Inclusion Body Myositis: Symptoms, Causes, Treatments, and Natural Approaches

Although rare, affecting roughly 25,000 Americans, inclusion body myositis is a debilitating disease often overlooked until its advanced stages.

Inclusion body myositis is an insidious disease that leads to muscle weakness and atrophy. Illustration by The Epoch Times, Shutterstock

Inclusion body myositis (IBM) is one of a group of muscle diseases called inflammatory myopathies. These conditions are marked by long-term muscle inflammation that deteriorates muscle over time, leading to weakness. The presence of inclusion bodies distinguishes this type of myositis from similar conditions, such as polymyositis. Inclusion bodies are clumps of proteins misfolded tightly together in a round shape, found in neurons and various tissue cells.

IBM is one of the most prevalent inflammatory muscle diseases affecting people over 50, with an estimated annual incidence ranging from one to nearly eight cases per 1 million Americans. One estimate suggests that around 25,000 individuals in the United States are affected by IBM.

What Are the Symptoms and Early Signs of IBM?

Each individual’s myositis has distinct features and treatments, but all cases share the common feature of chronic muscle inflammation. IBM typically starts with the slow progression of weakness in the skeletal muscles. This weakness progresses over months or years and impacts both proximal muscles (neck, shoulders, thighs) and distal muscles (hands, feet). The asymmetric and distal muscle involvement and insidious onset of the condition are two distinguishing features of IBM compared to other inflammatory myopathies.

Although it typically presents in one’s 50s, it can appear earlier. In one study, IBM patients’ symptoms appeared between the ages of 20 and 73, with an average age of 47 years.

Early signs and symptoms may include:

• Frequent tripping and falling: This can be due to buckling of the knees due to thigh weakness and may be the first sign of IBM.
• Weakness in the wrists and fingers: This may lead to challenges with pinching, buttoning, and holding onto objects.
• Struggling to rise from a seated position.
• Difficulty ascending stairs.
• Feeling fatigued after prolonged standing or walking.
• Dysphagia, or difficulty swallowing. At least 40 percent of IBM patients report this condition. It can also cause liquids to come out of the nose and lead to breathing in food or drink into the lungs. Weakness in throat muscles, known as dysphonia, can also make it difficult to speak.
• Muscle cramping and pain.

Other common signs and symptoms that may develop later include:

• Asymmetrical and distal muscle weakness: This condition sometimes affects only one side of the body, accompanied by an extremely gradual progression of IBM.
• Myalgia: Myalgia refers to pain and discomfort in the muscles and soft tissues of the body. This pain is typically dull and can affect one or multiple muscles.
• Muscle atrophy: Atrophy, the thinning or loss of muscle bulk, may occur most often in the forearm and quadriceps muscles of the legs.
• Difficulty lifting the arms.
• Weakness in the quadriceps, hands, forearms, and ankles.
• Unstable knees.
• Decreased walking ability.
• Impaired hand dexterity.
• Drop foot: A patient may have trouble lifting the front of their foot.

As a slowly progressing disease, IBM typically does not significantly affect life expectancy. Most people who have it experience a progressive decline in function over several years, eventually leading to disability. The rate of progression tends to be faster in people who were older at the onset of IBM. While most individuals can still walk, they may need a cane, wheelchair, or other assistive devices for longer distances. In some cases, more severe symptoms may require full-time wheelchair use within 10 to 15 years of symptom onset.

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What Causes IBM?

IBM appears to involve a complex interaction between inflammation, immune responses, abnormal protein processing, and muscle degeneration. During IBM’s development, some of the muscle fibers become damaged by invading immune cells, while muscle fibers show signs of degeneration without a clear cause. The exact mechanisms driving these processes and their interplay are still not fully understood, highlighting the complexity of the condition.

The following are several of the possible mechanisms involved in IBM:

• Inflammation: The inflammatory aspect involves immune cells—particularly cytotoxic CD8+ T-cells and macrophages, which normally eliminate faulty cells—becoming misdirected and invading healthy muscle fibers. These immune cells and CD4+ T-cells incite an inflammatory response within the muscles. This immune activation is likely driven by specific antigens (toxic or foreign substances), as suggested by the presence of numerous antigen-presenting cells (APCs) within muscle fibers. However, it remains unclear whether this is a primary inflammatory disorder or if the inflammation is secondary.
• Degeneration: On the degenerative side, abnormal processing of proteins associated with aging can lead to the deposition of toxic polymers (large, long-chain, organic molecules made up of repeating smaller units called monomers) in the muscles, causing damage. The presence of degenerative protein beta amyloid in the muscle fibers of IBM patients supports the idea of a degenerative pathway. This beta-amyloid protein has been shown to stimulate the production of interleukin-6 by human myoblasts (immature muscle cells), which can further aggravate the local immune response.
• Genetics: Genetic inclusion body myopathies can be inherited via dominant or recessive patterns. Dominant disorders need only one genetic flaw to manifest, while recessive require both parents to pass on the flaw in the same gene. The disease is not directly inherited in s-IBM patients, but an increased presence of the human leukocyte antigen (HLA) DR52 and DR3 genes suggests a potential autoimmune predisposition. Thus, while some individuals may have a genetic predisposition to IBM, the condition is generally not inherited.

In IBM, inflammatory cells invade muscle tissue, leading to the formation of vacuoles (bubbles of empty space) and clumps of proteins called inclusion bodies. These inclusion bodies and vacuoles degrade the muscle, resulting in weakness. Illustration by The Epoch Times, Getty Images

What Are the Types of IBM?

Inclusion bodies are present in two related but distinct conditions. While their symptoms and diagnosis may appear similar, they have different origins. They are:

• Sporadic inclusion body myositis (s-IBM): Most IBM cases are s-IBM, whose cause is unknown. It involves an autoimmune component, where the body attacks its own tissues. However, other factors may contribute, and the exact triggers remain unidentified. A subtype of s-IBM called familial inflammatory sIBM affects at least two siblings.
• Hereditary inclusion body myopathy (h-IBM): H-IBM comprises a diverse range of disorders inherited through either autosomal recessive or dominant patterns. H-IBM cases are rare and associated with genetic factors. Unlike myositis (hence the name “myopathy”), muscle inflammation is not typically a significant feature of h-IBM. Its symptoms often appear much earlier than those of s-IBM—sometimes in a person’s 20s. Thigh muscles are usually spared until the disease reaches advanced stages. In addition, the term “hereditary inclusion body myopathy” is becoming less used, as specific disorders are nowadays named based on their underlying genetic mutations. For instance, h-IBM type 2 is now called GNE myopathy due to its association with a mutation in the GNE gene.

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Who Is More Likely to Develop IBM?

The following factors may put a person more at risk of developing IBM:

• Age: IBM symptoms typically start appearing after the age of 50.
• Sex: IBM has a higher male-to-female ratio, estimated at around 3:1, in contrast to other autoimmune-related diseases.
• Genetics: Genetics, such as the HLA DR3 gene, can predispose some people to develop IBM.
• Certain conditions: Research has shown that individuals with a history of high blood pressure, high cholesterol levels, heart attacks, heart failure, pneumonia, anemia, or diabetes are at higher risk of developing IBM. Those infected with HIV may develop myositis, as can those with the human T-cell leukemia virus type 1 (HTLV-1 virus). In addition, some cases of myositis have been associated with Coxsackie B virus infection.
• Some medications: Certain medications may also trigger IBM. For instance, dasatinib, considered a safe drug for treating chronic myeloid leukemia, can lead to IBM in rare cases. Cholesterol-lowering statins such as atorvastatin, simvastatin, and rosuvastatin may induce autoimmune myopathy and cause IBM. Colchicine, used to prevent or treat gout, familial Mediterranean fever, cirrhosis, primary biliary cirrhosis, and pseudogout, has also been suspected in IBM cases. Interferons, used in treating viral infections, autoimmune diseases (e.g., multiple sclerosis), and certain cancers, may also induce s-IBM.

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How Is IBM Diagnosed?

Diagnosing IBM can be difficult due to symptoms not specific to the condition. Therefore, it’s important to consider a differential diagnosis. The conditions that share overlapping symptoms with IBM include:

• Acid maltase deficiency
• Chronic inflammatory demyelinating polyradiculoneuropathy
• Late-onset distal myopathies
• Motor neuron disease
• Myofibrillar myopathies
• Overlap myositis
• Post-polio syndrome

When symptoms first appear, IBM is often misdiagnosed as arthritis or polymyositis. Polymyositis is another inflammatory myopathy that can lead to muscle weakness and breakdown over time.

Muscle weakness is a common condition among older people. As it is often attributed to aging, it may be overlooked. Due to the rarity of IBM, many cases remain undiagnosed or misdiagnosed for years after symptoms begin. Few doctors have experience with IBM, making it important to consult a specialist if the condition is suspected.

A specialist may use a combination of the following approaches to diagnose IBM:

• Evaluation of physical symptoms and medical background: A specialist will first consider an individual’s personal and family medical history and check symptoms to document the pattern of weakness in the muscles.
• Blood tests: A blood test can check the level of creatine kinase (CK), an enzyme that leaks out of damaged muscle fibers. In IBM, CK levels may be only slightly increased, moderately increased up to 10 times the normal level, or even within the normal range. This is different from other inflammatory myopathies, where CK levels are typically very high, often reaching 15 times the normal level. In addition, a newer blood test can detect an antibody called anti-cN1A or anti-NT5C1A in the blood. This test is positive in about 50 percent of IBM patients and can help differentiate IBM from polymyositis. The test can also detect other autoimmune diseases. However, it may not be widely available.
• Nerve conduction studies: Nerve conduction studies may be performed to evaluate the speed of nerve impulse transmission and detect disruptions in nerve signals. During a nerve conduction study, electrodes are placed on the skin to stimulate a nerve with a mild electrical impulse. Another electrode records the response, and the resulting electrical activity is measured. This process is repeated for each nerve being tested. The speed of nerve impulses is calculated by measuring the distance between electrodes and the time it takes for electrical signals to travel between them. A nerve conduction study is often used along with electromyography to tell the difference between a nerve disorder and a muscle disorder.
• Electromyography (EMG): Related to the nerve conduction study, EMG evaluates the electrical activity of muscles and their controlling nerves. In IBM, abnormal electrical impulses may be observed, and EMG may rule out neurological disorders. While EMG can aid in confirming muscle involvement, it does not provide a definitive diagnosis. Results can be misleading, suggesting neurological disorders such as motor neuron disease in some cases.
• Imaging tests: Muscle imaging using magnetic resonance imaging (MRI) or computerized tomography (CT) scans can reveal distinct patterns of muscle involvement linked to IBM. This information aids in confirming an IBM diagnosis and differentiating it from other types of myositis.
• Muscle biopsy: The definitive test for IBM is a muscle biopsy, which entails extracting a small muscle sample and examining it under a microscope. Various stains are applied to emphasize different muscle components. In IBM, inclusion bodies are typically found within muscle cells.
• Genetic testing: Genetic tests may identify potential genetic factors.

Several diagnostic criteria have been suggested for IBM, but their clinical utility is limited due to low sensitivity. The European Neuromuscular Centre (ENMC) 2011 criteria have a very high specificity, exceeding 99 percent, implying that they can accurately identify those who don’t have IBM. However, these criteria still have a low sensitivity of around 57 percent, similar to other diagnostic criteria, meaning it’s not as effective at correctly identifying all IBM cases.

The following are the ENMC 2011 Diagnostic Criteria for IBM:

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Required criteria:

• Onset of symptoms after age 45
• Duration of symptoms exceeding 12 months
• Serum creatine kinase levels less than 15 times the upper limit of normal levels

Clinical criteria:

• Knee extension weakness is greater or equal to hip flexion weakness
• Finger flexion weakness is greater than shoulder abduction weakness

Pathological criteria:

• Presence of endomysial inflammatory infiltrate: Inflammatory cells within the connective tissue envelop individual muscle fibers.
• Presence of rimmed vacuoles: Rimmed vacuoles are localized areas of muscle fiber destruction.
• Protein accumulation or 15- to 18-nanometer filaments.
• Upregulation of major histocompatibility complex (MHC) class 1: There is an increase in the expression or production of MHC class 1 molecules on the surface of cells.

Classification:

• Clinicopathologically defined IBM: Required criteria + one or both clinical criteria + first three pathological criteria
• Clinically defined IBM: Required criteria + both clinical criteria + one or more, but not all, pathological criteria
• Probable IBM: Required criteria + one clinical criterion + one or more, but not all, pathological criteria

What Are the Complications of IBM?

The complications of IBM include:

• Inability to walk, necessitating assistive tools such as wheelchairs.
• Dysphagia.
• Aspiration pneumonia: The risk of aspiration pneumonia is highest for individuals with inflammatory myopathies such as IBM. Aspiration pneumonia has relatively high rates of recurrence and mortality.
• Compromised breathing due to diaphragm weakness and other respiratory complications, such as respiratory failure.
• Stumbling during walking and injurious falls.
• Development of pressure ulcers, muscle wasting, and other mobility-related issues.
• Challenges with everyday activities.
• Decreased self-reliance.
• Depression due to reduced quality of life.

In addition to complications, patients with IBM have increased risks of certain associated conditions compared to the general population, such as:

• Peripheral neuropathy: IBM patients are 2.7 times more likely to develop peripheral neuropathy. Peripheral neuropathy includes various conditions characterized by damage to the peripheral nervous system, which serves as a communication network transmitting signals between the brain, spinal cord (central nervous system), and the rest of the body.
• Sjögren’s syndrome: IBM patients are 6.2 times more likely to have Sjögren’s syndrome, a chronic autoimmune condition where the immune system targets and attacks the glands responsible for producing moisture in the eyes, mouth, and other areas, resulting in dryness.
• Blood cancers: Individuals with IBM are 3.9 times more likely to experience hematologic malignancies, particularly T-cell large granular lymphocytic leukemia, but are not at higher risk of other cancers.

Despite the heart being a muscle, IBM is not linked to a higher risk of heart abnormalities.

What Are the Treatments for IBM?

Although there are similarities in tissue appearance under the microscope, IBM’s clinical symptoms, treatment methods, and expected outcomes are notably different from those of other inflammatory myopathies.

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There is no cure for IBM that can reverse or eliminate it. The current treatment options primarily focus on managing symptoms. While IBM involves an autoimmune aspect, it typically does not show significant improvement with immunotherapy. However, immunotherapy might benefit some patients, particularly those with concurrent autoimmune conditions.

1. Medications

Most experts typically do not recommend medications for IBM except under specific circumstances. However, the following drugs may be used to treat IBM:

• ABC008: Biotechnology company Abcuro is currently conducting a phase 2/3 clinical trial for ABC008, an antibody aimed at targeting highly cytotoxic T-cells found in the muscles of individuals with IBM. These T-cells are believed to contribute significantly to muscle damage in the disease. ABC008 selectively eliminates the majority of highly cytotoxic T-cells while sparing protective T-cells and white blood cells, thus minimizing potential harm. The U.S. Food and Drug Administration (FDA) has granted an Orphan Drug Designation for ABC008 for the treatment of IBM.
• Alemtuzumab: A small clinical trial involving 13 IBM patients tested alemtuzumab, a drug typically used for leukemia and multiple sclerosis. The drug, which depletes specific immune cells, showed promising results in slowing IBM progression and improving strength in some patients. However, further research is needed to confirm its effectiveness.
• Arimoclomol: Arimoclomol is a substance thought to help fix specific proteins in muscle cells, preventing them from clumping. In a pilot study with IBM patients, the treatment was safe and well-tolerated. It also reduced important markers of IBM in mouse lab models representing different aspects of the disease and improved disease characteristics and muscle function of the mice. However, recent results from a large, randomized controlled trial showed the drug did not improve outcomes.
• Azathioprine: Immunosuppressive and immunomodulating drugs such as azathioprine have been used to address IBM’s inflammatory and muscle-wasting aspects. However, they weren’t able to reverse or slow the progression of the disease, and many clinicians believe their possible side effects outweigh the potential benefits, particularly for patients who also have other autoimmune diseases.
• Bimagrumab: Bimagrumab, or BYM338, is a human antibody that addresses muscle loss and weakness. In a pilot trial with s-IBM patients, it appeared to increase muscle mass and function. If the drug is approved, bimagrumab’s potential off-label use for s-IBM will be considered.
• Follistatin: Follistatin, also referred to as AAV1-FS344, is a protein delivered through gene therapy that enhances muscle strength and performance. It blocks certain proteins in the body that slow muscle growth and cause muscle loss, so it’s being explored as a potential treatment to improve muscle health and counteract muscle wasting in IBM.
• Glucocorticoids: Glucocorticoids are a type of corticosteroid with anti-inflammatory and immunosuppressive properties that some doctors may consider. These properties make them useful in treating conditions related to inflammation and immune system dysfunction. However, corticosteroids typically do not effectively treat this disease.
• Intravenous immunoglobulin (IVIG): IVIG therapy involves using blood plasma to manage dysphagia symptoms in some individuals. It is administered through an infusion that takes several hours. The treatment typically spans up to four months, including an induction phase and three maintenance cycles, to assess improvement in swallowing difficulties. If no benefit is observed, IVIG therapy is usually discontinued.
• Methotrexate: Limited evidence indicates that methotrexate, an immunosuppressive drug, can potentially lead to disease stabilization or modest improvement in some IBM patients.
• Sirolimus: Sirolimus, or rapamycin, is usually used to prevent kidney transplant rejection. A previously conducted phase 2b clinical trial investigated its use for IBM with promising results, and a phase 3 trial to further evaluate its efficacy is currently underway.

When prescribing medications for IBM, it’s crucial to reassess their effectiveness after a brief trial and discontinue them if no improvement is observed. The primary goal is to enhance or stabilize physical function, although this can be challenging due to the slow and unpredictable progression of the disease.

Continued medication use can be inappropriate, as long-term immunosuppressive drugs may potentially worsen outcomes in some cases. Assessing treatment efficacy based solely on creatine kinase levels is unreliable, as it doesn’t accurately reflect disease progression. Instead, evaluating the patient’s functional abilities can help determine the true impact of therapy.

2. Physical, Speech, and Psychological Therapies

Physical therapy involves exercises and techniques designed to maintain and improve strength, flexibility, and mobility in individuals with IBM. Physical therapists may create personalized exercise programs focusing on specific muscle groups to counteract weakness and prevent muscle atrophy.

Regular movement is especially important for people with IBM to prevent muscle loss, especially early in the disease. IBM specialists typically recommend cardiovascular exercise and regular low-resistance exercises while cautioning against heavy weights to avoid injury. Popular exercises include recumbent bicycle and aquatic exercises with reduced joint stress and improved mobility in water. In addition, stretching and range-of-motion exercises also play a key role in maintaining muscle function and flexibility. Taking precautions when exercising is essential to prevent overwork, falls, and injuries.

Patients with IBM commonly experience weakness in their quadriceps and anterior tibialis muscles, which can lead to foot drop and an increased risk of falls, often due to knee collapse or tripping. While studies on the use of orthoses (braces) in IBM are limited, bracing could potentially reduce falls in this group, but braces may also lead to slower walking speed and rhythm.

The following are other therapy options that may be helpful:

• Occupational therapy: Occupational therapists provide advice and specialized equipment to address daily challenges for individuals with IBM. Equipment includes utensils with ergonomic handles for better grip, tools to aid in climbing stairs, ramps for accessibility, walking aids, lift chairs, and guidance on optimizing bathroom facilities.
• Speech therapy: Swallowing difficulties in IBM can lead to food or liquid entering the windpipe, causing coughing, chest infections, and weight loss. Speech therapists can help manage these swallowing issues.
• Psychological therapy: Due to IBM’s chronic nature, psychological therapy or consulting a rehabilitation psychologist may be beneficial.

3. Adjuvant Therapies

In one case, a 70-year-old woman underwent a three-month comprehensive treatment involving platelet-rich plasma injections, hyperbaric oxygen therapy, and glutathione infusions. This patient found success with the first two treatment approaches, as she experienced significant improvement in muscle strength, mobility, flexibility, and functional ability. Platelet-rich plasma (PRP) therapy is a cell-based treatment where a person’s blood is extracted, processed to isolate platelets, and then injected into specific areas of the body to promote healing and regeneration. The process involves separating platelets from red blood cells using a centrifuge machine after collecting a small blood sample.

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Hyperbaric oxygen therapy (HBOT) involves breathing pure oxygen in a pressurized chamber with higher-than-normal air pressure. This increased pressure allows the lungs to gather more oxygen, which can aid in healing and sometimes combatting specific infections by delivering more oxygen to the tissues requiring it. The authors of this case report suggested further research exploring PRP injections and HBOT as possible adjuvant therapies for IBM was warranted.

4. Surgery

Surgical interventions for severe dysphagia in IBM include cricopharyngeal myotomy, where an incision is made through the throat’s cricopharyngeus muscle to facilitate easier opening of the pharynx during swallowing, and cricopharyngeal dilation, where the muscle at the top of the esophagus is stretched for easier food passage. A gastrostomy (abdominal feeding) tube might be necessary in advanced cases. One review suggested about one-quarter of those studied (26 total) received a feeding tube but still died due to aspiration. The researchers wondered whether receiving the tube earlier may have prevented this, though they noted the tube does not wholly prevent aspiration.

5. Possible Future Treatments

IBM typically does not respond well to any currently accessible therapies, and its rate of advancement seems unaffected by these treatment approaches. However, there are some new and promising treatments under development, including:

• Reducing endoplasmic reticulum stress: The endoplasmic reticulum (ER) is a compartment within a cell that plays a significant role in protein synthesis and folding. ER stress can occur when misfolded proteins accumulate in the ER, leading to cell dysfunction and IBM. Reducing ER stress involves decreasing protein overload and removing misfolded proteins.
• Promoting autophagy: Autophagy is a process where cells degrade and recycle damaged or unnecessary components to maintain cellular health, similar to a cellular self-cleaning mechanism. In muscles, a lack of autophagy can cause muscle atrophy and the accumulation of harmful materials within cells. In s-IBM, autophagy appears to be defective.
• Removing toxic protein aggregates: IBM involves the invasion of T-cells and the formation of protein aggregates such as rimmed vacuoles and inclusion bodies. Protein aggregates can also trigger immune responses and inflammation, and persistent immune activation can lead to T-cell large granular lymphocytic leukemia that resists treatment, possibly explaining the progression from polymyositis to IBM. These protein aggregates can hinder cell functions, spread within cells like an infectious agent, and prevent muscle cell repair after damage, ultimately causing weakness and muscle shrinkage. Therefore, treatments centered on removing these protein aggregates may be an area of future exploration.

How Does Mindset Affect IBM?

IBM can progress into a debilitating condition that severely impacts quality of life. It can be highly upsetting to have to rely on others for simple tasks, leading to negative feelings like guilt and sadness. However, mindset can affect how individuals cope with IBM and manage symptoms. Psychological support and strategies for cultivating a positive attitude can be beneficial for these people and may help prevent depression and despair.

A positive mindset can contribute to better adherence to treatment plans, rehabilitation exercises, a healthy lifestyle, and overall self-care. It can also help individuals maintain a sense of hope and resilience despite the long-term, worsening challenges IBM poses. Conversely, a negative mindset characterized by feelings of helplessness or hopelessness can impact motivation and willingness to engage in necessary activities for managing the condition and general wellness.

What Are the Natural Approaches to IBM?

Limited research has been done on the effectiveness of the following natural remedies in treating IBM, but they may have some effect on symptoms. Therefore, before adopting any of the see remedies, consult your doctor and IBM specialist first.

1. Medicinal Herbs

While research hasn’t discovered any specific medicinal herbs for treating IBM, the following may aid in increasing muscle strength or mass:

• Schisandra (Schisandra chinensis): In addition to Schisandra’s antioxidant, anti-allergen, antidepressant, and anti-anxiety properties, it decreased muscle cell inflammation and promoted autophagy in animal studies. It also improved muscle strength and stamina in rats.
• Turmeric (Curcuma longa): Turmeric can reduce inflammation and promote muscle recovery, but consuming it may lead to diarrhea, headache, and rash.
• Ashwagandha (Withania somnifera): Revered in the Indian Ayurvedic tradition as a tonic, particularly for the nerves, Ashwagandha is used for a wide range of health conditions. It is an anti-inflammatory and improves mitochondrial health and energy levels, but it may cause side effects such as rhinitis, constipation, and decreased appetite.
• Ginseng (Panax ginseng): Ginseng can enhance physical endurance, focus, and memory, boost immune system function, delay aging effects, and alleviate symptoms related to various health issues such as respiratory and heart conditions, depression, and anxiety. However, consuming it may affect sleep quality and blood sugar levels.

2. Supplements

IBM experts sometimes recommend certain over-the-counter supplements, including:

• Creatine monohydrate: Athletes often use creatine monohydrate (creatine for short) to enhance muscle strength and size. Our bodies naturally produce creatine, and it’s found in foods such as meat and fish. Supplementation can boost muscle creatine levels, which is particularly beneficial for vegetarians. A daily dosage of around 3 grams is commonly advised for optimal effects. The supplement is generally considered safe.
• Mitochondrial cocktail: Some supplements are believed to support mitochondria, the energy-producing units in our cells often affected in IBM. A combination of such supplements called the “mitochondrial cocktail,” which includes Coenzyme Q10, L-carnitine, B-complex vitamins, and antioxidants, has been proposed as a potential treatment. However, these supplements haven’t been extensively researched and can be costly. It’s essential to consult your doctor before using them.

3. Diet

Maintaining a balanced diet is essential for managing IBM, as it supports muscle health. Consume sufficient fruits, vegetables, and high-quality proteins while limiting sugar and refined starches. Adequate protein intake is crucial for muscle maintenance and repair, as muscles are constantly remodeling. Weak muscles can strain joints, leading to pain and instability, particularly in those with IBM. In addition, a healthy diet can help prevent overweight and obesity, which can cause metabolic changes that further promote muscle wasting.

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The ketogenic diet, often called the “keto” diet, is characterized by low carbohydrate intake and high fat consumption. It has a long history of being used to address specific medical conditions such as diabetes, polycystic ovary syndrome, and epilepsy. The ketogenic diet has the potential to reduce inflammation, improve cell energy production, address mitochondrial issues, and promote autophagy, which may be advantageous in managing IBM. 

In one case, a 52-year-old woman with progressive IBM followed a customized ketogenic diet (60 percent fat, 30 percent protein, 5 percent fiber, and 5 percent net carbohydrate by weight) for one year. Before adopting the diet, the patient suffered from frequent falls despite using a walking stick, along with swallowing problems, musculoskeletal pain, and depression. After following the keto diet for a year, the patient regained the ability to walk independently, and the aforementioned other symptoms resolved. Her strength improved, and she showed progress in various functional tests, leading to an enhanced quality of life. In addition, her blood creatine kinase levels also decreased. Any adverse effects from the diet were mild and resolved within three weeks after starting it.

The ketogenic diet should only be pursued if advised by your health care professional.

4. Mind-Body Practice and Acupuncture

Meditation, yoga, and mindfulness-based stress reduction (MBSR) classes can train the mind to be calm and aware, thus helping alleviate IBM patients’ worry, improve their concentration, and enhance their quality of life. Meditation and yoga can also be easily integrated into daily life.

Acupuncture can relieve various types of pain, including muscle pain in IBM. In some cases, acupuncture may even be as effective as nonsteroidal anti-inflammatory drugs (NSAIDs) in pain management. Acupuncture’s pain-relief mechanism is attributed to the increased release of beta endorphin, a natural painkiller. In addition, endorphins may also interact with cytokines such as interleukin-10, which can reduce inflammation in different disorders, potentially including IBM.

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How Can I Prevent IBM?

Since the exact causes of IBM are not fully understood, no known methods exist to prevent this condition. However, we can adopt a healthy lifestyle for overall muscle health and well-being and hope for the best. The following lifestyle factors will help promote overall health and support you if you do develop IBM:

• Regular exercise: Regular cardiovascular and strength-training exercises will discourage muscle wasting.
• Healthy diet: Choosing high-quality, whole foods over processed ones is essential.
• Stress management: Controlling stress will lower your odds of weakening your immune system and reduce systemic inflammation.
• Regular health checkups: Early detection and management of IBM can help maintain muscle function as much as possible.
• Sleep hygiene: Get seven or eight hours of sleep as often as possible and maintain a consistent bedtime routine.
• Avoid harmful substances: Avoiding smoking, limiting alcohol, and reducing exposure to toxins wherever possible will contribute to resilience.