also common. Even the light touch of bedsheets can be unbearable. Disability: Nerve damage can make daily tasks difficult or impossible. Foot ulcers and amputation: About 30 percent of diabetics develop foot ulcers during their lifetime, with a high risk of recurrence. They are serious complications that can go unnoticed due to nerve damage, leading to infections or gangrene. Poor circulation and high blood sugar hinder healing, with over half of ulcers becoming infected, often resulting in lower limb amputation. Autonomic dysfunction or failure: Damage to autonomic nerves can cause cardiovascular issues (irregular heart rate or blood pressure), digestive problems, difficulty swallowing, urinary issues (incontinence, frequent infections), and difficulty regulating body temperature. While these complications can be serious, there are steps that patients and their families can take to prevent or manage some of them effectively and improve quality of life. Here are some practical strategies: Foot care: Inspect feet daily and immediately address foot injuries; wear clean, dry socks and closed-toed shoes. Driving safety: Regularly assess whether driving is safe. Fall prevention: Be aware of surroundings, install railings, remove throw rugs and trip hazards, and install nightlights. Burn prevention: Set the water heater at 125 degrees Fahrenheit or lower to avoid burns. Health checkups: Get regular checkups to help manage blood pressure, digestive issues, and body temperature regulation. What Are the Treatments for Peripheral Neuropathy? Treating PN can be complex due to its many underlying causes and symptoms. The primary goal is to address the identified cause, such as managing blood glucose in diabetics or correcting vitamin deficiencies. In about 20 percent of cases, no cause is identified. However, symptoms can still be treated to improve quality of life, according to studies in Norway and the Netherlands, as mentioned in a 2020 paper in Neurological Research and Practice. Traditional painkillers are typically ineffective for nerve pain, so other medications are generally utilized. Unfortunately, these medications do not work for everyone; they do not address the underlying cause of PN and often come with significant side effects. 1. Anticonvulsants Despite limited effectiveness and significant safety concerns, gabapentin is widely prescribed as a first-tier treatment for neuropathic pain. Some researchers recommend reconsidering its use. A Cochrane Review found that gabapentin provided over 50 percent pain relief to about 38 percent of people with painful DPN. Safety concerns arise when gabapentin is taken with drugs like benzodiazepines and opioids. In a study of accidental mixed-drug deaths involving opioids, gabapentin was present in about 25 percent of cases. Adverse effects include daytime sleepiness, weight gain, edema, and dizziness, with additional concerns about cognitive impairment, dementia risk, addiction, abuse, misuse, and illegal distribution. Another option is pregabalin. However, research shows that for the majority of people with painful DPN, pregabalin provides little relief. At a dosage of 300 milligrams, only one in 22 people experienced a reduction in pain of 50 percent or more. 2. Antidepressants Antidepressants, such as tricyclic antidepressants (e.g., amitriptyline, nortriptyline) and serotonin-norepinephrine reuptake inhibitors (SNRIs) (e.g., duloxetine), are effective in treating neuropathic pain. Duloxetine has been shown to provide better pain relief than pregabalin. These medications work by increasing levels of norepinephrine and serotonin in the nervous system, which helps reduce pain signals. Be sure to discuss the potential side effects with your prescribing practitioner. 3. Analgesics Controlled-release oxycodone has been found to be an effective treatment in painful DPN with significantly improved quality of life. Tramadol, tapentadol, and other opioids may also be effective and are sometimes prescribed for severe neurologic pain. However, they should be used cautiously due to the associated high risk of addiction, misuse, illegal distribution, and when used with coexisting severe psychiatric conditions. 4. Corticosteroids, Plasma Exchange, and Intravenous Immune Globulin These treatments are used for severe neuropathies caused by inflammation or immune attacks on nerves, like chronic inflammatory demyelinating polyradiculoneuropathy (CIDP). Steroids reduce inflammation. Plasma exchange (PE) removes harmful antibodies from plasma and replaces it with a substitute solution. Intravenous immune globulin (IVIG), made from pooled antibodies from healthy donors, helps regulate the immune system. 5. Other As for topical medication, lidocaine patches or capsaicin cream may provide localized relief with few systemic side effects. Other potentially effective treatments include surgery for cases of nerve compression, transcutaneous electrical nerve stimulation (TENS), spinal cord stimulation (SCS), physical and occupational therapy, acupuncture, and low-level laser therapy. Studies show that combining traditional Chinese medicine (TCM) with Western medicine can improve effectiveness and nerve function. Emerging therapies such as ARA 290, a peptide, are also being explored for potential benefits in managing PN associated with sarcoidosis. How Does Mindset Affect Peripheral Neuropathy? Peripheral neuropathy can significantly affect a person’s daily life, affecting mood, sleep, and overall quality of life. Chronic pain, numbness, and other symptoms associated with PN can lead to sleep disturbances, which in turn can exacerbate the perception of pain, creating a vicious cycle. Additionally, the financial burden of associated direct and indirect costs can create stress that further degrades quality of life. While PN symptoms can influence mental state, mindset also plays a significant role in how individuals experience and manage their condition. A large study on various pain conditions found that certain thought patterns, such as thinking the worst about pain, fearing pain, and being overly aware of pain, are strongly linked to negative emotions, anxiety, depression, higher pain intensity, and greater interference with daily activities. This research underscores the importance of addressing mindset in PN management. A positive mindset can be a powerful tool in coping with PN and potentially improving outcomes. Here are key aspects of how mindset influences PN Pain perception Research has shown that mindset can influence how the brain processes pain signals. A more positive outlook may help reduce the perceived intensity of pain. Fear: Fear of falling can lead to decreased physical activity, which causes muscle weakness and loss of balance, further reducing mobility. This inactivity creates a vicious cycle, increasing the risk of falls. Other fears can play a role in this cycle, such as the fear of not being taken seriously or the fear of becoming disabled. Addressing this fear through mindset techniques and building confidence in safe movement can improve both physical and mental health. Impact on physical health The stress and anxiety resulting from fear can trigger the body’s “fight-or-flight” response, leading to increased cortisol levels. Chronic high cortisol levels can contribute to inflammation, suppress immune function, and impair healing processes. These physiological changes can exacerbate neuropathy symptoms and hinder recovery. Adopting stress-management techniques and maintaining a calm mindset can help mitigate some of the adverse effects of stress on nerve function. Treatment adherence: A proactive mindset can improve adherence to treatment plans, including medication regimens, physical therapy, and lifestyle modifications. Coping strategies A resilient mindset can help individuals develop and implement effective coping strategies, leading to improved quality of life despite PN symptoms. What Are the Natural Approaches to Peripheral Neuropathy? While many people use natural and herbal remedies, scientific evidence supporting their effectiveness is often limited. What works for one person may not work for another. Natural products can cause adverse reactions, interact with medications, or be contraindicated with certain medical conditions. Consult your health care provider or pharmacist for personalized advice. Natural approaches to peripheral neuropathy can complement conventional treatment effectively. The first step is to eliminate or minimize the causative agent. Before starting any necessary chemotherapy, optimizing nutritional status may help prevent PN or lessen its severity. Since nerves regenerate slowly and the body does not produce new nerves, patience is essential, especially with natural approaches, as damage can become irreversible over time. Below are some natural approaches backed by peer-reviewed research 1. Exercise Research demonstrates that aerobic exercise can improve symptoms of PN, whether performed alone or in combination with resistance or balance training. A minimum of three weekly sessions of activities such as walking, cycling, or swimming is recommended. Simple exercises, including leg stretches and balance movements, can also enhance nerve function and reduce pain. Regular exercise can potentially delay progression, improve symptoms, and, in some cases, even reverse symptoms. It can also enhance blood flow, reduce cellular damage, and stimulate nerve regeneration. 2. Gluten-Free Diet A gluten-free diet (GFD) can effectively reduce neuropathic symptoms and improve quality of life in those with gluten neuropathy, a type of peripheral neuropathy linked to gluten sensitivity. A small study found that those who strictly followed a GFD experienced better pain management and overall health compared to those who continued eating gluten. Gluten is incompletely digested and can cause inflammation by increasing intestinal permeability, even in individuals without gluten sensitivity. 3. Health-Promoting Fatty Acids Omega-3 fatty acids help reduce inflammation, regulate blood pressure, glucose tolerance, and nervous system development and function. Eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) are two important omega-3 fatty acids primarily found in fatty fish. EPA is known for its anti-inflammatory properties, while DHA is crucial for brain health. A small pilot study found that supplementing with 1,000 milligrams of DHA and 200 milligrams of EPA for three months helped reduce pain in DPN. One study found that gamma-linolenic acid (GLA) was as effective as alpha-lipoic acid (ALA) in reducing pain, although ALA may work more quickly in those with better kidney function. It is found in borage, evening primrose, and blackcurrant seed oils. 4. Additional Nutritional Support Research has shown that supplementing with certain vitamins, minerals, and other nutrients can improve symptoms and quality of life for those with peripheral neuropathy. These beneficial nutrients include: Vitamin E: This vitamin may reduce the occurrence and severity of chemotherapy-induced PN and synergize with pyrroloquinoline quinone (PQQ). Mitochondrial support: PQQ and Coenzyme Q10 (CoQ10) have been shown to support mitochondrial function. PQQ has neuroprotective properties and promotes nerve regeneration by increasing nerve growth factor synthesis. CoQ10 has antioxidant properties, potentially improving energy production and reducing oxidative stress. Vitamin D: This vitamin is essential for nerve health, with deficiency linked to an increased risk of DPN. Supplementation may improve symptoms. B-complex vitamins: These include B1 (thiamine), B12 (methylcobalamin), folate (methylfolate), and B6 (pyridoxal-5-phosphate). Benfotiamine: This is a synthetic form of vitamin B1 that is more effectively absorbed and better at raising thiamine levels in the body. It can potentially reduce nerve pain and improve function in diabetic neuropathy. Magnesium: Magnesium deficiency is common. The mineral is required for normal thiamine functions. Copper: A copper deficiency can cause symptoms similar to vitamin B12 deficiency, such as nerve damage and sensory issues. This may occur in someone with a history of bariatric surgery, multiple nutritional deficiencies, or high zinc exposure, such as from supplements or certain denture pastes. Antioxidants: Antioxidants fight free radicals and balance ROS. Glutathione and ascorbic acid (vitamin C) are well-known for enhancing nerve regeneration. Melatonin, another powerful antioxidant, protects nerve cells, reduces inflammation at injury sites, and stimulates the growth of new nerve fibers. Alpha-lipoic acid (ALA): Another antioxidant, ALA, given both intravenously and orally, can help reduce pain and improve quality of life in people with DPN. It is found in beef heart and kidney, tomatoes, spinach, and Brussels sprouts. N-acetylcysteine (NAC): A precursor to glutathione, this neuroprotective agent promotes nerve cell survival by stabilizing cell membranes and helping prevent cell death. Fibrinolytic enzymes: Bromelain (found in pineapple) and lumbrokinase may help reduce pain and inflammation, improve circulation, and support nerve healing. Lumbrokinase may help prevent excessive scar tissue formation and promote regeneration. Hypericum (St. John’s wort): This natural antidepressant has anti-inflammatory and neuroprotective effects and potential benefits in reducing neuropathic pain. L-glutamine: Oral supplementation may reduce the occurrence and severity of chemotherapy-induced peripheral neuropathy. Curcumin: This is a compound in turmeric that may reduce DPN severity and lower blood sugar levels, along with various other health benefits. Nano-curcumin, a highly absorbable form, has shown promise in studies. Individual supplementation or a professional formulation may be necessary to achieve therapeutic doses. While most B vitamins are safe in high doses, excess vitamin B6 can damage nerves and induce or worsen neuropathy.    How Can I Prevent Peripheral Neuropathy? Preventing peripheral neuropathy involves maintaining good metabolic, vascular, and nerve health. Just as the risk of peripheral neuropathy increases with each component of metabolic syndrome, the protective benefits increase with each healthy diet and lifestyle change. Here are some key strategies: Maintain good blood sugar control: This is essential for diabetics, but keeping blood glucose levels in check can prevent nerve damage in everyone. Exercise regularly: Movement is critical, so rather than stressing over which exercises to do, it may help to seek guidance from a professional to choose safe and appropriate activities. Even simply walking can make a significant difference. Follow a healthy diet: Consume a balanced diet rich in organic fruits and vegetables, naturally raised lean meats, and omega-3 fatty acids found in foods like wild-caught salmon. Ensure adequate nutrient intake: Obtain sufficient amounts of vitamins, minerals, and other essential nutrients through a balanced diet and supplementation as necessary. Consult a nutrition professional for assistance. Avoid toxic exposures: Eat organic foods to avoid pesticides and chemicals. Limit alcohol consumption and avoid smoking, as these can contribute to nerve damage. Manage other health conditions: Keep blood pressure under control and maintain a healthy weight. Avoid prolonged pressure on nerves: Be mindful of repetitive motions or prolonged positions that compress nerves. Manage stress: Practices like yoga, meditation, or deep breathing exercises can help manage stress, which may exacerbate neuropathy symptoms.

Epoch Health Pancreatic Cancer Pancreatic cancer is one of the most challenging forms of an already difficult disease. Despite relatively low incidence levels, it ranks seventh among causes of global cancer deaths in industrialized countries and was the third most common cause of cancer mortality in the United States in 2020. Because patients seldom experience symptoms until the disease has reached an advanced stage, pancreatic cancer remains challenging to treat successfully. According to Johns Hopkins Medicine, 80 percent of cases aren’t diagnosed until later, difficult-to-treat stages. Thus, despite advancements in detection and management, the five-year survival rate is still only 5 to 10 percent. What Are the Common Types of Pancreatic Cancer, or also known as Cancer of the Pancreas? There are two categories of pancreatic cancer—those that affect the exocrine cells in the pancreas and those that affect the endocrine cells. Exocrine cells are glands that secrete hormones and other substances through ducts in the body, whereas endocrine cells secrete hormones directly into the bloodstream. The pancreas has both types of cells. Exocrine Pancreatic Cancers Pancreatic adenocarcinoma: This is the most prevalent form of pancreatic cancer, accounting for about 90 percent of all diagnoses. It affects the exocrine cells in the pancreas ducts that produce digestive enzymes. Squamous cell carcinoma: This extremely rare cancer forms in the pancreatic ducts from squamous cells not naturally present in the pancreas. This type is so rare that there have not been enough reported cases for its origins to be wholly understood. Rarely discovered early, it has a very poor prognosis. Adenosquamous carcinoma: Accounting for 1 to 4 percent of exocrine pancreatic cancers, this rare pancreatic cancer presents elements of both ductal adenocarcinoma and squamous cell carcinoma. Compared to adenocarcinoma, adenosquamous carcinoma is more aggressive and has a poorer prognosis. Colloid carcinoma: Comprising only 1 to 3 percent of exocrine cases, this rare form typically develops from a particular type of benign cyst, an intraductal papillary mucinous neoplasm (IPMN). Because a pancreatic colloid tumor consists of malignant cells suspended in a gelatinous substance known as mucin, it spreads more slowly, is easier to treat than other pancreatic cancers, and has a much better prognosis. Neuroendocrine Pancreatic Cancer This type accounts for 5 percent of pancreatic cancer diagnoses. It starts in the endocrine cells, which produce hormones affecting many body processes from metabolism to blood sugar to mood. Survival and recovery rates for this type of cancer are better than those for adenocarcinoma. Pancreatic Cancer Benign Precancerous Lesions Cysts and other benign tumors, including IPMNs, can form in the pancreas, and some can result in pancreatic cancer. IPMNs and other benign lesions are often discovered while a patient is being scanned for an unrelated condition. Depending on the type of growth and location, your doctor may recommend surgical removal of the lesion or continued monitoring. What Are the Symptoms and Early Signs of Pancreatic Cancer? Pancreatic cancer typically doesn’t cause symptoms until it reaches advanced stages. Thus, reliable, early signs are hard to detect. As it progresses, pancreatic cancer can express the following symptoms: Loss of appetite Unplanned weight loss Abdominal pain that can radiate to the back Lower back pain Blood clots (often in the legs, which can manifest as redness, pain, and swelling) Jaundice Depression Light-colored or slimy stools Dark-colored urine Itchy skin Nausea and vomiting Sudden-onset diabetes or the exacerbation of preexisting diabetes Note that a range of less-serious conditions can cause the above symptoms. Consult your doctor if you have any of these symptoms. Despite the poor prognosis, pancreatic cancer is potentially curable if diagnosed early. According to Johns Hopkins Medicine, up to 10 percent of patients diagnosed early become disease-free posttreatment. The pancreatic cancer survival-time average is three to three-and-a-half years for patients diagnosed before the tumor grows or spreads. For people in families with a history of or genetic susceptibility to pancreatic cancer ( pdf ), it may be helpful to test even if symptoms are absent. Typically, the preventative tests are either an endoscopic ultrasound or an MRI. Absent symptoms, such testing is only conducted when genetic or hereditary elements indicate a higher risk for the individual. Doctors have sometimes identified early, treatable pancreatic cancers in high-risk individuals with these tests. What Causes Pancreatic Cancer? Your pancreas is a gland in the abdomen, between the stomach and spine. It produces hormones that regulate blood sugar levels and enzymes that aid digestion. Pancreatic cancer occurs when the DNA in your pancreas cells develops mutations. A cell’s DNA contains the blueprints for cell development and death. Such cancerous mutations instruct cells to grow without limit and to persist after normal, healthy cells would perish. In some rare cases, these mutations can be inherited. The affected cells can then become a tumor. Undetected or untreated, cancer cells can spread to adjacent organs and blood vessels and, over time, to other parts of the body. Who Is More Likely to Develop Pancreatic Cancer? These factors are associated with an increased risk for pancreatic cancer: Smoking and use of all forms of tobacco Obesity, particularly belly fat Excessive alcohol consumption Diabetes, especially type 2 diabetes. Sudden-onset diabetes can be a sign of pancreatic cancer. Chronic pancreatitis, inflammation of the pancreas Exposure to certain chemical toxins, such as pesticides and petrochemicals Family history of genetic vulnerability, such as BRCA1 or BRCA2 genes inherited from a parent Blood type other than O What Are the Tests to Detect Pancreatic Cancer? If a person exhibits symptoms associated with pancreatic cancer, specific tests and procedures will assist in diagnosis. If cancer is detected, follow-up tests will help assess the extent of the cancer. Imaging tests: These diagnostic tools give doctors an image of your pancreas and surrounding organs. Techniques used include magnetic resonance imaging (MRI), ultrasound, computerized tomography (CT scan), and positron emission tomography (PET scan). Endoscopic ultrasound (EUS): A tube is passed down the esophagus to provide images from within the abdomen of the pancreas and other adjacent organs. Biopsy: A small sample of tissue is collected either through a tool inserted into the EUS or, more rarely, via a pin inserted into the pancreas via the abdomen. Blood test: This test looks for specific proteins in the blood shed by pancreatic cancer cells. The test looks for a particular marker, CA 19-9. This marker may help indicate how well you will respond to treatment. However, not all patients with pancreatic cancer test positive for these markers, so the test’s diagnostic power is limited. Genetic testing: If you are diagnosed with pancreatic cancer, consider getting genetic testing done. This can determine if there’s a hereditary susceptibility in your family to the condition. It can also help your doctors chart a course of treatment for you. If a diagnosis of pancreatic cancer is confirmed, your doctor will seek to determine the extent (stage) of the cancer, which helps indicate which treatments are most likely to help. Stages of cancer range from zero to 4. The lower stages mean the cancer is confined to the pancreas. In later stages, cancer has metastasized to other parts of the body. Finally, if you are a direct relative—parent, child, or sibling—of someone diagnosed with pancreatic cancer, consider genetic testing for yourself and your family members. The results can tell you if you have the BRCA1 or BRCA2 gene mutation that increases the risk for this and other types of cancer. Of course, having this mutation doesn’t mean you’ll develop cancer. But knowing your risk can help improve your chances of an early diagnosis. What Are the Complications of Pancreatic Cancer? Pancreatic cancer can develop several complications, typically involving the organs of the digestive system and the nerves surrounding the pancreas. Bowel Obstruction A pancreatic tumor can obstruct the duodenum (the initial passage of the small intestine), blocking the movement of digested food from the stomach into the intestine. In this case, your physician may recommend inserting a stent into your small intestine to keep it unobstructed. In some situations, you may need to undergo surgery to have a temporary feeding tube placed or to have the attachment of the stomach relocated to a lower point of the intestines not blocked by cancer. Jaundice Pancreatic cancer can block the liver’s bile duct, causing jaundice. The signs of jaundice include yellow skin and eyes, pale stools, and dark urine. Your doctor may recommend inserting a stent (a plastic or metal tube) into the bile duct to keep it unobstructed. Pain A growing tumor may impinge on nerves in your abdomen, resulting in pain that may become severe. Pain medications may be prescribed to manage this pain. In addition, radiation and chemotherapy treatments may slow tumor growth and relieve some pain. In more severe cases, your physician may recommend a procedure to inject alcohol into the abdominal nerves (a celiac plexus block). This procedure interrupts pain signals sent from this area to the brain. Weight Loss Several aspects of pancreatic cancer can cause weight loss. Weight loss might occur as the cancer disrupts the body’s metabolism. Nausea and vomiting caused by treatments or a tumor putting pressure on the stomach may make eating solid food difficult or impossible. Also, the body may not be able to fully process food because the pancreas isn’t producing enough digestive juices. What Are the Treatments for Pancreatic Cancer? Pancreatic cancer treatment depends upon the cancer’s stage and location and the patient’s overall health and personal preferences. Treatment can involve surgery, radiation, or chemotherapy. In late-stage cancer, treatment may focus on palliative (supportive) care. Surgery Surgery aims to remove the cancerous tumor(s) from the organ. The procedure used will depend upon the location of the cancer in the pancreas. Pancreaticoduodenectomy (“Whipple procedure”): This procedure is used when the cancer is in the head of the pancreas. The operation requires surgical skill to remove the head of the pancreas, the duodenum, the gallbladder, part of the bile duct, and adjacent lymph nodes. Sometimes part of the stomach and colon are removed as well. Then, the surgeon reattaches the remaining parts of these organs to allow the patient to digest food. Distal pancreatectomy: This procedure removes the pancreas’ left side (body and tail). The procedure may also involve removing your spleen. Total pancreatectomy: As the name implies, this procedure completely removes the pancreas. While you can live relatively normally without this organ, you will need lifelong insulin treatments and enzyme replacement therapy. Surgery for tumors affecting nearby blood vessels: If the tumor(s) involve nearby blood vessels, you may not be a candidate for the above surgical interventions. In that case, at some state-of-the-art medical centers, surgeons may offer operations that include removing and reconstructing the affected blood vessels. Each of these surgeries carries the risk of significant complications and requires a long recovery. You'll remain in the hospital for several days after surgery and then continue recovery for several weeks at home. Research shows pancreatic cancer surgery tends to cause fewer complications when performed by experienced surgeons at centers that have handled many of these operations. Ask about your surgeon’s experience with pancreatic cancer surgery. If you have doubts, consider a consultation with another doctor affiliated with a hospital known for its pancreatic surgery success. Chemotherapy Chemotherapy uses drugs that are toxic to cancer cells. The drugs are administered as pills or through an IV. Chemotherapy may be combined with other treatments or used as a stand-alone treatment, especially in advanced cancer cases. It can also be used before surgery to shrink a tumor or after surgery as a follow-up to eliminate any cancer cells not removed by the procedure. Radiation Therapy Radiation therapy directs high-energy X-rays at the tumor to kill cancer cells. It is typically combined with chemotherapy. It may also be used for advanced patients who are not eligible for surgery to ease symptoms. Targeted Therapy In this treatment, drugs are used to target specific proteins that determine the spread and growth of the cancer. This therapy may also be combined with other modes of treatment. For example, erlotinib, olaparib, larotrectinib, and entrectinib are common medications for targeted therapy. Pain Management Pancreatic cancer can involve nearby nerves, which can be very painful. Your doctor may prescribe oral medications, steroid injections, or nerve blocks to manage the pain. If you have pancreatic cancer, talk to your doctor to determine a treatment to ease your symptoms if you’ve started experiencing severe and enduring pain. The National Cancer Institute offers an interactive chart that provides in-depth details on various treatment options, including the procedures involved and the relative efficacy and risks. Radiation therapy, for instance, is sometimes employed, but its efficacy for pancreatic cancer is a source of controversy. How Does Mindset Affect Pancreatic Cancer? According to the American Cancer Society, research has not shown that attitude, mood, or mind-body therapies impact cancer survival rates. Some recent research challenges that assessment, pointing out that “studies of the placebo effect are revealing that our mindsets can even leverage endogenous opioid and neuroimmune pathways, thereby directly changing physiology and shaping objective markers of health. During cancer treatment, mindsets about the meaning of illness (e.g., whether it is a catastrophe, a manageable challenge, or an opportunity to make positive life changes) are important.” However, it is important to note that there is no medical evidence to conclude that the patient “brought cancer upon themselves” through negative thinking or due to a particular personality type.Less controversial in the research is the recognition that interventions like biofeedback, meditation, support group attendance, therapy for depression, and visualization can help manage symptoms, discomfort, and the mental challenges associated with such a diagnosis. A pancreatic cancer diagnosis is undoubtedly a difficult and life-altering experience. Talk to your health care provider about your options for addressing the mental and lifestyle issues surrounding living with cancer. Consider joining a support group for people with pancreatic cancer; your health care provider can provide leads on both online and in-person groups. Spending time with others experiencing the same challenges can improve your mental and emotional health. You may also want to meet with a therapist or social worker to address the feelings that arise. What Are the Natural Approaches to Pancreatic Cancer? There is limited peer-reviewed research on natural approaches to pancreatic cancer. One notable exception is a promising study that showed one of the active ingredients of Nigella sativa oil (black seed oil), thymoquinone, kills pancreatic cancer cells in vitro and interferes with their replication process. Further research is underway to try to isolate and enhance the oil’s active properties for the development of pharmaceutical treatment. A literature review published in 2021 looked at natural compounds used in several traditional Asian medicines, including Korean, Thai, and Chinese, and found that several compounds showed evidence of contributing to the death of cancer cells, including Eucalyptus microcorys, a species of Eucalyptus native to Australia and commonly known as tallowwood, as well as Moringa and coix seed (Job’s tears), which are known for their anti-inflammatory properties. How Can I Prevent Pancreatic Cancer? There is no surefire method to prevent pancreatic cancer, but there are steps you can take to reduce your risk. Dr. Ryoichi Nakahara, who holds a doctorate in surgery from the University of Tokyo, Japan, suggested in an interview with The Epoch Times that better prevention of pancreatic cancer can be achieved through management in the following six areas: Quit smoking: Smoking cigarettes is believed to cause roughly 25 percent of pancreatic cancers. Nicotine impacts the secretion of the pancreas. Smoking can cause the carcinogen N-nitrite to enter the bile duct and then reflux into the pancreatic duct, thus inducing pancreatic cancer. Balanced diet: Eat a light, low-fat diet, emphasizing cereals, beans, fish, and shrimp, vegetables such as radishes and green vegetables like broccoli and cabbage, and fruits such as grapes, kiwis, figs, and so forth. Outdoor aerobic exercise: Engage in regular exercise such as walking, cycling, and swimming. Exercise promotes vitality and immunity and exercises bones and muscles, which supports optimal tissue and organ functioning. It also prevents cancer due to its ability to mobilize the immune system and enhance T-cell function. In July 2022, a research team at the New York University School of Medicine published a study in the international oncology journal Cancer Cell. Researchers found that in mice afflicted with pancreatic ductal adenocarcinoma, aerobic exercise slowed tumor growth. Regular physical checkups: Regular physical examination and screening improve the detection rate of early pancreatic cancer, enhancing one’s prognosis and allowing physicians to use the full spectrum of treatments, including surgery, which is crucial to the long-term survival of this disease. Self-protection at work: If you work in an environment where you are exposed to chemicals, take all necessary precautions to reduce exposure, including wearing masks, gloves, and, where applicable, hazard suits. Develop a healthy mood: Stress can lead to an impaired immune system as well as metabolic and endocrine dysfunction. Impairments in these systems create a more inviting environment for cancer to develop and aggressively advance.

NIH Article Cancer cell visualized In the 1920s, Otto Warburg observed that tumor cells consume a large amount of glucose, much more than normal cells, and convert most of it to lactic acid. This phenomenon, now known as the ‘Warburg effect,’ is the foundation of one of the earliest general concepts of cancer: that a fundamental disturbance of cellular metabolic activity is at the root of tumor formation and growth. In the ensuing decades, as it became apparent that abnormalities in chromosomes and eventually individual genes caused cancer, the ‘metabolic’ model of cancer lost a good deal of its appeal, even as emerging technologies were exploiting the Warburg effect clinically to detect tumors  in vivo . We now know that tumor suppressors and proto-oncogenes influence metabolism, and that mutations in these genes can promote a metabolic phenotype supporting cell growth and proliferation. Thus, these advances have unified aspects of the metabolic and genetic models of cancer and have stimulated a renewed interest in the role of cellular metabolism in tumorigenesis. This review reappraises the notion that dysregulated cellular metabolism is a key feature of cancer and discusses some metabolic issues that have escaped scrutiny over the years and now deserve closer attention. The Warburg effect, also known as aerobic glycolysis , is defined as a high rate of glucose (Sugar energy) utilization and lactate production despite the presence of sufficient oxygen to oxidize glucose carbon in the mitochondria. Recognition of this unusual metabolic phenomenon stems from experiments performed by the German physiologist Otto Warburg, starting in the 1920s. In those experiments, Warburg compared the metabolism of rapidly proliferating mouse ascites tumor cells to that of differentiated, quiescent cells from organs of the adult animal. He proposed that a fundamental impairment of cellular respiratory capacity was the root cause of all cancer, a bold and controversial claim that was ultimately rejected despite his continued writing and lecturing on the subject for some 40 years. Nevertheless, appreciation of the Warburg effect as a feature of tumor cell metabolism has survived its namesake by a long stretch. Today, the glycolytic activity of tumors is not only accepted, but exploited clinically by F-deoxyglucose positron emission tomography (FDG-PET), which detects tumors precisely by virtue of their enhanced ability to take up and metabolize glucose compared to normal tissue. The Warburg effect remains the most frequently cited evidence that tumors display dysfunctional metabolism. Recently, interest in tumor metabolism has enjoyed a renaissance as an ever-growing number of reports uncovers the molecular connections between transformation and cell metabolism, and as technological improvements increase the feasibility of studying tumor metabolism  in vivo . The field seems poised to offer significant insights into tumor biology over the next decade. As such, it is worth re-examining the evidence for a  bona fide  connection between altered cellular metabolic state and tumorigenesis: does the notion of such a connection stand up to our current understanding of tumor biology and cancer genetics? If there is such a link, then the following should be true: 1.     Tumor cells should have metabolic activities that differ from non-transformed, quiescent cells, and these activities should be required for tumor growth; 2.     The mutations in tumor suppressors and proto-oncogenes that promote cancer should regulate the metabolic activities observed in tumors; and 3 .    Mutations in metabolic enzymes should, in at least some cases, promote tumorigenesis.   DO TUMOR CELLS HAVE METABOLIC ACTIVITIES THAT ARE DIFFERENT FROM QUIESCENT CELLS AND ARE REQUIRED FOR TUMOR GROWTH? Cancer & Metabolism   Most studies on tumor metabolism have been motivated by one of two general concepts about the way cell metabolism is regulated. The first is that tumor metabolism is primarily a response to stresses imposed upon cells during tumor growth. There is abundant evidence that some stresses, particularly hypoxia, exist in the tumor microenvironment and exert effects on metabolism3–5. But the high glycolytic flux in tumors can appear even when oxygen is abundant, and the metabolic consequences of hypoxia include specific impairments of protein and lipid synthesis that are counterproductive to cell growth and proliferation6–8. These observations suggest that the cellular responses to tumor hypoxia, including enhanced glycolysis, serve to facilitate tumor cell survival, not growth. This is also true in non-transformed cells, which rely on glycolysis to survive periods of hypoxia9. When oxygen delivery improves and rapid cell growth resumes, the persistence of glycolysis is likely due to other factors. Alternatively, one can presume that tumor cell metabolic activities function primarily to support the unusually high rates of cell growth and proliferation found in tumors. Since each round of replicative cell division requires a doubling of protein, lipids and nucleic acids, it stands to reason that tumor cell metabolism must provide the energy and biosynthesis needed to meet this challenge. Rapid tumor growth requires the ability to capture nutrients and process them in the appropriate metabolic pathways to convert their carbon and nitrogen into macromolecules. All of the activities discussed in this section (the Warburg effect, fatty acid synthesis and mitochondrial glutamine metabolism) occur during cell growth, and evidence suggests that the three pathways cooperate in such a way as to maximize the production of macromolecules in proliferating cells. Glutamine metabolism  is second only to the Warburg effect in terms of historical significance to the study of tumor cell metabolism. Glutamine is the most abundant amino acid in human plasma and participates in many metabolic pathways required for normal cell function. In addition to its role in protein synthesis, it provides nitrogen for the synthesis of nonessential amino acids, purines, pyrimidines and hexosamines, and is the major source of glutamate used for glutathione synthesis. Tumor cells have long been known to consume glutamine at high rates  in vivo  and to require high concentrations of glutamine to survive and proliferate  in vitro . Classical studies on tumor cell metabolism in culture demonstrated that glutamine is an important carbon source since most of the glutamine consumed is used as a respiratory substrate in the mitochondria rather than for protein synthesis 31 . More recent experiments have demonstrated that suppressing mitochondrial glutamine metabolism can alter gene expression, accelerate apoptosis and stimulate cellular differentiation. Therefore, glutamine metabolism has the potential to integrate a large number of cellular activities that support tumorigenesis. WHERE DO WE GO FROM HERE? At present, the data on tumor cell metabolism make a compelling argument that during the process of transformation, cells acquire a fairly stereotyped set of metabolic characteristics that enable them to grow and proliferate with reduced dependence on extracellular signals, and that the mutations in tumor suppressors and proto-oncogenes that cause cancer contribute to this ‘metabolic transformation.’ There are a number of important questions that still need to be addressed before we can appreciate fully the role of metabolism in the development, progression, and treatment of cancer. Below are six areas that are in particular need of attention. First , there is still a large gap between our understanding of tumor cell metabolism in vitro and tumor metabolism in vivo. The inhibitor and RNA interference experiments cited above demonstrate the requirement of certain enzymes for tumorigenesis, but the ability to observe the metabolism of live tumors would provide a much richer understanding of the biochemical aspects of tumor growth and would support more rigorous examination of the effect of tumorigenic mutations on metabolic flux. The use of 18FDG-PET and conventional NMR spectroscopy have provided some validation of the Warburg effect and other pathways in live tumors but are currently best suited to give snapshots of metabolism rather than robust measurements of metabolic flux. The application of more sensitive methods such as the use of probes labeled with hyperpolarized 13C may ultimately support flux analysis in vivo. Second , the regulation of anaplerosis and of glutamine metabolism in general has not been carefully studied with respect to cell signaling. While glutamine consumption is a general metabolic feature of cell proliferation, it is unknown whether all tumor cells must use glutamine as the major source of carbon for anaplerosis. In a few cases, cellular biosynthesis and growth have been correlated with the induction of alternative anaplerotic pathways that do not involve glutamine metabolism, and thus the universality of glutamine-based anaplerosis is debatable. Furthermore, while stimulation with mitogens can enhance glutamine utilization in various cell types, neither the signaling pathways responsible for this activity nor the specific pathways of glutamine metabolism (e.g. glutaminolysis vs. glutamine-based anaplerosis) have been characterized. Resolving these issues will go a long way towards integrating our understanding of cell signaling and the metabolism of cell growth. Considering that glucose and glutamine play complementary roles in proliferating tumor cells, it will be interesting to test whether they are co-regulated by the same signaling pathways and affected by the same tumorigenic mutations. Third , many studies have sought to unravel the complex relationships between oxidative stress, cellular transformation and cancer. At the level of cell metabolism, there are many open questions about how NADPH-producing systems are regulated and whether these mechanisms are altered in tumor cells. Rapidly proliferating tumor cells require NADPH both to maintain pools of reduced glutathione and to support the reductive biosynthetic reactions needed for anabolic metabolism. The two NADPH-producing systems discussed above, G6PD and cytosolic malic enzyme, are expressed in tumors of various histological types, and in some cases their activities are almost equal in proliferating tumor cells, implying equivalent contributions to the NADPH pool. It is interesting that G6PD deficiency, a common X-linked condition, does not alter the risk of death from cancer. This suggests that malic enzyme or other systems can provide sufficient NADPH to support tumorigenesis in G6PD-deficient cells, and that selective inhibition of malic enzyme in individuals with G6PD deficiency might suppress tumor growth. Conversely, maintaining an NADPH pool and a robust response against oxidative stress is critical in preventing tumorigenesis, as emphasized by recent studies on the transcription factor NF-E2-related factor-2 (Nrf2). Nrf2 is sequestered in the cytosol through association with its repressor Keap1 (Kelch ECH associating protein 1). Exposure to oxidative and other stresses allows Nrf2 to translocate to the nucleus, where it heterodimerizes with small Maf-family proteins and binds promoters containing antioxidant response elements, thus inducing expression of genes that serve antioxidant functions. This protects cells from apoptosis during exposure to oxidizing agents, UV irradiation and other stresses. Knockout mice lacking Nrf2 have enhanced susceptibility to cancer when exposed to chemical mutagens. Future studies will be aimed at exploiting the Nrf2 pathway as a strategy to prevent cancer, and at understanding other mechanisms by which normal cells and tumor cells respond to oxidative stress. Fourth , almost all previous studies on tumor cell metabolism have been performed in unsynchronized populations of cells distributed throughout the cell cycle, so that the resulting data represent average cell metabolic activity throughout the cycle. The temptation is to assign the greatest biological importance to the pathways that appear to be the most active, but such an interpretation could miss the significance of pathways that are transiently induced at specific, critical points of the cell cycle. One can envision two ways to identify these activities: by performing flux analysis in synchronized populations of cells or by using inhibitors and genetic models to determine the effect of disrupting candidate metabolic activities on progression through the cell cycle. There is already strong evidence that interfering with metabolism profoundly affects the cell cycle. In fibroblasts, glucose deprivation imposes an AMPK- and p53-dependent G1/S phase arrest, and in Drosophila, elimination of ETC components stimulates several distinct signaling pathways that culminate in arrest at the G1/S transition. These efforts are relevant to metabolically directed cancer therapy, especially if such therapies are used as adjuvants to existing strategies that already exert cell cycle-specific effects. For example, if ionizing radiation is most effective on cells at the G2/M transition, then a metabolic therapy targeting a G2-specific activity might increase the fraction of cells at that stage, thereby increasing the overall efficacy of treatment. Fifth , it is possible that normal but genetically defined variation in the expression of metabolic enzymes could influence cancer risk and progression. Microarray analysis of gene expression in cells from healthy individuals has shown that some metabolic enzymes and transporters are highly variable in their mRNA abundance, and that the variance is defined genetically. Currently, the association between disease states and variance of expression in these genes is unknown. But the abundance of certain metabolic enzymes in tumors is correlated with poor clinical outcome in various forms of cancer. If an individual’s cells have an unusually high expression of a key enzyme(s) at baseline, then the acquisition of a transforming mutation in those cells might translate into enhanced growth and clinically aggressive features of the resulting tumor. Since the variance in expression of the enzyme would not independently cause cancer, the genes responsible for the variance would probably not be identified in linkage studies to find cancer-causing genes. Finally , it will be interesting and important to fit tumor metabolism back into the context of the entire cancer patient. Regardless of the increased metabolic autonomy of tumor cells, tumor growth still relies on the metabolism of the host both to provide nutrients and to remove secreted waste products. Yet the issue of how tumors influence whole-body metabolism is still very much an open question, and one that relates directly to the health of cancer patients. For example, the phenomenon of cancer cachexia has been appreciated for centuries, but its causes are only partially understood and include processes that raise whole-body energy expenditure and stimulate catabolism in both the fat and muscle. Does the catabolic response function in part to provide nutrients to the tumor? In rats, tumor growth was associated with progressive increases in the synthesis and release of glutamine from muscle, ultimately resulting in decreased glutamine stores in the face of relentless tumor growth, consistent with glutamine ‘steal’ by the tumor. Other studies have demonstrated markedly enhanced Cori cycle metabolism to convert lactate back to glucose in the liver of cancer patients who were suffering from progressive weight loss. These studies demonstrate the interconnected nature of whole-body metabolism in patients with cancer. They also underscore the fact that any hope for rational, metabolically directed cancer therapies depend on the development of a comprehensive understanding of metabolism in the host as well as in the tumor.

Epoch Health Article As the 10th most common cancer in the United States, leukemia will affect up to 2 percent of Americans at some point in their lifetime. Lekemia Spotting Leukemia occurs when the proliferation of abnormal blood cells outpaces that of healthy blood cells. Leukemia is a general term for cancers affecting blood cells. The specific type of leukemia is determined by the type of blood cell involved and the rate at which the cancer progresses. In the United States, the incidence rate of leukemia cases was 14.1 per 100,000  people annually, with a mortality rate of 5.9 per 100,000, based on data from 2017 to 2021 for cases and 2018 to 2022 for deaths. Leukemia is most commonly found in adults over 55, but it is also the most prevalent cancer in young people under 15. What happens in your body What Are the Types of Leukemia Cancer? leukemia begins in blood stem cells, which are formed in the bone marrow and develop into various types of cells. Blood stem cells develop into either lymphoid or myeloid stem cells. Lymphoid stem cells produce lymphocytes, a type of white blood cell that fights infections, while myeloid stem cells produce red blood cells, platelets, granulocytes, and monocytes, with the latter two also being white blood cells. Before maturing into blood cells, lymphoid and myeloid stem cells first differentiate into blast cells, such as lymphoblasts and myeloblasts, which are immature blood cells. In leukemia, abnormal blast cells are overproduced and do not mature into functional blood cells. These leukemia cells often grow and survive more effectively than normal cells, gradually crowding out and suppressing the production of healthy blood cells. The progression and impact on normal cells vary depending on the type of leukemia. This article will discuss the four main types of leukemia. 1. Acute Myeloid Leukemia (AML) Acute myeloid leukemia is characterized by the presence of over 20 percent myeloid blasts. AML was estimated to account for 34 percent of all leukemia cases in the United States in 2023. It is the most prevalent type of leukemia in adults but is less common among children. It is the most aggressive cancer, with its prognosis varying depending on the molecular subtypes, and usually urgent treatment is needed. Cancer cells can rapidly spread to other parts of the body, including the central nervous system, liver, and lymph nodes. AML primarily affects white blood cells, although in very rare cases, it can involve red blood cells or platelets, as seen in acute erythroid leukemia and acute megakaryoblastic leukemia. 2. Chronic Myeloid Leukemia (CML) Chronic myeloid leukemia is a slow-growing cancer of the bone marrow and blood, with less than 20 percent myeloid blasts. It occurs when two parts of our DNA get mixed up, creating an abnormal chromosome called the Philadelphia chromosome, an acquired chromosomal abnormality that develops after birth. This leads to the production of a faulty protein that causes certain blood cells to malfunction. These dysfunctional cells are mostly neutrophils, basophils, and eosinophils—all white blood cells. CML was estimated to account for 15 percent of all leukemia cases in the United States in 2023. CML can sometimes progress into AML, which is difficult to treat. 3. Acute Lymphoblastic Leukemia (ALL) Acute lymphoblastic leukemia involves the blastic transformation of B- and T-cells, which are lymphocytes. The bone marrow produces too many of these abnormal lymphocytes, which cannot effectively fight against infections, while crowding out the healthy cells. It can spread to the brain, liver, lymph nodes, spine, and spleen. ALL is the most common leukemia in children, making up about 80 percent of cases in this age group. Most children with ALL have the B-cell subtype. It was estimated to account for 11 percent of all leukemia cases in the United States in 2023. In about one-quarter of adults with ALL, the leukemia cells have the Philadelphia chromosome. 4. Chronic Lymphocytic Leukemia (CLL) Chronic lymphocytic leukemia occurs when a specific type of white blood cell called a monoclonal lymphoid cell grows out of control. It mostly affects people between the ages of 60 and 70. CLL usually progresses slowly, so not everyone with it will need treatment right away; treatment typically starts when symptoms become noticeable. It was estimated to account for 31 percent of all leukemia cases in the United States in 2023. What Are the Symptoms and Early Signs of Leukemia? Leukemia often doesn’t have early signs or symptoms. It might not be discovered until a person undergoes a routine checkup. Symptoms and signs vary by the type of leukemia. The following are more common across any type: Anemia:  Anemia (insufficient red blood cells) may present as fatigue, weakness, pallor (pale skin), malaise, dyspnea on exertion (shortness of breath with activity), tachycardia (rapid heartbeat), and chest pain during exertion. Thrombocytopenia:  Thrombocytopenia (insufficient platelets) can lead to bleeding from mucous membranes, easy bruising, purpura (small red or purple spots on the skin), nosebleeds, bleeding gums, and heavy menstrual periods. Spontaneous bleeding, including in the brain or abdomen, may also occur. Granulocytopenia or neutropenia:  Neutropenia (insufficient neutrophils, a type of white blood cells) increases the risk of infections from bacteria, fungi, and viruses. Symptoms may include fevers and severe or repeated infections. The exact cause of the fever is often unclear, but granulocytopenia (insufficiency in a type of white blood cell) can lead to rapidly worsening and serious bacterial infections. Pancytopenia:  Pancytopenia is characterized by low levels of all three above types of blood cells. Swelling of the lymph nodes, liver, or spleen:  When leukemic cells infiltrate organs, it can enlarge the liver, spleen, and lymph nodes. Fever and chills. Unexplained weight loss. Night sweats. Loss of appetite. Joint pain. Bone pain. What Causes Leukemia? Leukemia occurs when there are changes in the DNA of bone marrow cells, but the reason for these genetic changes is not understood. Leukemia development is influenced by various genetic and environmental risk factors, which vary depending on the type of leukemia. What Are the Stages of Leukemia? Each type of leukemia is staged  differently. The types are staged accordingly: ALL  is staged according to leukemia cell maturity and the type of lymphocyte involved. AML  is staged using the French-American-British (FAB) system, which accounts for how many leukemia cells there are and what size, number of healthy cells, chromosome changes, and other genetic issues. CLL  is staged with the Rai system, which considers the blood’s lymphocyte count, the degree of spleen, lymph node, and liver enlargement, and whether there is anemia or low platelet count. CML  is staged according to how many diseased cells are in the blood and bone marrow. Who Is at Risk of Leukemia? The following factors raise one’s risk of developing leukemia: Age:  Age is a risk factor that differs among types. The highest incidence rates for ALL occur in children and adolescents under 15 years old, and children to middle-aged people are more at risk for CML. However, adults 50 years or older are more at risk for AML and CLL. Sex:   Men  are more at risk for all four types of leukemia than women. Genetic syndromes:  These include Down syndrome, Fanconi anemia, Bloom syndrome, ataxia-telangiectasia, neurofibromatosis type 1, Shwachman-Diamond syndrome, congenital dyskeratosis, Kostmann syndrome, Wiskott-Aldrich syndrome, Li-Fraumeni syndrome, Klinefelter syndrome. Genetics and family history:  Inherited genetic mutations present from birth may increase the risk of developing AML. Race:  In the United States, ALL is more common among whites and Hispanics, and CLL is more common among whites than other races. Gene alterations:  Most DNA changes associated with AML develop during a person’s lifetime rather than being inherited at birth. Changes in specific genes such as FLT3, c-KIT, and RAS  are common in AML cells. These changes can prevent bone marrow cells from maturing properly or cause them to grow uncontrollably. Smoking:  Smoking is associated with about a 50 percent  increased risk of leukemia, possibly due to the presence of the carcinogen benzene in tobacco. Radiation exposure or chemotherapy:  People who have received radiation therapy or chemotherapy (e.g., with drugs called etoposide and alkylating agents) have a higher risk of leading to AML, known as treatment-related or therapy-related AML. People exposed to very high levels of radiation, such as survivors of atomic bomb blasts or nuclear reactor accidents, are also at increased risk of AML and CML. Leukemia from radiation exposure takes many years to develop, and most people treated with radiation for cancer do not develop the disease. CML has also been reported in those who have undergone excessive diagnostic X-rays or CT scans. Benzene exposure:  Benzene is present in unleaded gasoline and is used in the chemical industry. People can be exposed to benzene through their work, the environment, or by using certain products. It is found in paint strippers, adhesives, forest fire smoke, and volcanic gas. Blood and bone marrow disorders:  People with certain blood disorders, such as myelodysplastic syndrome and myeloproliferative disorders, and bone marrow diseases are at higher risk for developing AML and CLL. HTLV-1 infection:  Infection with the human T-cell leukemia/lymphoma virus, type 1 (HTLV-1) raises the risk of developing T-cell ALL, a rare form of ALL. Epstein-Barr virus (EBV):  EBV is associated with a type of ALL. In the United States, EBV is the virus that commonly causes infectious mononucleosis. Weakened immune system  due to immunosuppressive drugs. Exposure to herbicides:  Researchers have identified a possible link between CLL and exposure to herbicides such as Agent Orange  used during the Vietnam War. The U.S. Department of Veterans Affairs provides disability compensation to those exposed to this herbicide. Chromosome changes:  In most cases of CLL, changes are found in chromosomes, commonly involving deletions such as the loss of part of chromosome 13. Other affected chromosomes can include 11 and 17, and occasionally there is an extra chromosome 12 (trisomy 12). How Is Leukemia Diagnosed? The doctor will inquire about one’s health history, which includes symptoms, risk factors, and past medical events. He or she may also inquire about any family history of leukemia. A physical exam helps the doctor check for signs of leukemia. A series of tests, which may include blood tests, cytogenetic and molecular studies, and imaging tests, are performed to diagnose specific types of leukemia and for staging purposes. Blood Tests Complete blood count (CBC):  A complete blood count measures the number and quality of white blood cells, red blood cells, and platelets. The presence of immature blood cells (blasts) in the blood, which are not normally seen, may lead doctors to suspect leukemia. Blood chemistry tests:  Blood chemistry tests measure specific chemicals in the blood to help identify liver or kidney issues caused by leukemia and help stage the disease. In leukemia, levels of certain chemicals, such as blood urea nitrogen, creatinine, phosphate, alanine aminotransferase, and uric acid, may be elevated. Blood clotting tests:  Blood clotting tests evaluate how well the body can clot blood, as abnormal levels of clotting factors can be associated with leukemia. Key tests include fibrinogen level, prothrombin time (PT), partial thromboplastin time (PTT), and international normalized ratio (INR). Kidney function panels. Liver function panels. Peripheral blood smear:  Blood cells are stained and examined under a light microscope to reveal their number, size, shape, and type, as well as the pattern of white blood cells and the ratio of blast cells to maturing and mature white blood cells. Quantitative immunoglobulin test:  The quantitative immunoglobulin test measures the concentration of antibodies (immunoglobulins) in the blood, which are produced by B-cells to help protect the body from infections. Other Tests Bone marrow tests:  Bone marrow testing typically involves two steps that are usually done simultaneously. These samples are usually taken from the hip bone and examined to detect chromosomal and cellular changes. First, during bone marrow aspiration, a liquid sample is collected. Next, a bone marrow biopsy removes a small bone piece with marrow. Immunophenotyping (flow cytometry):  Immunophenotyping is a technique that uses fluorescent labels to sort and classify cells. This method allows doctors to quickly examine many antibodies on thousands of cells in a single sample, and it’s useful for identifying unique features of leukemia cells. Imaging tests:  Doctors use imaging tests such as X-rays, computed tomography (CT) scans, magnetic resonance imaging (MRI), or ultrasounds to rule out other causes of symptoms and to check for leukemia cell masses in the chest that could affect breathing or blood circulation. Spinal tap:  A spinal tap (lumbar puncture) involves using a needle to collect cerebrospinal fluid, which is then examined for cancer cells. Cytogenetic and Molecular Studies Cytogenetic karyotyping:  Cytogenetic karyotyping identifies chromosomal abnormalities, helping doctors confirm a leukemia diagnosis and determine its type or subtype. These results also assist in planning the appropriate treatment. Fluorescence in situ hybridization (FISH):  FISH uses fluorescent DNA probes to detect chromosomal abnormalities and genetic changes in leukemia cells. It helps differentiate between leukemias with similar appearances but distinct genetic profiles. Polymerase chain reaction (PCR):  PCR is a very sensitive test that can find a single  leukemia cell among 100,000 cells. It amplifies specific gene segments to detect DNA mutations, inversions, or deletions associated with certain leukemia types. It aids in diagnosing leukemia and assessing its prognosis. Quantitative polymerase chain reaction (qPCR):  The qPCR test is a highly sensitive method used to find and measure the amount of a specific gene, BCR::ABL1 (related to the Philadelphia chromosome), in blood or bone marrow samples. It can detect even tiny amounts of this gene, which may not be visible with other tests. Biomarker testing:  Biomarker testing or molecular/genomic testing analyzes the DNA or RNA sequence in cancer cells to identify genetic changes. This information helps assess risk, predict prognosis, and guide treatment decisions, including the need for intensive or novel therapies. DNA sequencing:  DNA sequencing tests blood or marrow samples for mutations in certain genes. Identifying mutations or their absence helps assess the patient’s prognosis. Beta-2 microglobulin test (B2M):  Beta-2 microglobulin is a small protein produced by various cells and can be measured through a blood chemistry test. What Are Possible Complications of Leukemia? Complications of leukemia include the following: Disseminated intravascular coagulation (DIC):  DIC is a leukemia complication where blood clotting proteins malfunction, causing both clotting and bleeding. It is commonly linked to acute promyelocytic leukemia but can occur with other leukemia types. Regular lab monitoring and fibrinogen replacement with cryoprecipitate are crucial for patient survival. Severe infections:  Immunosuppression due to chemotherapy, stem cell transplantation, or the leukemia alone raises the risk of severe infections. Other cancers:  Leukemia survivors have an increased risk of developing subsequent cancers. Research has found a 5.6 percent risk of any cancer occurring within 30 years after leukemia. The most frequent second cancers in childhood leukemia survivors are other types of leukemia or lymphoma. Organ dysfunction:  Leukemia cells can invade organs. Death. What Are the Treatments for Leukemia? Some types of leukemia can be cured. Treatment for leukemia depends a lot on the specific type of leukemia and individual factors such as age and other health conditions. Conventional treatments include: Chemotherapy:  Chemotherapy uses anti-cancer drugs, either injected or taken orally, to target fast-growing cells, affecting both cancerous and healthy cells. It’s the primary treatment for many types of leukemia. The typical treatment for AML is known as the “7+3” regimen, where patients receive cytarabine continuously for seven days and an anthracycline drug (either daunorubicin or idarubicin) for three days. Targeted therapy:  In recent years, new drugs have been developed that specifically target certain parts of cancer cells. These targeted drugs work differently from traditional chemotherapy and usually have different side effects. Imatinib, nilotinib, dasatinib, bosutinib, and ponatinib are tyrosine kinase inhibitors (TKIs) that block the abnormal protein produced by the Philadelphia chromosome. Most patients respond well to TKIs, which are the standard treatment for CML, so acute chemotherapy is usually only necessary if the disease progresses to an accelerated phase or blast crisis. These drugs have also been successful in combination with chemotherapy for treating the blast phase, which previously had a poor prognosis. Stem cell transplant:  For some patients in remission who can handle intensive chemotherapy, the doctor might suggest a stem cell transplant during the consolidation phase. Interferon therapy:  Interferons are natural substances produced by the immune system, and interferon-alpha is a manmade version that mimics this natural substance. Interferon therapy helps slow the growth of leukemia cells. Active surveillance:  CLL progresses more slowly than other types of leukemia and usually doesn’t significantly shorten a person’s lifespan. Early treatment isn’t helpful unless the patient meets specific criteria for starting therapy. Radiation therapy:  Radiation therapy uses high-energy radiation to destroy cancer cells. It is used to treat a person with CLL with an enlarged lymph node, spleen, or other organ. ******The above treatments are what Oncologists will give and they will not look at Natural products. Below are the Natural treatments from my book: Sulforaphane Leukemia CSCs (Cancer Stem Cells) were first reported in liquid tumors, such as leukemias, with CD34+/CD38− cancer cells capable of initiating and promoting tumorigenesis in immunodeficient mice injected with cells derived from Acute Myeloid Leukemia (AML) patients. Later, another group showed evidence that AML would follow a hierarchical development pattern with CSCs on the top and giving rise to differentiated cancer cells by asymmetric division, originating the heterogeneity observed in AML patients SFN was found to inhibit the proliferation of AML stem-like cells in vitro and in vivo, by possibly decreasing the transcriptional and protein levels of components of the SHH pathway, one of the embryonic signaling pathways found to be dysregulated in CSCs. By impairing SHH, SFN decreased the self-renewal of AML stem-like cells, thus affecting their proliferation. Fenbendazole and Mebendazole both work by cutting off the energy intake. ·       Mebendazole induces autophagy in endothelial cells, likely impairing angiogenic activity  via decrease in Wnt/β-catenin axis and VEGFR-2 levels. ·       Autophagy promotes invasion of cancer stem cells through TGF-1β dependent epithelial-mesenchymal transition. Ivermectin Hairy Cell Leukemia ·       Mitochondria has been a promising target in blood cancer given their unique dependencies on mitochondrial functions compared to normal hematopoietic cells. In line with this concept, we show that an anthelminthic drug Ivermectin selectively kills chronic myeloid leukemia (CML) cells via inducing mitochondrial dysfunctions and oxidative stress. ·       Ivermectin is significantly more effective in inducing caspase-dependent apoptosis in CML cell line K562 and primary CML CD34 than normal bone marrow (NBM) CD34 cells. ·       Ivermectin also augments in vitro and in vivo efficacy of standard CML tyrosine kinase inhibitors. ·       Mechanistically, Ivermectin inhibits respiratory complex I activity and suppresses mitochondrial respiration in K562 and CML CD34 cells. ·       In addition, Ivermectin also induces mitochondrial dysfunctions in NBM CD34 cells in a similar manner as in CML CD34 cells whereas NBM CD34 cells are significantly less sensitive to Ivermectin than CML CD34 cells. As there are no Hairy Cell studies yet it would be very surprising, given Ivermectins results on other Leukemia cancer cell would not be replecated in Hairy Cell Leukemia! https://www.sciencedirect.com/science/article/abs/pii/S0006291X18302869 How Does Mindset Affect Leukemia? While mindset doesn’t play a role in the development of leukemia, it can influence how leukemia patients cope with the disease, its treatment, and treatment outcomes. A positive mindset can help patients handle the emotional challenges of leukemia, potentially leading to better overall well-being. It can also encourage patients to stick with their treatment plans and follow medical advice. Similarly, a constructive mindset can help in managing stress, which may improve how patients respond to treatment, and it can encourage patients to seek support from family, friends, and health care providers. ****I have not studied the below "Remedies" well enough to comment on their efficacy, however, I will be researching these more and do a wrte up on them. What Are the Natural Approaches to Leukemia? While some natural remedies are available, more research and clinical studies are necessary to confirm their safety and effectiveness. Consult a doctor before trying any of them. Medicinal Herbs Feverfew (Tanacetum parthenium):  Feverfew, also known as bachelor’s button , is a daisy-like plant commonly found throughout North America. Malignant stem cells play a key role in the development and persistence of AML. The compound parthenolide , derived from feverfew, has been found to selectively trigger the death of these AML stem cells, unlike standard chemotherapy, which often misses these vital cells and leaves the root cause of leukemia unaddressed. However, parthenolide’s effectiveness in medical treatments was limited as the body didn’t absorb it well. In 2019, researchers at Birmingham University developed a new parthenolide derivative  that is better absorbed by the body and has promising effects against leukemia based on in vitro and in vivo studies. So far, clinical trials haven’t been completed on this derivative’s effectiveness in treating leukemia. Korean red ginseng:  A 2009 study  found that treating U937 human leukemia cells with Korean red ginseng extract slowed their growth and triggered cell apoptosis (programmed cell death). A 2016 study  tested a water extract of Korean red ginseng on a leukemia tumor model created by transplanting T-cell lymphoma cells (RMA cells) into mice. When given orally, the extract reduced the size of the tumors, increased the levels of certain enzymes involved in cell death, and decreased another enzyme linked to cancer metastasis. Although the extract boosted the presence of CD11c+ immune cells, it did not directly kill the cancer cells. Based on cell line studies and mouse models, other medicinal herbs that can inhibit leukemia cell growth or trigger their apoptosis include: Euphorbia formosana Moringa oleifera Typhonium flagelliforme Acupuncture As per a 2022 review , the evidence for acupuncture’s effectiveness in alleviating leukemia symptoms is strongest in its ability to reduce pain and nausea/vomiting. Its effectiveness is less certain for symptoms such as peripheral neuropathy, fatigue, constipation, insomnia, night sweats, and itching (pruritus). How Can I Prevent Leukemia? With many risk factors being uncontrollable, there is no guaranteed way to prevent leukemia. However, you can take steps to lower your risk by: Avoiding smoking Limiting exposure to radiation (e.g., X-rays) and harmful chemicals (e.g., benzene) Maintaining a healthy lifestyle by getting enough sleep, being physically active, and eating a balanced diet that is restrictive of processed foods Preventing HTLV-1 and EBV infection Getting regular checkups

Epoch Health Article Ranking among the top causes of cancer-related deaths globally, liver cancer affects approximately 25,000 men and 11,000 women in the United States each year. Liver Cancer What Are the Symptoms and Early Signs of Liver Cancer? In the early stages, liver cancer may not manifest with obvious symptoms. As it progresses, symptoms such as those listed below may become noticeable. However, as these symptoms can also be attributed to other health issues, if you experience any, consult your doctor. They are: Unintentional weight loss Loss of appetite Early satiety after small meals Nausea and vomiting Swelling in the legs and feet due to fluid retention Abdominal lump or mass on the upper-right side Persistent pain in the upper-right abdomen or right shoulder blade Abdominal bloating or swelling Yellowing of the skin or eyes (jaundice) Swollen belly (ascites) caused by fluid buildup in the abdomen Itching Fever Easy bruising or bleeding Severe fatigue or weakness Pale, clay-colored stools Dark urine Some liver cancers produce hormones that may cause other signs or symptoms, including: Increased blood calcium levels possibly resulting in constipation, nausea, and confusion Decreased blood sugar levels that may lead to fatigue or feelings of faintness Enlarged breasts or testicular shrinkage in males Increased red blood cell count that might cause facial redness What Causes Liver Cancer? Cancer, in general, occurs when a change in DNA creates cellular mutations, and those mutated cells multiply uncontrollably. Liver cancer typically develops due to chronic inflammation. Several factors cause chronic liver inflammation and make it more likely that a person will develop cancer, including: Cirrhosis:  Cirrhosis is scarring of the liver. It occurs when scar tissue obstructs blood flow in the liver, impairing its function. Cirrhosis is mainly caused by chronic alcoholism and hepatitis infections. However, those with hepatitis C-related cirrhosis face a greater risk of developing liver cancer compared to those with cirrhosis from hepatitis B or alcohol consumption. Most people diagnosed with the main type of liver cancer in the United States also have cirrhosis. Chronic hepatitis B virus infection (HBV):  Hepatitis B virus can spread through body fluids. Chronic HBV infection is the primary cause of liver cancer in Asia and Africa. Transmission can occur from mother to child during childbirth, through sexual contact, or by sharing needles. Chronic hepatitis C virus infection (HCV):  Transmission of HCV is very similar to that of HBV. HCV can result in cirrhosis and is the primary cause of liver cancer in North America, Europe, and Japan. Nonalcoholic steatohepatitis (NASH):  NASH is a severe type of nonalcoholic fatty liver disease (NAFLD, although now, it is often called metabolic dysfunction-associated steatotic liver disease, or MASLD) that can lead to cirrhosis, characterized by an abnormal accumulation of fat in the liver, possibly resulting in inflammation and liver cell damage. Liver Cancer What Are the Types of Liver Cancer? There are two main categories of liver cancer: primary and secondary. 1. Primary Primary liver cancer originates from the cells, bile ducts, blood vessels, or connective tissue within the liver. The following are different types of primary liver cancer: Hepatocellular carcinoma (HCC):  Hepatocellular carcinoma, also known as hepatoma, originates from hepatocytes, the liver’s primary cells. HCC makes up approximately 80 percent to 90 percent of primary liver cancer cases and ranks as the third most common cause of cancer-related death globally. It’s frequently associated with cirrhosis. All other primary liver cancers are rare. Cholangiocarcinoma (bile duct cancer):  Although cholangiocarcinoma is considered another major type of liver cancer, it is relatively rare, making up about 15 percent  of liver cancer cases. The major bile ducts connect the liver and gallbladder to the small intestine while carrying bile produced by the liver to help with fat digestion. Cancer originating in the ducts outside the liver is called extrahepatic cholangiocarcinoma, while that within the liver is intrahepatic cholangiocarcinoma. Cholangiocarcinoma is a slow-growing type of cancer. Angiosarcoma:  Angiosarcoma, also known as hemangiosarcoma, is a rare type of soft tissue sarcoma that starts in the liver’s blood vessels. It accounts for 2 percent of all primary liver cancers. It is primarily diagnosed in older people, and its cause is usually unidentified. Hepatoblastoma:  While rare overall, hepatoblastoma is typically diagnosed in children under 2 years old. Sometimes, it can develop in older children and lead to the production of hormones that can cause precocious puberty. The cause of this cancer remains unknown. Fibrolamellar carcinoma:  Fibrolamellar carcinoma typically affects adults in their 20s and 30s, and it is not linked to cirrhosis, hepatitis B or C, or other known risk factors. Compared to other types of liver cancer, people with fibrolamellar carcinoma may have a better prognosis if detected early, with many living for several years after the tumor is removed. Fortunately, most liver growths (tumors) are benign. Treatment for benign tumors is often unnecessary unless they grow significantly, cause discomfort or pain, can be seen and are unsightly, press on other organs, or release hormones affecting bodily functions. 2. Secondary Secondary liver cancers, also known as metastatic liver cancers, are caused by cancer cells breaking away from their original site and traveling through the bloodstream or lymphatic system to the liver, where they form new tumors. Various types of tumors can metastasize to the liver, such as colorectal, breast, lung, and pancreatic cancers. What Are the Stages of Liver Cancer? HCC can be staged using various systems, including the tumor, node, and metastasis (TNM) and Barcelona Clinic Liver Cancer (BCLC) systems and Okuda criteria. The most commonly used, BCLC, comprises five stages: Stage 0:  Very early; there is one small tumor less than 2 centimeters in size that is asymptomatic and hasn’t invaded the major blood vessels in the liver. Stage A:  Early; there can be as many as three tumors, each smaller than 3 centimeters. There are still no symptoms or invasion into the major liver blood vessels. Stage B:  Intermediate; there are multiple tumors in the liver, either more than three or one to three tumors, with at least one being larger than 3 centimeters. There are still no symptoms or invasion into the major liver blood vessels. Stage C:  Advanced; the cancer has either invaded the major blood vessels in the liver or metastasized to other parts of the body, with noticeable symptoms. Stage D:  End-stage; the cancer has either invaded the major blood vessels in the liver or metastasized to other parts of the body, and there is severe liver damage. The TNM system is based on the following criteria: T:  Number of primary tumors, their size, and whether or not they have spread to nearby organs N:  Spread of cancer to nearby lymph nodes M:  Metastasis to other organs Increasing severity is indicated by adding numbers zero to 4 after T, N, and M. Who Is at Risk of Liver Cancer? The risk of developing liver cancer increases as individuals accumulate multiple risk factors. The following factors put a person more at risk: Sex:  Men are twice as likely to develop liver cancer than women for unknown reasons. This may be because men drink more alcohol than women. Age:  In the United States, primary liver cancer typically affects individuals aged 60 and older. Race:  Liver cancer rates are highest among Asian Americans and Pacific Islanders in the United States, followed by Hispanic and Latino, American Indian, Alaska Native, African American, and white populations, in that order. Hepatitis infections:  HBV and HCV infections are the biggest risk factor for liver cancer. However, clearing the acute hepatitis B or C virus results in complete recovery from the infection, and the increased risk of liver cancer is only present in individuals who do not clear the virus and experience persistent infection. Metabolic disorders:  Obesity leads to fat accumulation in the liver, causing nonalcoholic fatty liver disease (NAFLD). NAFLD and its association with Type 2 diabetes pose significant risk factors for hepatocellular carcinoma in the United States. Smoking:  The risk of developing liver cancer rises in correlation with the quantity of cigarettes smoked and the number of years the person has smoked. Fortunately, the risk of liver cancer decreases over time following smoking cessation. Environmental carcinogens:  Exposure to specific chemicals such as vinyl chloride and plutonium or consumption of aflatoxin-contaminated food can increase liver cancer risk. Aflatoxin is produced by mold on stored nuts and grains. This risk is lower in the United States but more prevalent in regions such as sub-Saharan Africa, Southeast Asia, and China. Excessive alcohol consumption:  This is a risk factor for liver cancer, particularly when an individual has cirrhosis or HBV/HCV infection. Specifically, heavy drinkers with cirrhosis have a 10-fold higher risk of developing liver cancer than those without. Betel chewing:  A 2009 Taiwanese study found that chewers of betel nut (used as a mild stimulant) without HBV/HCV infection had higher risks of cirrhosis and HCC, and these risks were combined with those associated with viral hepatitis infections synergistically. There is also some evidence that betel quid, a combination of betel leaf, areca nut, and slaked lime, causes liver cancer with or without tobacco, but more research is needed to confirm this. Family history:  People with relatives with liver cancer could be more at risk. Long-term steroid use:  Anabolic steroids, male hormones used by athletes for muscle strength and size, slightly raise the risk of HCC with long-term use. However, cortisone-like steroids such as hydrocortisone, prednisone, and dexamethasone do not pose the same risk. HIV infection or AIDS:  People with HIV or AIDS face a higher risk of liver cancer, likely due to their compromised immune system’s reduced ability to combat infections. Liver fluke infection:  Liver flukes are parasitic worms. Infections typically occur due to consuming contaminated food or water. Birth control pills:  The use of oral contraceptives for five or more years, especially older formulas, is associated with a slightly increased risk of liver cancers in women, but research has been controversial. Certain genetic conditions:  Inherent medical conditions that may increase the risk of liver cancer include hereditary hemochromatosis, alpha-1 antitrypsin deficiency, glycogen storage disease, and Wilson’s disease. Genomic instability, which can involve changes in chromosomes or single DNA building blocks, also plays a significant role in liver cancer development. Specific genes such as TERT promoter, TP53, CTNNB1, ARID1A, and FGF, along with signaling pathways such as JAK/STAT, WntB-catenin, and PI3K-AKT-mTOR, are key drivers in causing HCC. Primary sclerosing cholangitis:  This condition can result in inflammation and scarring of the bile ducts, leading to intrahepatic cholangiocarcinoma. How Is Liver Cancer Diagnosed? Liver cancer screening involves checking for cancer in people without symptoms. Early detection through screening can aid in identifying cancer at a stage where treatment may be more effective. While there isn’t a standard or routine screening test for liver cancer in the United States, the following tests are often used: Alpha-fetoprotein testing:  Alpha-fetoprotein (AFP), a protein produced by liver tumors, is the most commonly used tumor marker for liver cancer detection. Tumor markers, or biomarkers, are substances tumors produce that can be detected in blood, fluids, or tissues. However, in addition to liver cancer, increased AFP levels can also occur in pregnancy, hepatitis, and other cancers, so AFP testing is controversial. High-risk cirrhotic patients, such as those with hepatitis C, hepatitis B, or hemochromatosis, may undergo AFP level checks every three to four months. Computed tomography (CT) scan:  This may reveal a tumor. Ultrasound scan:  Ultrasonography every six or 12 months is a standard screening option. However, in obese individuals, ultrasound is much less sensitive, so alternating ultrasound with MRI or CT scans should be considered. Liver cancer diagnosis typically involves a physical examination, blood and imaging tests, and occasionally a liver biopsy for confirmation. The following may be performed: Physical examination:  HCC patients usually have an enlarged liver. In infants, doctors typically suspect hepatoblastoma when they detect a sizable mass in the upper right area of the abdomen, especially if the infant’s health is declining. Blood tests:  Liver function tests (LFTs), tests for viral hepatitis, blood chemistry tests (which measure the levels of various substances in the blood), complete blood count, and kidney function tests may help diagnose liver cancer. In addition, the CA 19-9 test checks for this particular marker associated with bile duct cancers in the blood and assists in predicting liver cancer prognosis. Imaging tests:  The imaging tests listed above, as well as magnetic resonance imaging (MRI) and angiography, which visualize the arteries that provide blood to a liver tumor, may also be used. Another test, positron emission tomography (PET), is a nuclear medicine imaging method in which a small amount of radioactive sugar is injected into the body, highlighting abnormalities such as tumors. This scan can help detect bile duct cancer and is often done concurrently with a CT scan for a more comprehensive evaluation. Endoscopic procedures:  Diagnosing cholangiocarcinoma in the bile ducts outside the liver typically involves specialized X-ray methods. Typically, upper endoscopy passes an endoscope fitted with a camera through the patient’s mouth into the esophagus so that images can be seen on a monitor during the procedure. In the case of endoscopic retrograde cholangiopancreatography (ERCP), an upper endoscopy is performed to inject dye directly into the bile ducts while taking external X-rays to illuminate the course of the dye. Cholangioscopy involves using a specialized endoscope called a cholangioscope to see and biopsy tumors inside the bile duct; it’s often performed during an ERCP procedure. Percutaneous transhepatic cholangiography involves inserting a needle through the skin into a liver bile duct and injecting contrast material to visualize the biliary tree with X-rays. Liver biopsy:  If AFP levels are notably high and a tumor is visible on imaging scans, a diagnosis of liver cancer can be made. However, if the tests listed above are inconclusive, a liver biopsy may be recommended since it provides a definitive diagnosis. During a biopsy, liver tissue is extracted for analysis in a pathology lab to confirm cancerous tissue. What Are the Complications of Liver Cancer? The complications of liver cancer include the following: Hepatic encephalopathy  is a reversible condition marked by a range of neuropsychiatric issues caused by neurotoxic substances building up in the bloodstream and brain. Common symptoms include confusion, personality changes, disorientation, and reduced consciousness levels. Portal vein thrombosis  refers to the constriction or obstruction of the portal vein due to a blood clot. Variceal bleeding  occurs in the large esophageal veins. Obstructive jaundice  occurs when the bile duct or pancreatic duct becomes narrowed or blocked, hindering the usual flow of bile from the liver to the intestines. Pyogenic liver abscess  refers to a collection of pus enclosed within the liver. Intraperitoneal bleeding  is internal bleeding in the abdominal cavity, the area between organs and the inner lining of the abdominal wall. Metastasis to other organs and tissues. Portal hypertension refers to increased pressure within the portal venous system, which includes the portal vein leading to the liver. Infection of the biliary tree (i.e., cholangitis)  is a complication of cholangiocarcinoma and subsequent duct obstruction. Anemia. ***The following are the “Standard Treatments” given to people. Of course there are very bad side effects, whereas the Natural Products do not produce these side effects and I believe that more research is needed. It is interesting to note that An anti-parasitic drug, when combined with a standard treatment halted all tumor growth in tumors that had still grown with the standard treatment drug. This shows that Natural products can be used to help stop highly advanced tumors from progressing further and then help to start remission in Liver cancer. In other cancers, as shown in my 588 page book, can be stopped, as mine was and which made me a cancer survivor in 3 months! *** What Are the Treatments for Liver Cancer? The only confirmed curative approach in liver cancer is surgery, either resection or transplant. However, 70% of patients are not eligible for surgery. Surgery is the preferred treatment for liver cancer in patients without cirrhosis and metastasis. Depending on the patient’s health condition, the following treatment options may be available: 1. Surgery Liver resection:  Liver resection, also known as partial hepatectomy, removes the tumor along with a surgical margin of healthy tissue. This procedure is considered if the patient has no portal hypertension, normal bilirubin levels, and enough remaining healthy liver tissue post-surgery. Liver resection offers several surgical options, including resecting an entire lobe, multiple lobes (i.e., extended lobectomy), or part of a lobe (i.e., segmental resection). After the removal of cancerous tissue, a healthy liver can regrow to its normal size in about six months, but cirrhosis limits its regeneration capacity. Liver transplant:  If the patient cannot receive a liver resection, a liver transplant may be considered. A liver transplant can be whole or partial (e.g., a split-liver transplant). 2. Ablation Therapy Ablation therapy uses extreme heat or cold to eliminate abnormal tissue growth. Radiofrequency ablation (RFA)  uses electrical currents to generate heat to eliminate cancerous cells. At temperatures above 194 degrees Fahrenheit, the tumor starts to disintegrate. Percutaneous ethanol injection (PEI)  involves injecting concentrated ethanol alcohol directly into a liver tumor using a needle. This method is often used for tumors located near major blood vessels in the liver. Microwave ablation (MWA)  uses electromagnetic waves to generate heat to eradicate cancer cells. Neither RFA nor MWA can be used if the tumors are near major blood vessels. 3. Radiation Therapy External radiation therapy might be suggested if targeted therapy or immunotherapy isn’t feasible due to the patient’s health condition. The following are types of radiation therapy: Conformal radiation therapy  uses computer technology to create a three-dimensional image of the tumor, thus customizing radiation beams to match its shape precisely. This targeted approach delivers a high radiation dose to the tumor while minimizing harm to surrounding healthy tissues. Proton beam radiation therapy  uses high-energy protons to target and eliminate tumor cells. It is known for its precision in sparing surrounding healthy tissue from radiation exposure, and it’s especially useful if the tumor is located near critical structures or in sensitive areas. Stereotactic body radiation therapy (SBRT) administers highly concentrated beams of radiation directly to liver tumors. It is also considered the most effective radiation therapy for liver cancer. 4. Embolization Embolization is a therapy that obstructs or reduces blood flow (and oxygen) to tissues or organs to eliminate cancer cells. The following are types of embolization that may be used in liver cancer: Transarterial chemoembolization (TACE):  Chemoembolization combines blocking the tumor’s blood supply with delivering chemotherapy drugs to the cancer. TACE is a form of chemoembolization that targets branches of the hepatic artery to treat liver cancer. It is the usual treatment for those with healthy liver function, overall good health, and no major issues such as portal hypertension or portal vein thrombosis. It is also the most frequently performed procedure to address inoperable liver tumors or for liver cancer patients awaiting a transplant. Transarterial radioembolization (TARE)  is a form of embolization therapy that administers radioactive microspheres into specific tumor arteries, where they become caught and continue to irradiate the tumor. 5. Immunotherapy The immune system usually prevents itself from attacking healthy cells by using proteins called checkpoints, which cancer cells use to hide from the immune system’s attacks. Immunotherapy boosts the immune system to combat cancer with immune checkpoint inhibitors, monoclonal antibodies that block checkpoints, thus allowing the immune system to recognize and attack liver cancer cells. 6. Other Cryotherapy:  Also known as cryosurgery, cryotherapy involves freezing and destroying cancer cells using a specialized instrument. Chemotherapy:  Although chemotherapy is not very effective in treating HCC, it can be used to treat cholangiocarcinoma, and it’s also available for other types of liver cancer. Endoscopic retrograde cholangiopancreatography (ERCP):  ERCP can be used to manage bile duct obstruction in cholangiocarcinoma. It involves using an endoscope equipped with a camera and surgical tools to unblock bile ducts and place a stent. This stent helps open up the duct, allowing bile to drain into the intestine, improving the patient’s quality of life and alleviating symptoms such as jaundice. Palliative care:  Palliative care is specialized medical care aimed at relieving suffering and enhancing the quality of life for individuals with life-limiting illnesses that cannot be cured. It focuses on managing pain and symptoms, providing support to patients and their families, and ensuring dignity and comfort throughout the illness. How Does Mindset Affect Liver Cancer? Although there is no scientifically validated evidence from studies demonstrating that an individual can influence the progression of their cancer solely through mindset or mental control, mindset can influence liver cancer outcomes in several ways, such as: Providing psychological resilience:  The psychological burden is high in liver cancer patients, and many experience depression and anxiety. Psychological interventions and improved emotional resilience can help patients cope better with the stress and challenges of liver cancer diagnosis and treatment. Improved adherence to treatment:  A proactive and resilient mindset can lead to better adherence to treatment plans, including medication schedules, follow-up appointments, and lifestyle changes. Higher quality of life:  Improved mood can contribute to a higher quality of life during cancer treatment by elevating overall health and energy levels and even reducing pain. This is because mindsets can impact endogenous opioid and neuroimmune pathways, thus directly influencing physiology and affecting measurable health indicators. Offering coping mechanisms:  A positive mindset often leads to the adoption of effective coping strategies, such as seeking social support and maintaining a healthy lifestyle. Supporting the immune system:  Research suggests that positive attitudes and optimism may benefit the immune system, thus potentially supporting the body’s natural defenses against cancer. What Are the Natural Approaches to Liver Cancer? While aforementioned liver cancer treatments all face limitations such as cancer recurrence, potential ineffectiveness, and adverse reactions, some natural approaches have shown promise in improving patients’ symptoms and survival rates. However, please consult your health care provider before using any of them. Certain plants contain unique bioactive compounds that can disrupt the pathways leading to the development of HCC associated with the risk factors, potentially delaying or preventing HCC. 1. Medicinal Herbs and Herbal Medicines Milk thistle (Silybum marianum):  Milk thistle, also known as silymarin , has been used as a remedy for liver, kidney, and gallbladder issues for two millennia. Research indicates that compounds in milk thistle may help protect the liver. Among them, a flavonoid called dihydroquercetin can decrease fat accumulation in the liver, especially in individuals who consume alcohol, thus helping prevent fatty liver. Silymarin can protect the liver from toxins. In a pooled analysis of studies involving cirrhosis patients, milk thistle treatment was linked to a notable decrease in liver-related mortality. However, study results have been mixed regarding whether milk thistle improves liver function tests. In addition, individuals allergic to ragweed may also have an allergy to milk thistle. Wolfberry (Lycii fructus):  Wolfberry, also known as goji berry, is a fruit from the Lycium barbarum plant and is often used in traditional Chinese medicine (TCM). The most important component of wolfberry is Lycium polysaccharide (LPP), which has various health benefits such as regulating the immune system, acting as an antioxidant, protecting nerve cells, controlling blood sugar levels, and anti-cancer effects. One 2008 study discovered that drinking juice containing polysaccharides from wolfberries can increase antioxidant biomarkers in humans. LPP was also found in a 2006 study involving both rat and human HCC cell lines to hinder the growth of liver tumor cells and prompt their death, suggesting its potential use as an anti-cancer agent. Zingiberaceae (ginger):  In one 2010 study, a daily dose of 50 milligrams per kilogram of ginger extract effectively treated experimental cancer in rats by decreasing growth factors and the levels of alpha-fetoprotein, a liver tumor marker, indicating that ginger extract might protect against early stages of liver cancer in such rat models. Lesser galangal (Alpinia officinarum) is a member of the ginger family with antioxidant, anti‐inflammatory, antimicrobial, and cytotoxic properties. In one 2012 study, its extract and components demonstrated anti-cancer properties against lab-cultured HCC cancer cells. Some researchers have suggested that Alpinia officinarum rhizome extract might be used as a chemopreventive agent against HCC in rats. Huaier granules:  Huaier granules are commonly used in TCM for liver cancer treatment. They contain Trametes robiniophila Murr, a medicinal fungus rich in organic compounds and minerals with polysaccharide protein as its active component. Research shows that Huaier granules target various factors and pathways in liver cancer. They inhibit growth and induce death in certain cancer cells. In addition, they interfere with signaling pathways related to tumor angiogenesis (new blood vessel formation). Fufang Banmao capsules (FFBMs):  Fufang Banmao capsules are a highly recognized cancer drug composed of 11 traditional Chinese medicines. Their main ingredient, Banmao, contains cantharidin, which has anti-cancer properties. In one 2011 study, FFBMs were given to HCC patients either before they received TACE treatment or one week or one month after the treatment. This combined treatment significantly enhanced the immune functions of the patients with HCC. 2. Diet Broccoli sprouts:  Broccoli sprouts are a rich source of health-promoting plant-based bioactive compounds, including polyphenols, minerals, and vitamins A, C, K, and B6, essential for overall health. Sulforaphane, a nutrient found in cruciferous vegetables such as broccoli, has been shown to have anti-cancer properties by inducing cell cycle arrest and cell death in human cancer cell cultures. One study found that broccoli sprouts significantly assisted in the suppression of liver HeP-G2, an HCC cell culture . *** I grow sprouts for use in Sandwiches, Salads and just to munch on. It is in my book and in much greater detail than here!”*** Black currants:  Black currants are packed with plant-based nutrients, antioxidants, vitamins, healthy fats, and minerals, including a type of rare and healthy omega-6 fat. In a 2011 rat model, black currant skin extract reduced the occurrence, number, size, and spread of early liver cancer tumors in rats in a dose-dependent way. Asparagus:  Asparagus polysaccharide is used in clinical settings to treat different types of cancers such as breast cancer, leukemia, and lung cancer. One 2014 laboratory study found that asparagus polysaccharide can slow the growth of specific liver cancer cells, such as HeP-G2 and HeP-3B, without harming healthy liver cells, such as 7702 cells. Green tea (Camellia sinensis):  Green tea has been used to prevent liver diseases in Asia for a long time. The main polyphenol in green tea, epigallocatechin-3-gallate (EGCG), was tested on mice with liver damage and showed promising effects in reducing injury, inflammation, and oxidative stress in the liver. Tea polyphenols may help prevent and fight liver cancer by halting cancer cell growth, promoting cancer cell death, and reducing inflammation and oxidative stress in the liver. At present, moderate doses seem helpful, while excessive doses with supplement extracts showed evidence of toxicity to healthy cells. Coffee:  Coffee consumption has been linked to protective factors against HCC. According to a 2019 systematic review of four studies, coffee has a weak to strong inverse association with liver cancer. The researchers concluded that the Japanese population was likely to experience a decrease in the risk of primary liver cancer due to coffee consumption. 3. Supplements Berberine:  Berberine, an alkaloid from Coptidis rhizoma, has been shown to have significant antibacterial, anti-inflammatory, antioxidant, anti-apoptotic, and anti-autophagic properties. Reports indicate its potential in treating cancer and inflammation. In one 2010 study, berberine exhibited anti-cancer effects on human HCC cell cultures by promoting cancer cell death and suppressing tumor cell proliferation. ***I use Berberine as part of my protocol and it is in my book in greater detai*** Resveratrol:  Resveratrol is a natural compound in red grapes known for its potent antioxidant and anti-inflammatory abilities, making it highly valued in herbal medicine. Cancer cells change how they obtain energy, favoring a process called aerobic glycolysis, which helps them grow and survive. One 2015 study of four different HCC cell lines discovered that resveratrol encouraged liver cancer cell death and reduced the activity of a protein called hexokinase 2 (HK2), linked to aerobic glycolysis. Resveratrol also worked well with conventional treatments such as sorafenib to slow cancer cell culture growth. The study’s researchers concluded that blocking HK2 with resveratrol could be a promising way to treat liver cancer and stop its metastasis. 4. Alternative Medicine and Mind-Body Practices Acupuncture and moxibustion:  Pain relief is crucial for liver cancer treatment. Acupuncture therapy is a popular pain management method used in liver cancer patients, especially in China. It can also help relieve drug-induced vomiting and other gastrointestinal reactions during liver cancer treatment, along with moxibustion. Meditation and yoga:  Meditation and yoga can be used as relaxation methods to reduce stress in liver patients, and meditation can also relieve pain for some patients. How Can I Prevent Liver Cancer? Avoiding known risk factors can prevent many cases of liver cancer. Here are steps you can take to minimize your risk: Limit alcohol consumption. Avoid or quit smoking. Consider getting vaccinated against hepatitis B. Practice safe sex and avoid having multiple sexual partners to reduce the risk of hepatitis B and C infection. Avoid sharing needles or using illicit drugs. Treat hepatitis B and C infection, cirrhosis, and other medical conditions that may lead to liver cancer. Maintain a healthy weight and exercise regularly. Eat a balanced diet with plenty of fruits, vegetables, and whole foods. Avoid exposure to aflatoxins. Follow safety guidelines when handling chemicals or toxins that may affect the liver. Get regular checkups and screenings for liver health, especially if you belong to at-risk groups.

Originally on Urology times May 5, 2014 PSA TEst I recently read a very disturbing book that I wanted to share with everyone, as it presented a point of view that I, as a urologist, do not commonly encounter. “The Great Prostate Hoax: How Big Medicine Hijacked the PSA Test and Caused a Public Health Disaster,” by Richard Ablin and Ronald Piana (Palgrave Macmillan) ( cancer prostate icd 10) was only recently published, but a quick Google search shows just how much publicity it is receiving. Note that this blog is not a review of the book. For that I recommend reading either the review by The Economist (“Prostate cancer: Help or harm,” March 8, 2014) or the one by The New York Post (“Why the prostate cancer test is useless,” March 1, 2014). The first is a balanced review while the second is less balanced but informative in its own right. The book was brought to my attention by a patient sent to me for evaluation of an elevated PSA. He seemed an ideal patient to have his PSA checked: He had a family history of prostate cancer, was in his mid-60s, and was very healthy. His primary care doctor had been checking PSAs yearly and when the value jumped from about 3.5 to over 5.0 ng/mL (even after rechecking a month later), he was sent to me. During our conversation regarding what to do next (I highly recommend Dr. Hollingsworth’s excellent Urology Times article on talking about PSA to patients), he asked me about this book. While not buying into the book’s conspiracy theories, he was very alarmed at the limitations of the test that the book highlights. “The Great Prostate Hoax” begins with a historical perspective on the discovery of PSA and its acceptance by the FDA and the urology community, first in 1986 to monitor those with prostate cancer and later in 1994 to screen for the disease. This passage summarizes the remainder of the book: “But in a large sense, the situation dramatized by John [a patient described earlier as having been harmed by PSA screening] illustrates the grim reality of the health care system itself: encouraged by perverse incentives, many of the tests and procedures that doctors do are unnecessary, and quite a few are downright harmful.” The Great Prostate Hoax: How Big Medicine Hijacked the PSA Test and Caused a Public Health Disaster" by Richard J. Ablin and Ronald Piana Middle-aged men know the story: the PSA (prostate-specific antigen) test is an essential early-warning system for cancer. Elevated PSA levels mean cancer, which in turn means you should probably make the gutsy but necessary decision to prolong your life by having your prostate removed. Except this story is rubbish. Says who? Says the pathologist who first observed the PSA, back in 1970. Despite losing his own father, agonizingly, to prostate cancer at age 67, Richard J. Ablin (who is in his 70s) hasn’t had a PSA test done on himself and doesn’t intend to. There is, he says, no reason to do so on a healthy man, he explains in his book “The Great Prostate Hoax.” Because PSA, contrary to what you’ve been told, doesn’t work as a cancer indicator. That’s why a New England Journal of Medicine joint study of results from the US and Europe concluded, “PSA-based screening results in small or no reduction in prostate cancer-specific mortality.” Two years later the US Preventive Services Task Force declared that healthy men should not have a routine PSA test. Look at it this way: If you had a PSA test in 2009, and it led to a biopsy, a cancer diagnosis and treatment for that cancer, there is, according to Dr. Peter Bach, a health-care policy specialist at Sloan-Kettering Cancer Center, a 1 in 50 chance that by 2019 or later, you will have been saved from dying of prostate cancer. But there is a 49 in 50 chance that you will have been treated unnecessarily. Another approach, from cognitive psychologist Hal Arkes: Picture two auditoriums with 1,000 men in each. Auditorium One is filled with men who had PSA tests. In Auditorium Two, no one had a PSA test. Eight men in each room will die of prostate cancer. The upside of a PSA test is small to nonexistent. But let’s not forget about the huge downside. A man who falsely believes he is about to die of prostate cancer and goes along with a surgeon’s recommendation that the gland be removed may pay a devastating price. Incontinence and impotence are bland sounding words but imagine your quality of life if you were forced to wear a diaper forever and could never have sex again. A radical prostatectomy robs a man of much of what made him himself. And these complications are exceedingly common: The prostate is located amid a tightly strung nest of important nerves that is difficult to keep intact during surgery. Ablin’s book is a gripping disaster tale about how hype, profit-chasing, hysteria, and intransigence to reality reinforced one another in producing a horrendous mass medical error. When the protein called PSA was first discovered (T. Ming Chu of the Roswell Park Cancer Institute was also involved), with higher quantities of it possibly linked to cancer, the medical community had hopes that a PSA test might turn out to be the male equivalent of a pap smear, which is a highly effective means of detecting pre-cancerous cells in the cervix. But the PSA protein is present in every prostate, and though a reading above four (nanograms per millilitre) is often called a warning sign, you could have a reading of 0.5 and have cancer, or a reading of eleven and be cancer-free. Even if the test could reliably inform you whether you have cancer, it’d still be more or less useless. Prostate cancer is both extremely common (by the time a man is in his 40s, he already has a 40% chance of having prostate cancer, and the odds increase from there) and extremely likely to be harmless. Think of prostate cancer as existing in two entirely different forms. It can be either a rabbit eager to burst out of its box (and into other parts of the body) or a turtle that just sits there, barely moving at all. You should worry about the rabbit, not the turtle. The PSA test won’t tell you which kind you have. Yet a huge industry swung into action behind the PSA. One expert cited by Ablin says perhaps half of the urologists in the United States would go bankrupt without the gold rush of prostate-removal surgery that followed the PSA discovery. Now that the worth of the PSA test has been questioned, the industry is looking for a follow-up version, but Ablin is wary of whatever replacement is found. *“When a 50-year-old man went for his yearly physical,” explains Ablin, “he routinely had a PSA test, quite often without his knowledge. The level of his PSA could propel him into the prostate cancer industry . . . the prostate gland is at the epicenter of a worldwide trillion-dollar industry and the PSA test as its kingpin. Think of PSA as oil. If the test were made irrelevant, an industry would crumble. *“You don’t have to be a conspiracy theorist to grasp what the stakeholders will do to keep this Prostate Cancer Hoax industry booming.” ( cancer prostate icd 10) ***** The authors paint a picture of doctors, motivated by greed and malevolence, diagnosing patients with prostate cancer simply so they can be treated. Clearly, Ablin and Piana have never seen a man expire from metastatic prostate cancer. I marked the last paragraph because the medical system is motivated by greed, however, it is not motivated by doctors as much as it is by the big pharmaceutical companies, the researchers who have no morals and the lobbyists who see only money. We must always remember that we, as people searching for alternatives….they do NOT work in our best interests! The natural cures that I will present, in the next chapters, will highlight the cheap alternative drugs that are widely available, that work better most times than the Chemotherapeutics and Radiotherapy they push, and are far cheaper than the ‘Wonder Drugs” they push on us. The problem is that these alternatives cannot be patented so there is no money to be made, and they then quash the idea that we can heal ourselves, they direct the research, and they publish only research that fits their agenda of making $$Billions off our illnesses. I have decided to not play their game, and I am in the process of healing myself and ensuring that my cancer will not come back. It is a conscious choice that I made after much research, thousands of hours in fact, followed by thousands of hours in putting this book together. I wanted a quality of life that the doctors, specialists, and pharmaceutical companies could not guarantee me. Share

Glaucoma is a group of eye diseases that can lead to vision loss or blindness by damaging the optic nerve at the back of the eye. This damage typically occurs due to increased pressure caused by fluid buildup in the front part of the eye, harming the optic nerve over time. Glaucoma ranks as the second most common cause of blindness globally (next to cataracts), affecting over 3 million Americans. What Are the Types of Glaucoma? There are two main categories of glaucoma: primary and secondary. Primary refers to cases where the exact cause of the condition is unknown. When other medical conditions cause glaucoma, it’s called secondary glaucoma. Primary Primary open-angle: Open-angle glaucoma is the most common type in the United States, comprising 90 percent of all glaucoma cases. It is characterized by damage to the optic nerve, a wide anterior chamber angle  (the space between the cornea and the iris surface), and increased intraocular pressure (IOP; eye pressure) of over 21 millimeters of mercury (mmHg). This type of glaucoma is a significant cause of blindness, particularly among African Americans, where it accounts for nearly 20 percent of all cases. Normal-tension:  Normal-tension glaucoma is a form of open-angle glaucoma that occurs in people with regular eye pressure (below 21 mmHg). In the United States, between one-third and one-half of people with glaucoma have this type. Angle-closure:  Also called narrow-angle or acute glaucoma, angle-closure glaucoma is a medical emergency. It accounts for approximately 10 percent of all glaucoma cases in the United States. The “angle” is where the iris and cornea meet  at the outer edge of the anterior chamber. Angle-closure glaucoma occurs when the outer edge of the iris obstructs fluid drainage from the front of the eye, leading to rapid fluid buildup and a sudden rise in pressure. Without prompt treatment, this type of glaucoma can result in severe vision loss or blindness within a few days. Chronic angle-closure glaucoma progresses gradually and may not exhibit symptoms other than vision loss. Primary congenital: Primary congenital glaucoma is a rare condition resulting from improper development of the aqueous drainage system before birth. It affects approximately 0.01 percent of babies born in the United States.    Secondary Other medical conditions, such as cataracts, tumors, diabetes, eye surgery complications, and the use of certain medications can also cause the following glaucomas: Neovascular:  Neovascular glaucoma occurs when excessive blood vessel growth obstructs the eye’s drainage area, typically due to underlying medical conditions such as diabetes or high blood pressure. Pigmentary:  Pigment dispersion syndrome occurs when pigment rubs off from the back of the iris, potentially increasing eye pressure and causing pigmentary glaucoma. Exfoliation:  Exfoliation glaucoma, also known as pseudoexfoliation glaucoma, is a form of secondary open-angle glaucoma occurring in individuals with exfoliation syndrome. This syndrome leads to the accumulation of cellular material on various parts of the eye, thus obstructing fluid drainage. Uveitic:  Uveitic glaucoma is a common complication of uveitis, which causes eye swelling and inflammation. Around 20 percent of people with uveitis develop uveitic glaucoma. Experts believe inflammation and scar tissue formation in the eye’s middle region may block fluid drainage, leading to increased eye pressure, uveitic glaucoma, and eventual vision loss. Secondary childhood: Secondary childhood glaucoma results from an eye developmental anomaly unrelated to the aqueous drainage system, a syndrome, or another eye condition. Some individuals may have increased eye pressure without visible damage. These patients are called “glaucoma suspects” as they have an increased risk of developing glaucoma later on. Even those with normal eye pressure may be considered glaucoma suspects if their optic nerve shows unusual characteristics. However, most glaucoma suspects do not experience symptoms, underscoring the importance of regular monitoring by an ophthalmologist. What Are the Symptoms and Early Signs of Glaucoma? Glaucoma often begins without noticeable signs, so 50 percent  of those affected are unaware of their condition. As it progresses, vision loss typically begins with peripheral vision, which may go unnoticed initially due to its slow development. Without intervention, glaucoma can lead to blindness. The specific symptoms also vary depending on the type of glaucoma, as indicated in the following: Primary open-angle :  This type is nicknamed “the silent thief of sight” as patients often experience no symptoms until vision damage becomes significant when blind spots start developing in the side vision. The symptoms include increased IOP and tunnel vision. Normal-tension : Patients typically don’t experience symptoms until it’s too late, which is the same for people with open-angle glaucoma (except open-angle exhibits elevated IOP). Patients may also experience bleeding in the nerve fiber layer of the optic disc. Angle-closure : Symptoms include severe eye pain, nausea, red eye, and blurred vision. If you suddenly experience these symptoms, seek medical attention immediately. Primary congenital :  Children diagnosed with congenital glaucoma often exhibit cloudiness in their eyes, light sensitivity, abnormally high tear production, and possibly larger-than-normal eye size. Neovascular : Symptoms include eye pain or redness and loss of vision. Pigmentary : Individuals with pigment dispersion syndrome or pigmentary glaucoma may experience halos (rainbow-colored rings around lights) or blurred vision following activities such as jogging or playing basketball. Exfoliation : While exfoliation glaucoma shares the same symptoms as primary open-angle, it can advance more rapidly and frequently results in increased eye pressure. Uveitic : Uveitic glaucoma can damage the optic nerve and induce a loss of visual field. Patients with it experience symptoms of both uveitis and glaucoma, including red eyes, pain, sensitivity to light, spots in vision, and blurred vision. What Causes Glaucoma? In glaucoma, retinal ganglion cells and nerve fibers in the optic nerve are gradually lost. This leads to a telling appearance of the optic nerve head and progressive vision decline. The pattern of peripheral vision loss is a key feature that sets glaucoma apart from other eye conditions. Researchers believe that glaucoma occurs when there’s too much aqueous humor , the fluid that nourishes the eye, leading to high pressure (IOP) inside the eyes. Usually, this fluid moves like water filling a sink. The faucet (the ciliary body) produces it, and drains (drainage canals) remove it from the eye to maintain a normal fluid level. As drainage canals become clogged, the fluid doesn’t drain properly, resulting in an imbalance. When pressure becomes abnormally high, it harms the optic nerve, leading to glaucoma. Low- or normal-tension glaucoma can occur when eye pressure is within the normal range but still too high for the optic nerve. Glaucoma in Eye Normally, aqueous humor drains through drainage canals in the eye. With glaucoma, the drainage canals become blocked, resulting in elevated pressure that affects the optic nerve and impairs vision. Illustration by The Epoch Times, Shutterstock Certain factors put people at higher risk, including: Age:  African Americans 40 years old and above and people of all ethnicities who are 60 years old and above (particularly Hispanics) are at a higher risk of developing glaucoma. Males in their 30s are at the highest risk for pigmentary glaucoma, with the ratio of males to females ranging from 2:1 to 5:1, depending on the study. Ethnicity:  African Americans have a significantly higher risk of developing glaucoma—about six to eight times—than whites. Normal-tension glaucoma seems to affect those of Japanese ancestry more. Higher risks for angle-closure glaucoma are seen in Asian and Inuit populations, with lower risks in European and African populations. High intraocular pressure: Intraocular pressure (IOP) is the leading risk factor for glaucoma. Family history of glaucoma:  Researchers have identified specific genes that may affect people’s risk of glaucoma. Identical twins with the same genes are more likely to have glaucoma than fraternal twins, hinting that genetics play a role. Eye structure:  Thin corneas, thinning of the optic nerve, concave iris, posterior iris insertion, and flat corneas are risk factors for pigmentary glaucoma. Cardiovascular issues,  like heart conditions and abnormal blood pressure. Eye-related conditions, such as reduced optic nerve tissue, retinal detachment, eye tumors, and eye inflammation, can make one more prone to glaucoma. Retinal ischemia and systemic vascular conditions put one at risk of neovascular glaucoma. Farsightedness or nearsightedness. Eye injury. High blood pressure increases your risk of open-angle glaucoma. Diabetes  is a risk factor for open-angle glaucoma. Low blood pressure  can make one more likely to develop normal-tension glaucoma. Low birth weight  can increase the risk of primary congenital glaucoma. Maternal history of seizure increases one’s risk of inheriting primary congenital glaucoma. Medications:  In addition to people with uveitis, people taking steroids, which can treat uveitis, can develop uveitic glaucoma. Also, a new study found a link between attention-deficit/hyperactivity disorder (ADHD) medications and angle-closure and open-angle glaucoma’s. Lifestyle:  Some lifestyle activities that can raise IOP include playing high-wind instruments, drinking coffee, practicing specific yoga poses, wearing tight neckties, and lifting heavy weights. One 2022 study found a link between snoring, daytime sleepiness, insomnia, and both short and long sleep durations and the risk of developing glaucoma. Stress is also a factor, as chronic stress can affect various organs, and the eyes are no exception. Glaucoma patients often link severe emotional stress to their vision problems; this connection is supported by research showing that stress can increase eye pressure and cause vascular issues in the eye and brain, potentially leading to reduced oxygen and glucose levels (which can hurt eye health). While nerve cells may not die outright, they may become inactive and negatively affect vision. Heavy metal toxicity: The connection between glaucoma and certain neurodegenerative disorders suggests that heavy metal (e.g., cobalt, lead, mercury) toxicity could contribute to glaucoma development. Ionizing radiation: Ionizing radiation can potentially contribute to the development of glaucoma, particularly in cases of high doses of prolonged exposure. How Is Glaucoma Diagnosed? Primary care physicians, typically optometrists or ophthalmologists, can screen for glaucoma using visual field tests such as frequency-doubling technology (FDT), perimetry, and ophthalmoscopic evaluation of the optic nerve. When glaucoma is suspected, your doctor will conduct a comprehensive eye examination to confirm the diagnosis. Such an eye exam consists of: Tonometry : Tonometry uses a tonometer to measure the pressure inside the eye. During the test, your doctor applies a small amount of anesthetic and dye to the eye’s front, then shines a light into the eye and gently touches its surface with the tonometer. Some optometrists use a puff-of-air instrument that doesn’t touch the eye. Normal eye pressure ranges from 11 to 21 mmHg, with readings above 21 mmHg considered high. Serial tonometry involves taking multiple pressure measurements over a period of time and observing how eye pressure changes throughout the day. Optic nerve evaluation :  To check for changes in the optic nerve, your doctor uses an ophthalmoscope, which consists of a light source and magnifying lenses, to see inside the eye. Sometimes, other tools are used, such as optical coherence tomography, a scan that uses special light rays to create an image of the back of your eye. This optic nerve assessment can show if glaucoma has caused any damage. Visual field testing :  A visual field test, also known as perimetry or a peripheral vision test, assesses for any areas of vision loss. During the test, you’ll see a series of light spots, with some appearing at the edges of your vision, to test your peripheral vision, which is typically affected first by glaucoma. If you can’t see these spots in your peripheral vision, it could indicate vision damage from glaucoma. Gonioscopy : Gonioscopy uses a special lens to inspect the eye’s drainage canals to determine whether the glaucoma is open-angle or closed-angle. Corneal thickness measurement :  Your doctors will also assess corneal thickness, as thinner corneas may increase the risk of glaucoma. Corneal thickness can also affect the accuracy of eye pressure readings. Thinner corneas might lead to underestimated readings, while thicker corneas may lead to higher readings. Visual acuity test :  A visual acuity test, often using an eye chart, assesses your ability to see clearly at different distances. Eye muscle function test :  An eye muscle function test assesses the muscles around your eyes for any issues. During the test, your doctor will move an object and ask you to track it with your eyes. Slit-lamp exam :  The slit-lamp examination assesses the front structures of the eye using a specialized microscope with a bright light. It helps doctors evaluate various eye parts, such as the eyelids, cornea, conjunctiva, sclera, and iris, in detail. Regular eye exams are crucial as they enable early detection by your ophthalmologist, helping prevent vision loss. Individuals over 40 and those with risk factors for glaucoma should undergo a comprehensive eye exam every one to two years. What Are the Complications of Glaucoma? Glaucoma complications may include: Blindness:  This is usually painless. Painful blind eye:  Having open-angle glaucoma increases the risk of a condition called central retinal venous occlusion, which may lead to a painful blind eye. Visual field loss. No light-perception vision: No light perception  refers to the most severe type of vision loss, with a complete inability to detect light. This condition usually indicates an advanced or end-stage disease, as all sensory input from the eye is lost.    What Are the Treatments for Glaucoma? Currently, there is no cure to reverse vision loss caused by glaucoma. However, treatment can help prevent additional damage and further vision loss based on the type and severity of the condition. In some cases, eye drops may not effectively control eye pressure. Your doctor might recommend an oral medication—often a carbonic anhydrase inhibitor—to help lower eye pressure. The goal of treatment is to lower your eye pressure by either enhancing the drainage of aqueous humor from the eye or decreasing the production of the fluid using the following methods: 1. Eye Drops Eye drops are commonly used as an early treatment for glaucoma; it’s crucial to use them regularly to manage eye pressure effectively. Usually, eye drops are initially applied to one eye (known as a one-eye trial). If there’s improvement in the treated eye within one to four weeks, then both eyes will receive treatment. Before using an eye drop, inform your doctor about any other medications or supplements you are taking, as the eye drops may interact with these substances. The eye drops that help in draining fluid from the eye to reduce eye pressure include: Prostaglandins:  Examples are latanoprost, travoprost, tafluprost, and bimatoprost. Possible side effects may include slight eye irritation, changes in eye color, and elongated eyelashes. Rho kinase inhibitors: Rho kinase inhibitors improve fluid drainage in the eye through a pathway called the trabecular meshwork. Examples include netarsudil and ripasudil. Possible side effects include redness and discomfort in the eye. Nitric oxides:  Nitric oxides help lower IOP by decreasing the production of aqueous humor, making it easier for fluid to flow out through a central drainage canal, and relaxing the trabecular meshwork cells. These functions improve the drainage of fluid from the eye. Examples include latanoprostene bunod and NCX 470. Miotic or cholinergic agents: Due to side effects such as head and eye pain and potential vision changes, as well as the need for their frequent use of up to four times daily, this type of medication is not commonly used anymore. One example is pilocarpine. Other categories of eye drops function by reducing the production of aqueous humor. They include: Alpha-adrenergic agonists: Typically, these medications are administered two or three times daily. Their possible side effects include irregular heart rate, increased blood pressure, red or itchy eyes, dry mouth, and fatigue. Examples are apraclonidine and brimonidine, with brimonidine being the anti-glaucoma alpha agonist of choice. Beta blockers: Potential side effects include decreased heart rate, reduced blood pressure, breathing difficulties, and fatigue. Examples include betaxolol and timolol. Carbonic anhydrase inhibitors: These medications are usually taken two or three times daily. Possible side effects may include a metallic taste, increased frequency of urination, and tingling sensations in the fingers and toes. Examples include dorzolamide and brinzolamide. 2. Laser Treatment When both eye drops and oral medications don’t suffice, laser treatment may be recommended, as it’s effective for certain types of glaucoma. It involves using a focused beam of high-energy light on your eye to reduce or prevent fluid buildup and lower the eye pressure. Different types of laser treatments include the following: Laser trabeculoplasty  involves using a laser to widen the drainage tubes in your eye, thus improving fluid drainage and lowering internal pressure. Cyclodiode laser treatment uses a laser to remove eye tissue that produces fluid to reduce eye pressure. Laser iridotomy is designed for individuals with angle-closure glaucoma. During this procedure, an ophthalmologist uses a laser to make a small hole in the iris to facilitate fluid flow to the drainage angle in the eye. You might notice flashes of bright green or red light during laser treatment. Most people experience minimal or no pain or discomfort throughout the procedure. After the treatment, you might experience swelling, soreness, occasional corneal scratching, and temporary pain. However, the pain typically diminishes rapidly as the cornea heals, and your doctor can provide eye drops for relief. Most people return to their everyday lives the day after the treatment. However, it may take four to six weeks to see if the treatment was successful. In addition, after a successful laser treatment, most people still need to take medications for the rest of their lives. 3. Surgery Many types of glaucoma surgery are available, including: Trabeculectomy:  This is the most common type of surgery used for glaucoma treatment. During the procedure, a surgeon makes a small flap in the sclera (the white part of the eye) to create a drainage path for fluid. This type of surgery, typically considered when other treatments have failed, may have complications such as vision loss, cataracts, infection, and droopy eyelids. Patients are often awake during this surgery, as only a local anesthetic is used, although general anesthetic is also available. Trabeculotomy:  Trabeculotomy is very similar to trabeculectomy, except it uses an electric current to cut the sclera. Viscocanalostomy:  Viscocanalostomy involves removing a portion of the sclera to facilitate easier fluid drainage from the eye. Glaucoma implant surgery:  A surgeon inserts a small tube (shunt) onto the eye’s sclera during this procedure. This shunt helps drain excess fluid. Minimally invasive glaucoma surgery (MIGS): MIGS is a newer approach for mild glaucoma with fewer risks and side effects than conventional surgeries. It reduces eye pressure to aid faster recovery. While showing promise for certain glaucoma types, MIGS is currently not considered universally superior to other treatments. Deep sclerectomy:  Deep sclerectomy widens the drainage channels in your eye, often achieved by inserting a small device into them. Cataract surgery:  Cataract surgery can often lower eye pressure in people with cataracts, making it a potential treatment for glaucoma in some cases. 4. Novel Treatment Methods in Development Researchers are developing several new treatment approaches for glaucoma, such as cell-based therapies for optic nerve regeneration. While promising, these approaches are in the early research stages and not yet ready for human clinical trials. Gene targeting to replace mutated genes responsible for genetic forms of glaucoma is also being explored. This approach is being studied in animal models but has not yet advanced to human clinical trials. How Does Mindset Affect Glaucoma? A positive mindset can play a role in managing glaucoma in several ways. Maintaining a positive mindset can reduce mental stress, a potential cause of glaucoma. It can also help lower eye pressure, a key factor in glaucoma management, and reduce vascular dysfunction. The findings of a 2021 study suggested that anxiety increases the risk of glaucoma progression and is also linked to IOP patterns and disk hemorrhage. A positive mindset can reduce anxiety by increasing resilience and strategic reframing, thus benefiting glaucoma management. A positive mindset can improve adherence to medication and treatment plans, potentially slowing glaucoma progression. Additionally, being proactive can encourage healthier lifestyle choices such as regular exercise, a balanced diet, and avoiding smoking, contributing to overall eye health and reducing glaucoma risk. What Are the Natural Approaches to Glaucoma? Several natural approaches to glaucoma exist. However, please consult your doctor before exploring any of them. 1. Medicinal Herbs According to a 2002 survey of 1,000 glaucoma patients, 5.4 percent used alternative treatments for their glaucoma, and 57.4 percent of those used herbal therapies. Some popular herbs for this condition include: Ginkgo (Ginkgo biloba):  A 2013 retrospective study assessed 42 patients with treated normal-tension glaucoma who were given 80 milligrams of ginkgo biloba extract twice daily. The extract slowed the progression of visual field damage in these patients. In a 2003 study, 27 patients with vision loss due to normal-tension glaucoma were given either ginkgo biloba extract or a placebo. The extract was taken orally, three times daily for four weeks, followed by an eight-week washout period, then four weeks of placebo. The researchers conducted visual field tests at different stages and discovered that the extract might help improve existing vision loss in some patients. Bilberry (Vaccinium myrtillus): Bilberry contains anthocyanin, a flavonoid that may protect nerve cells and help with glaucoma. It could improve blood flow to nerve cells, strengthen the optic nerve, make nerve cells more resistant to damage, and reduce eye inflammation. In one 2017 study, the retinal ganglion cells of mice given bilberry extract orally were protected from dying. The extract increased certain proteins related to cell protection, which may explain its ability to protect against eye injuries such as those in glaucoma. Another 2012 retrospective study involving 332 glaucoma patients found ginkgo and bilberry extracts beneficial for enhancing vision in certain people with normal-tension glaucoma. Chinese skullcap (Scutellaria baicalensis):  Chinese skullcap extract and its main active flavonoids, including baicalin, baicalein, and wogonin, have low toxicity and can protect nerves, fight oxidative stress, reduce inflammation, and even combat cancer. These flavonoids can protect against damage caused by reduced blood flow in the retina. One 2015 study discovered that baicalein treatment in animals lowered eye pressure by enhancing fluid drainage from the eye. Another 2016 study found that administering wogonin in a rat model with optic nerve crush decreased the loss of their retinal ganglion cells and prevented these cells’ apoptosis. Saffron (Crocus sativus): Crocin, crocetin, and safranal are the key components behind saffron’s beneficial health effects. These compounds can protect against DNA damage, act as antioxidants, fight cancer, reduce inflammation, prevent heart disease, control blood sugar and pressure levels, improve lipid profiles, and delay degenerative conditions. One 2019 study discovered that a type of saffron extract reduced inflammation and protected cells in the eye, particularly the retinal ganglion cells, in mice with high eye pressure. Erigeron breviscapus: Erigeron breviscapus is a flowering plant native to China that belongs to the Asteraceae family. A 2011 study showed that treating rabbits with chronic increased IOP with an Erigeron breviscapus extract for 60 days protected retinal nerve cells. Scutellarin, extracted from Erigeron breviscapus, possesses cardioprotective properties against conditions such as ischemia, heart attack, stroke, and diabetic complications. A 2021 study on mice with chronic IOP elevation found that oral scutellarin helped maintain the mice’s retinal structure and vision, suggesting that scutellarin could be a new treatment option for glaucoma. Qing Guang An Granule (QGAG): A 2020 study examined QGAG, a Chinese medicine used to treat glaucoma for over two decades, and identified 55 active compounds and 173 targets related to glaucoma treatment. Among them, 20 key targets were found to be involved in processes such as cell death, response to oxygen deficiency, and cell growth regulation. The researchers also discovered critical pathways suggesting that QGAG may offer the potential for further research and new drug development for glaucoma treatment. 2. Supplements Vitamin C:  Vitamin C, known to exist in high concentrations in the human eye, is believed to interact with oxygen in eye fluids. Since it can reduce oxidative damage in cells, vitamin C can potentially protect against retinal damage in glaucoma. A 1966 study found that intravenous glycerol-vitamin C (sodium salt) could lower pressure inside the eye. However, newer studies are needed to confirm vitamin C’s IOP-reducing function. Alpha-lipoic acid (ALA): Alpha-lipoic acid is an antioxidant derived from caprylic acid, a medium-chain fatty acid found in foods like coconut. It’s produced in the mitochondria and plays a role in breaking down nutrients. There’s ALA in red meat, beets, carrots, potatoes, spinach, and broccoli. In one 2013 study, researchers gave ALA to mice with glaucoma symptoms to see if it could stop the disease from deteriorating and to another group of mice before they developed glaucoma to see if it could prevent the disease. The results showed that both approaches increased eye cell protection, improved cell transport, and reduced oxidative stress, which is linked to glaucoma. Melatonin:  Melatonin is a hormone that our brains produce in the dark. Supplements can be used to treat jet lag, anxiety, and certain sleeping disorders. A 2006 review suggested that certain retinal ganglion cells play a role in the release of melatonin. Considering this connection, using drugs that affect melatonin could be a promising addition to the treatment of glaucoma, along with traditional methods that focus on managing eye pressure. 3. Other The following are other natural approaches that may help with glaucoma symptoms: Acupuncture:  One 2020 systematic review found that acupuncture might slightly reduce eye pressure. Another 2018 study showed that acupuncture targeting specific acupoints around the eyes can enhance blood flow in people with primary open-angle glaucoma. However, further research with better-designed trials is still needed. Changing sleeping position: The head-up position at 20 degrees is associated with lower nighttime eye pressure than lying flat (supine). Exercise:  Engaging in treadmill exercise and regular physical activity can lead to a temporary decrease in IOP. Achieving ideal BMI:  A 2020 study found that Korean women with low BMI had higher rates of glaucoma, possibly due to lower nutrient intake. Another study found that individuals with a BMI over 30 were more likely to develop primary open-angle glaucoma. Additionally, metabolically healthy obese people were at a lower risk than metabolically unhealthy non-obese people. Metabolic health is affected by things like diabetes, hypertension, and high cholesterol. Relaxation techniques: Meditation and other relaxation techniques may help lower stress and help optimize glaucoma treatment. How Can I Prevent Glaucoma? Glaucoma is not entirely preventable, as some cases are congenital and genetics have some role, but you can reduce your risk of developing it by following these measures: Eat more fruits and vegetables: One 2012 study found that consuming more fruits and vegetables (e.g., oranges, collard greens, and spinach) rich in vitamins A and C, along with carotenoids, might lower the risk of glaucoma in older African American women. A 2016 study linked the consumption of dietary nitrate and green leafy vegetables to a reduced risk of primary open-angle glaucoma. Stay physically active. Avoid head-down positions: Spending too much time upside down, like when using gravity tables, increases eye pressure, which raises glaucoma risk. Proactively manage stress. Stay current with annual comprehensive dilated eye exams:  If you are in a high-risk group or over 40, getting a complete yearly exam is recommended. Don’t smoke. Maintain oral health:  Some research suggests a link between gum disease and glaucoma. Wear protective eyewear when needed to avoid eye injury. Treat underlying medical conditions that may lead to glaucoma. Reevaluate the need for certain medications, like steroids, which raise your risk of glaucoma with prolonged use.

China was once renowned for its authenticity and morality. However, after the CCP took control in 1949, under its totalitarian rule, ethics became loose, and fears rose. Ever since the COVID-19 outbreak, the CCP has repeatedly delayed reporting and attempted to cover up the situation, hindering a coordinated global response. The regime has been doing the same with its persecution of people of faith. Regardless of the ultimate origin of the virus, the CCP’s totalitarian regime, lack of accountability, and opaque policies have led to the harm of millions of lives. They must be held accountable for their actions. Ultimately, the origins of COVID-19 remain unclear, although the argument for it being created in a lab is gaining traction. If it were created in a lab, this danger would align with the CCP’s modus operandi of covering up outbreaks and engaging in risky, gain-of-function research in Wuhan labs. At the very least, the Chinese government is complicit for trying to cover up the virus in the first place. The theory that the virus originated in a lab, however, also presents challenges. The chances of researchers having the skill and luck to create such a virus are very low. I think that the answer may be more universal—with both nature and science taking a role in its origin. COVID-19’s origin could also tap into a universal balance. Historically, plagues have arisen during times of spiritual persecution. The CCP is currently persecuting various ethnic and religious groups, including Christians and Falun Gong. The pandemic is a consequence of the CCP’s crimes against humanity, which they won’t acknowledge....yet the CCP Should Be Held Accountable and this needs to go before the world courts. International Court of Justice

The COVID-19 virus’s unprecedented features—pathogenicity and transmissibility—are beyond what any virologist or doctor has previously encountered. The original Wuhan COVID-19 virus could spread widely throughout the body, starting in the lungs and affecting various vital organs, including the brain, heart, blood vessels, liver, kidneys, and intestines. Other viruses, such as the SARS virus, can also affect multiple organs, though not as broadly or severely as COVID-19. Most SARS complications have been self-limiting or reversible, although serious illness can sometimes result. In contrast, lethal complications such as heart failure, acute cardiac injury, and pulmonary embolism have been more commonly reported in COVID-19 patients. The flu virus infects far fewer organs and is much less severe than the original Wuhan COVID-19 virus. The unprecedented virus-COVID-19 can attack almost every part of the body due to several key factors: ACE2 receptor binding: The virus has used its key—or spike protein—to bind to the angiotensin-converting enzyme 2 (ACE2) receptor, which is the gatekeeper of our cells, allowing the virus entrance. Inflammation and cytokine storm: Once inside, the spike protein triggers inflammation, which can cause an extreme immune response (cytokine storm) that can lead to multiple organ failure. Blood vessel damage: The spike protein can damage blood vessels, causing blood clots in vital organs that can lead to severe complications such as heart attack, stroke, and sudden death. Covid virus attacking body

The 2019 Military World Games—a kind of Olympics for soldiers—was held in Wuhan starting Oct. 18 and lasted nine days. Nearly 10,000 military athletes from more than 100 countries, including those from major European countries, participated. It is reported that athletes from Germany, Italy, France, and Sweden became ill after their trip to Wuhan. Notably, these countries were the hardest hit early in the pandemic. The Missing Pieces in Lab Origin and the potential answer for Covid-19 Put simply, the Chinese lab has been conducting risky studies. Additionally, the CCP appears to have been hiding the facts about when COVID-19 first started—as they have a record of doing with other outbreaks, such as the 2003 SARS outbreak. Therefore, many scientists have leaned toward the Wuhan lab leak hypothesis as the potential answer for Covid-19 virus origin. The reason a conclusion hasn’t been made is that there is no smoking gun-level evidence that WIV created the exact same virus as COVID-19, though they have similar features. One question that has been overlooked is whether people intending to do something can make it a success. Many people aim to conquer the world, yet few have successfully done so. Considering other possibilities doesn’t negate the Chinese regime’s unethical actions throughout the pandemic—such as hiding it from the world for months—but such consideration could potentially broaden our perspective and lead to other important insights. Though many scientists have leaned toward the Wuhan lab leak hypothesis, the lab-created coronaviruses were very different from the COVID-19 virus. Lab Leak Theory