FAQ

Dynamito MAPEs (Mitochondrial Activation Factors) can effectively improve the efficiency of the electron transport chain on mitochondria and increase energy generation. Additionally, they help maintain mitochondrial integrity, reduce mitochondrial membrane damage, significantly decrease the production of endogenous oxidative free radicals, making mitochondria less susceptible to damage and maintaining cell survival rates.

The effective ingredients of Dynamito MAPEs, by enhancing mitochondrial function within cells, increase cell activity, improve organ function, and reduce the occurrence of diseases. Scientifically proven effects of Dynamito MAPEs include anti-aging, reducing pulmonary inflammation and fibrosis, regulating the immune system, maintaining blood glucose and lipid stability, and neuroprotection.

The sources of Dynamito MAPEs can be found in herbal medicine and natural plants, which are extracted using special techniques to extract components that may activate mitochondria. Further, through a professional screening platform and evaluation model, the most effective components that activate mitochondria are identified.

To determine whether Dynamito MAPEs have the effect of activating mitochondria, a professional screening platform and evaluation model can be used to identify whether the components from herbal medicine and natural plants have functionality on mitochondria, and to assess the superiority and inferiority of Dynamito MAPEs based on this model.

Mitochondria are the energy factories within cells, and the condition of cells is governed by the function and activity of mitochondria. How can mitochondria be evaluated? Basically, mitochondrial quality testing can be evaluated based on the efficiency of mitochondrial energy production (mitochondrial operational efficiency; spare respiratory capacity, SRC) and capacity (mitochondrial energy generation; adenosine triphosphate, ATP). Additionally, the values obtained through mitochondrial testing platforms are transformed to present a comprehensive indicator of mitochondria, known as the Bioenergetic High-Risk Index (BHI), which is divided into five levels. The higher the level, the better the mitochondrial activity and function. Through the index scale, mitochondria can be more easily evaluated.

Dynamito MAPEs are mediators for mitochondrial activation, effectively increasing mitochondrial function and activity. By enhancing mitochondrial activity and function, through mitochondrial testing platforms, the improvement in mitochondrial function after consuming Dynamito MAPEs can be assessed.

Exercise plays a significant role in activating mitochondria. Here are some ways exercise helps activate mitochondria:

• Aerobic Exercise: Aerobic exercises such as jogging, swimming, and cycling can increase oxygen supply, thereby promoting mitochondrial function. By increasing respiratory and cardiovascular activity, aerobic exercise enhances cellular oxygen utilization, thus increasing mitochondrial energy production.
• High-Intensity Interval Training (HIIT): HIIT involves high-intensity exercise followed by rest periods. This training method increases cellular oxygen demand, promotes mitochondrial biosynthesis and energy production, and helps improve mitochondrial function.
• Strength Training: Engaging in strength training can increase muscle mass and metabolism, thereby increasing overall metabolic rate. This contributes to improved mitochondrial function, as muscle cells contain a large number of mitochondria, and mitochondrial energy production is crucial for muscle function.
• Endurance Training: Long-duration endurance training, such as long-distance running or cycling, can increase mitochondrial density and function within cells, thereby enhancing body endurance and stamina.
• Jumping Rope and brisk walking: These low-intensity aerobic exercises can effectively promote mitochondrial function while improving cardiovascular health and metabolism.

In summary, regular participation in various forms of exercise can increase mitochondrial density and function within cells, thereby enhancing metabolic rate, endurance, and overall health.

Diet also plays a crucial role in activating mitochondria. Here are some dietary suggestions to help activate mitochondria:

• Consume Sufficient Antioxidants: Antioxidants help reduce the production of free radicals, thereby lowering oxidative stress within cells and benefiting mitochondrial function. Consume plenty of vegetables, fruits, nuts, and whole grains rich in antioxidants such as vitamin C, vitamin E, and selenium.
• Moderate Intake of Healthy Fats: Healthy fats, especially Omega-3 fatty acids, are essential for maintaining cell membrane health and promoting mitochondrial function. Consume foods rich in Omega-3 fatty acids such as fish, flaxseeds, nuts, and olive oil.
• Limit Processed Foods and Sugars: Excessive consumption of processed foods and sugars can lead to increased inflammation and oxidative stress in the body, affecting mitochondrial function. Avoid processed foods, candies, and sugary beverages, and opt for fresh, natural foods instead.
• Increase Protein Intake: Protein is an essential component of cell structure and is also crucial for mitochondrial function. Adequate protein intake helps maintain cell structure and promotes mitochondrial biosynthesis.
• Moderate Intake of Vitamins and Minerals: Vitamins and minerals play vital roles in cellular function and metabolism. Ensure adequate intake of nutrients such as vitamin B, vitamin D, magnesium, calcium, and zinc to support healthy mitochondrial function.
• Proper fluid intake: Adequate hydration helps maintain balance within and outside cells, facilitating the transport of nutrients and metabolites, thereby supporting mitochondrial function.

Overall, a balanced diet and healthy eating habits provide the necessary nutrients and energy for mitochondria, helping maintain their normal function and promoting overall health.

Not all cases of decreased metabolic rate are due to poor mitochondrial function; other factors may be involved. For instance, prolonged exposure to high stress leads to the production of stress hormone cortisol, which competes with the precursor of thyroid hormone, reducing thyroid hormone secretion and lowering metabolic rate. Determining whether one has poor mitochondrial function requires a comprehensive organic acid metabolism analysis test in functional medicine. During the process of converting carbohydrates, lipids, or proteins into energy through mitochondria, various metabolites, known as organic acids, are produced and excreted through urine. By testing these organic acids in urine, one can assess the efficiency of mitochondrial energy conversion. If the conversion efficiency is poor, the likelihood of impaired mitochondrial function is higher.

Poor metabolic rate involves various possibilities, but how can one determine whether they have poor mitochondrial function? Professional physicians suggest that in clinical functional medicine, a comprehensive organic acid metabolism analysis test is still necessary for evaluation. During the process of converting carbohydrates, lipids, or proteins into energy through mitochondria, various metabolites, known as organic acids, are produced and excreted through urine. By testing these organic acids in urine, one can assess the efficiency of mitochondrial energy conversion. If the conversion efficiency is poor, the likelihood of impaired mitochondrial function is higher.

• Vibrant Energy, Clear Mind: Nurturing mitochondria leads to increased energy production, allowing better focus at work and enjoyment during leisure time!
• Normalized Metabolism, Balanced Physique: With healthy mitochondrial metabolism, fat accumulation decreases, maintaining a great physique without needing to hit the gym!
• Strengthened Immune Barrier, Repelled Pathogens: Mitochondria act as immune command centers; nurturing them enhances resistance, significantly boosting immunity!
• Elimination of Harmful Cells, Cancer Prevention: Cancer is the leading cause of death; mitochondria promote the apoptosis of aging cells, effectively eliminating cancer cells from the source!

Mitochondria act as the powerhouses of cells, providing the energy our bodies need. Nowadays, people advocate for anti-aging and antioxidant approaches, not just for youthful skin but also to maintain youthful organ functions. The seemingly tiny mitochondria inside cells are closely related to the secrets of aging and health. Degenerative diseases like dementia, Parkinson's disease, and cancer have been confirmed to be associated with mitochondria. Therefore, nurturing mitochondria has become a burgeoning science.

The mechanism of mitochondrial regeneration therapy involves providing healthy external mitochondria to the damaged area, where the mitochondria are taken up by cells through endocytosis. The external mitochondria then fuse with the damaged mitochondria inside the cell, repair the damaged mitochondria, and then remove and metabolize the damaged mitochondria through fission, thus restoring the number and function of mitochondria.

In addition to being the energy production center of cells, mitochondria also play an important role in cell survival and regulating physiological functions. However, with more and more research confirming the relationship between disease occurrence and mitochondrial damage, mitochondrial regeneration therapy has been shown to effectively improve cell damage in damaged organs, enhance damaged mitochondrial activity through external mitochondrial assistance, inhibit cell death, and treat diseases that are difficult to cure with drugs.

Alzheimer's Disease

Alzheimer's disease is a neurodegenerative disease caused by multiple factors, affecting many biochemical reactions in brain cells, including amyloid-β aggregation, neurofibrillary tangle formation, oxidative stress, and neuroinflammation, ultimately leading to neuronal death, hippocampal atrophy responsible for memory, and further brain lesions. Since neurons rely heavily on mitochondria to produce energy to maintain survival, mitochondrial damage can lead to the development of the aforementioned lesions.

Due to the complex pathogenesis of Alzheimer's disease, no drugs have been found to effectively treat Alzheimer's disease patients. In order to reduce the poor efficacy of single drugs in treating Alzheimer's disease, scientists have proposed transplanting active intact mitochondria as a method to treat the disease. Studies have found that Alzheimer's disease mice receiving mitochondrial reconstruction therapy showed significant increases in mitochondrial functional indicators such as citrate synthase and cytochrome c oxidase activity in brain cells, significant reductions in hippocampal neuron loss, decreased neuroglia, and reduced cognitive impairment. Therefore, mitochondrial regeneration therapy also offers new hope for Alzheimer's disease.

Parkinson's Disease

Parkinson's disease is characterized by the death of dopaminergic neurons in the substantia nigra of the brain, resulting in the inability to produce dopamine and leading to conditions such as motor dysfunction. Both genetic and environmental risk factors can cause the death of dopaminergic neurons, with mitochondria controlling cell fate. Under normal conditions, damaged mitochondria can be metabolized, but when the repair mechanism is damaged, mitochondrial damage accumulates, leading to increased oxidative stress and eventual inability of mitochondria to produce energy, causing the death of dopaminergic neurons. Current clinical treatments aim to directly or indirectly increase dopamine activity to alleviate motor dysfunction, but cannot rescue already dead dopaminergic neurons. Research has found that treating with external mitochondria significantly restores the number of dopaminergic neurons in Parkinson's disease rats, increases the functional proteins of mitochondria, and significantly improves the motor ability of Parkinson's disease rats, effectively reducing the motor dysfunction caused by Parkinson's disease, indicating that mitochondrial reconstruction therapy proposes a new direction for the treatment of Parkinson's disease.

Spinal Cord Injury

The spinal cord is the peripheral nervous system extending from the brain, and spinal nerves entering and exiting specific segments of the spinal cord control specific parts of the body. The upper part controls breathing, neck, and upper limb functions, while the thoracic spine is responsible for chest and abdominal movements, the lumbar spine regulates lower limb function, and the sacral spine controls defecation, urination, and sexual function. Spinal cord injury refers to acute traumatic injury to the spinal cord and nerves, usually resulting in varying degrees of damage depending on specific segments of the spinal cord. Injury to the cervical spine causes quadriplegia, while injury to the thoracic, lumbar, or sacral spine causes paraplegia. In addition to this, spinal cord injury also causes difficulty in urination, defecation, and sexual dysfunction, and may also affect respiratory problems and autonomic dysfunction. Because dead nerve cells are not easily regenerated, there is currently no effective treatment for spinal cord injury. Currently, many methods intend to increase nerve activity and transplant neurons. Among them, mitochondrial reconstruction therapy has been used to treat spinal cord injury, and preliminary results have shown that mice treated with mitochondrial therapy respond to mechanical tests with increased force.

Myocardial Infarction

When the heart is blocked due to vascular occlusion, blood cannot be transported to the heart tissue, causing the myocardium to lack oxygen and nutrients, resulting in damage to the mitochondria. Quickly damaged mitochondria can lead to myocardial death. Research has shown that directly extracting mitochondria from muscle tissue and then injecting them into ischemic myocardium results in increased mitochondrial activity and inhibition of myocardial cell death, further effectively improving cardiac contraction and relaxation function, and the therapy is also safe. In clinical trials, mitochondrial reconstruction therapy has also been shown to improve heart function in children with myocardial infarction after reperfusion.

Mitochondrial Therapy for Acute Lung Injury/Acute Respiratory Distress Syndrome

Research has found that mitochondrial damage increases significantly in lung cells in animals simulating lung injury, and damaged lungs further lead to multiple organ failure and death. However, when animals received mitochondrial reconstruction therapy, the damaged mitochondria in lung cells were repaired, effectively reducing lung cell death. In addition, under mitochondrial reconstruction therapy, immune cell infiltration and the production of inflammatory proteins were also reduced. Therefore, mitochondrial reconstruction therapy can maintain the barrier of alveolar epithelium, reduce a series of inflammatory reactions, reduce pulmonary edema, and reduce the symptoms of respiratory distress, thereby possibly reducing the high mortality rate of acute lung injury.

Diabetes

Diabetes has become a global health problem affecting the health of people worldwide. Type 1 diabetes is a hereditary disease caused by autoimmunity attacking pancreatic tissue, leading to pancreatic cell death. Type 2 diabetes is mainly caused by a high-sugar and high-fat diet, which weakens mitochondrial function and increases oxidative stress. With long-term high blood sugar, the pancreas gradually dies and cannot produce insulin. Both type 1 and severe type 2 diabetes patients are unable to produce insulin due to decreased or dead pancreatic function. In preclinical studies, co-culturing the pancreas with mitochondria has been shown to increase pancreatic activity and increase insulin release. In the future, mitochondrial reconstruction therapy may be applied in the clinical treatment of diabetes, including type 1 diabetes or type 2 diabetes, to increase the survival rate of pancreatic cells and the secretion of insulin.