PROTEIN TRIGGERS
- How to build up muscle?
- What is a maple syrup urine disease (MSUD)?
HOW TO BUILD UP MUSCLE?
The first question is about how to build up the muscle? So, firstly is by attempted to build up muscle by using androgen and insulin. The anabolic (nitrogen-retaining) effects of androgen on skeletal muscle cells enhance muscle mass by increasing amino acid flux into muscle and by stimulating protein synthesis. Exogenous insulin has the potential to increase muscle mass by similar actions and also by increasing the content of muscle glycogen.
The second way is by taking a diet in which the amount of protein required depends on personal weight and daily caloric intake. A few specific groups of people are at risk for being protein-deficient, including elderly women and people with illnesses or eating disorders. A protein deficiency is defined as eating 50% to 75% of the recommended amount of daily protein. While a diet in which protein makes up more than 30% of personal caloric intake causes a build up of toxic ketones.
The second way is by taking a diet in which the amount of protein required depends on personal weight and daily caloric intake. A few specific groups of people are at risk for being protein-deficient, including elderly women and people with illnesses or eating disorders. A protein deficiency is defined as eating 50% to 75% of the recommended amount of daily protein. While a diet in which protein makes up more than 30% of personal caloric intake causes a build up of toxic ketones.
WHAT IS MSUD?
Maple syrup urine disease (MSUD) is a rare, inherited metabolic disorder. With MSUD, the body cannot break down certain amino acids. Individuals who have the disease produce urine that has a distinctive maple syrup odor.
Special enzymes process the amino acids so they can be used to maintain all the body functions. If some of the necessary enzymes are missing or defective, the amino acids and their by-products, called keto acids, collected in the body. As the levels of these substances increase, neurological damage, coma, and life-threatening conditions can result. In MSUD, the body does not have enzymes from a group called the branched-chain alpha-keto acid dehydrogenase complex (BCKAD). BCKAD enzymes process three important amino acids: leucine, isoleucine, and valine.
This MSUD are caused by mutations, or changes, in the genes that tell your body to make certain enzymes. Gene mutations are inherited on the chromosomes that received from our parents. When the genes related to the BCKAD enzymes are defective, the BCKAD enzymes are not produced or work inaccurately.
MSUD is a recessive genetic disorder. Typically, parents of children with MSUD do not have the disease. They possess one mutated gene and one normal gene for MSUD. Though they carry the defective gene, they are not affected by it. The defective gene is called recessive. Parents of children with MSUD are called carriers.
Having MSUD means that we inherited one flawed gene for MSUD from each parent. Both parents must carry a mutation of the gene associated with MSUD to pass the disease on to their child.
There are four subtypes of MSUD. All are inherited genetic disorders. They only differ by their degree of enzyme activity, severity, and age when the disease appears.The first one is Classic MSUD. This is the most common form of this condition. In this form, the patient has little, if any, enzyme activity (about two percent or less than normal activity). This is the most severe form of MSUD. Symptoms are present in newborns within a few days of birth.
Then the Intermediate MSUD. Intermediate MSUD is a very rare form of the disease. It is a version of classic MSUD. The symptoms and age of onset of this type vary greatly. Individuals with intermediate MSUD have a higher level of enzyme activity than classic MSUD (about three to eight percent of normal activity).
Intermittent MSUD does not interfere with normal physical and intellectual growth and development. It is a milder form of classic MSUD. Individuals have more significant enzyme activity (about 8 to 15 percent of normal activity). Symptoms usually don’t appear until a child is between 1 and 2 years of age. The initial reaction often occurs when the child experiences stress, an illness, or an unusual increase in protein.
The last one is Thiamine-responsive MSUD. This type of MUSD is a rare form of the condition that often improves with large doses of thiamine, or vitamin B1. Symptoms in a child with thiamine-responsive MSUD usually occur after infancy. Even though thiamine can be beneficial, dietary restrictions also are necessary.
Special enzymes process the amino acids so they can be used to maintain all the body functions. If some of the necessary enzymes are missing or defective, the amino acids and their by-products, called keto acids, collected in the body. As the levels of these substances increase, neurological damage, coma, and life-threatening conditions can result. In MSUD, the body does not have enzymes from a group called the branched-chain alpha-keto acid dehydrogenase complex (BCKAD). BCKAD enzymes process three important amino acids: leucine, isoleucine, and valine.
This MSUD are caused by mutations, or changes, in the genes that tell your body to make certain enzymes. Gene mutations are inherited on the chromosomes that received from our parents. When the genes related to the BCKAD enzymes are defective, the BCKAD enzymes are not produced or work inaccurately.
MSUD is a recessive genetic disorder. Typically, parents of children with MSUD do not have the disease. They possess one mutated gene and one normal gene for MSUD. Though they carry the defective gene, they are not affected by it. The defective gene is called recessive. Parents of children with MSUD are called carriers.
Having MSUD means that we inherited one flawed gene for MSUD from each parent. Both parents must carry a mutation of the gene associated with MSUD to pass the disease on to their child.
There are four subtypes of MSUD. All are inherited genetic disorders. They only differ by their degree of enzyme activity, severity, and age when the disease appears.The first one is Classic MSUD. This is the most common form of this condition. In this form, the patient has little, if any, enzyme activity (about two percent or less than normal activity). This is the most severe form of MSUD. Symptoms are present in newborns within a few days of birth.
Then the Intermediate MSUD. Intermediate MSUD is a very rare form of the disease. It is a version of classic MSUD. The symptoms and age of onset of this type vary greatly. Individuals with intermediate MSUD have a higher level of enzyme activity than classic MSUD (about three to eight percent of normal activity).
Intermittent MSUD does not interfere with normal physical and intellectual growth and development. It is a milder form of classic MSUD. Individuals have more significant enzyme activity (about 8 to 15 percent of normal activity). Symptoms usually don’t appear until a child is between 1 and 2 years of age. The initial reaction often occurs when the child experiences stress, an illness, or an unusual increase in protein.
The last one is Thiamine-responsive MSUD. This type of MUSD is a rare form of the condition that often improves with large doses of thiamine, or vitamin B1. Symptoms in a child with thiamine-responsive MSUD usually occur after infancy. Even though thiamine can be beneficial, dietary restrictions also are necessary.