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Cancer as a Metabolic Disease

Cancer as a Metabolic Disease

Cancer is a complex disease involving numerous tempo-spatial changes in cell physiology, which ultimately lead to malignant tumors. Abnormal cell growth (neoplasia) is the biological endpoint of the disease. Tumor cell invasion of surrounding tissues and distant organs is the primary cause of morbidity and mortality for most cancer patients.

The biological process by which normal cells are transformed into malignant cancer cells has been the subject of a large research effort in the biomedical sciences for many decades. Despite this research effort, cures or long-term management strategies for metastatic cancer are as challenging today as they were 40 years ago.

Emerging evidence indicates that impaired cellular energy metabolism is the defining characteristic of nearly all cancers regardless of cellular or tissue origin.

In contrast to normal cells, which derive most of their usable energy from oxidative phosphorylation, most cancer cells become heavily dependent on substrate level phosphorylation to meet energy demands. Evidence is reviewed supporting a general hypothesis that genomic instability and essentially all hallmarks of cancer, including aerobic glycolysis (Warburg effect), can be linked to impaired mitochondrial function and energy metabolism. A view of cancer as primarily a metabolic disease will impact approaches to cancer management and prevention.

Evidence is reviewed supporting a general hypothesis that cancer is primarily a disease of energy metabolism. All of the major hallmarks of the disease can be linked to impaired mitochondrial function.

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Thomas M. Seyfried and Laura M Shelton

Glut1 DS as a Metabolic Disease

Glut1 DS as a Metabolic Disease

Glucose Transporter Type 1 Deficiency Syndrome (Glut1 DS) manifestations can be explained in terms of current understanding of glucose transport in the brain via the mechanism of glucose metabolism. Glucose is the principal fuel source for brain metabolism; the glucose transporter Glut1 (solute carrier family 2, facilitated glucose transporter member 1), the protein product of SLC2A1, is the fundamental vehicle by which glucose enters the brain.

The cerebral metabolic rate for glucose is low during fetal development and at birth. The rate increases linearly after birth, peaks around age three years, remains high for the remainder of the first decade of life, and gradually declines during the second decade of life to the rate ofglucose utilization seen in early adulthood. It thus appears that the risk for clinical manifestations during fetal development and the newborn period is low, whereas the risk is increased later in infancy and early childhood.

Glucose transporter type 1 deficiency syndrome (Glut1-DS) is characterized by infantile seizures refractory to anticonvulsants, followed by deceleration of head growth, delays in mental and motor development, spasticity, ataxia, dysarthria, opsoclonus, and other paroxysmal neurologic phenomena, often occurring prior to meals.

Affected infants appear normal at birth following an uneventful pregnancy and delivery. Birth weight and Apgar scores are normal. Affected children then experience infantile-onset epileptic encephalopathy associated with delayed neurologic development, deceleration of head growth and resulting microcephaly,ataxia, and spasticity [De Vivo et al 2002a, De Vivo et al 2002b].

Seizures usually begin between age one and four months, are the first clinical indication of brain dysfunction.

Apneic episodes and abnormal episodic eye movements simulating opsoclonus may precede the onset of seizures by several months. Five seizure types occur: generalized tonic or clonic, myoclonic, atypical absence, atonic, and unclassified. The frequency of seizures varies among affected individuals some experience daily events; others have only occasional seizures separated by days, weeks, or months; two individuals never had a clinical seizure [von Moers et al 2002, Leary et al 2003].

Other paroxysmal events including intermittent ataxia, mental confusion, lethargy or somnolence, hemiparesis, abnormalities of movement or posture such as dystonia, total body paralysis, sleep disturbances, and recurrent headaches have also been described [Overweg-Plandsoen et al 2003]. It is unclear whether these events represent epileptic or non-epileptic phenomena. These neurologic symptoms generally fluctuate and may be influenced by factors such as fasting or fatigue.

Varying degrees of cognitive impairment, ranging from learning disabilities to severe mental retardation, are characteristic.

Varying degrees of speech and language impairment are observed in all affected individuals. Dysarthria is common and associates with dysfluency (i.e., excessively interrupted speech). Both receptive and expressive language abilities are affected, with expressive language skills disproportionately affected.

Social adaptive behavior is an exceptional strength. Individuals with Glut1-DS tend to be comfortable in group and school settings and interact well with others.

Paroxysmal exercise-induced dyskinesias (PED) are involuntary intermittent movements triggered by prolonged physical exertion. Autosomal dominant inheritance may occur. Recently, mutations in the glucose transporter 1 (GLUT1) gene (chr. 1p35-p31.3) have been identified as a cause in some patients with autosomal dominant PED.

The diagnosis of Glut1-DS is established in neurologically impaired individuals with 1) reduced cerebrospinal fluid (CSF) glucose concentration (hypoglychorrhachia) that seldom, if ever, exceeds 40 mg/dL and 2) low ratio of CSF glucose concentration to blood glucose concentration (consistently -0.33-0.01; normal ratio: 0.65 -0.01). SLC2A1 is the only gene known to be associated with Glut1-DS.

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Alzheimer's as a Metabolic Disease

Glut1 DS as a Metabolic DiseaseNo effective treatments are currently available for the prevention or cure of Alzheimer's disease (AD), the most frequent form of dementia in the elderly. The most recognized risk factors, advancing age and having the apolipoprotein E Ɛ4 gene, cannot be modified or treated. Increasingly, scientists are looking toward other risk factors to identify preventive and therapeutic strategies. Much attention recently has focused on the metabolic syndrome (MetS), with a strong and growing body of research suggesting that metabolic disorders and obesity may play a role in the development of dementia.

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"What if there was a cure from Alzheimer's Disease... and no one knew?"- Mary Newport, M.D.

Diabetes as a Metabolic Disease

Diabetes is a disorder of metabolism— the way the body uses digested food for growth and energy. Most of the food people eat is broken down into glucose, the form of sugar in the blood. Glucose is the main source of fuel for the body.

After digestion, glucose passes into the bloodstream, where it is used by cells for growth and energy. For glucose to get into cells, insulin must be present. Insulin is a hormone produced by the pancreas, a large gland behind the stomach.

When people eat, the pancreas automatically produces the right amount of insulin to move glucose from blood into the cells. In people with diabetes, however, the pancreas either produces little or no insulin, or the cells do not respond appropriately to the insulin that is produced. Glucose builds up in the blood, overflows into the urine, and passes out of the body in the urine. Thus, the body loses its main source of fuel even though the blood contains large amounts of glucose.

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Brain Tumors as a Metabolic Disease...

Brain Tumors will be diagnosed in over 200,000 people in the U.S. over the next year. They are the leading cause of cancer deaths in children through high school. Brain tumors that are “benign” may be as debilitating as those that are malignant. Non-malignant brain tumors reoccur and may result in death. Brain tumors have a significantly lower than average cure rate than that of other types of cancer. Everyone is susceptible, and there is no prevention because their causes are still unknown!

Brain tumors are the leading cause of cancer deaths in young adult’s ages 20-39 years of age. They are difficult to treat, and often severely compromise the quality of a person’s life. The location of the tumor is likely to affect one's thought, emotion, and physical function.