File Name: the prime cause and prevention of cancer .zip
- The Prime Cause and Prevention of Cancer with two prefaces on prevention
- Cancer prevention and screening: the next step in the era of precision medicine
- What Causes Cancer?
The Prime Cause and Prevention of Cancer with two prefaces on prevention
Nicotinamide is a water-soluble amide form of niacin nicotinic acid or vitamin B3. Both niacin and nicotinamide are widely available in plant and animal foods and niacin can also be synthesized in the liver from dietary tryptophan.
Nicotinamide is also commercially available in vitamin supplements and in a range of cosmetic, hair and skin preparations. Niacin, nicotinamide and cancer. Niacin, also known as nicotinic acid, is an organic compound and is, depending on the definition used, one of the 20 to 80 essential human nutrients. Together with nicotinamide it makes up the group known as vitamin B3 complex .
It has the formula C6H5NO2 and belongs to the group of the pyridine-carboxylic acids. These are hydrolysed in the intestine and the resulting nicotinamide is absorbed either as such, or following its hydrolysis to nicotinic acid.
Nicotinamide is present in nature in only small amounts. Enzymatic hydrolysis of the co-enzymes can occur during the course of food preparation. The prime cause of cancer is the damage to the mitochondria in normal cells. Nearly all cancer cells contain damaged mitochondria and the basic reason behind this, is increasing the intracellular inflammation or basically the incline in Reactive Oxygen Species ROS produced by each mitochondrion in oxidative phosphorylation.
Increasing the ROS in a cell can cause damage to the DNA of the mitochondrion and also nucleus DNA, but another reason behind turning the normal cell into cancer cell is the chaos caused by the increasing of inflammation inside each cell and increasing the intracellular ROS.
These chaos causes some abnormal messaging between the DNA of the nucleus to stop the apoptosis and turning the oxidative phosphorylation to the fermentation in cytosol. Normally by damaging to the mitochondria, the cell should apoptosis. However; the nucleus sends wrong messages to stop the apoptosis and do fermentation process in cytosol to survive the cell.
Even some normal left mitochondria would be shut down and stop the oxidative phosphorylation. This is the main and the real reason how increasing intracellular inflammation can cause cancer. This research introduces the butterfly effect inside the normal cells is the basic reason behind the cause of cancer .
Low dietary niacin has also been associated with an increased frequency of oral, gastric, and colon cancers, as well as oesophageal dysplasia . In the Linxian trial in China, involving nearly 30, residents, 40 mg niacin and 3. Most human studies have examined the dietary intake or supplementation of niacin in combination with other micronutrients [10,11]. Some chemotherapeutic agents e. Maintaining an optimum nicotinamide level is therefore essential in cancer patients and individuals at risk of exposure to genotoxic agents .
The activation of nuclear enzyme PARP-1 by DNA strand breaks during cellular genotoxic stress responses leads to complex signaling pathway that can enhance DNA repair, result in apoptotic cell death, or cause cellular energy loss leading to necrotic cell death. Nicotinamide protected against UV-induced immunosuppression in mice and humans and UV-induced carcinogenesis in mice. However, extrapolation of these data to human, particularly when physiological regimes involved in human carcinogenesis, should be done cautiously.
There is a shortage of knowledge on the impact of niacin on cancer risk in human populations. It is known that cancer patients tend to be deficient in niacin at a time when they are exposed to large doses of genotoxic drugs during chemotherapy [21,22]. Although animal models suggest that niacin deficiency enhances this risk , there are no human data available to further define this risk. Although developed countries generally supplement niacin in cereal products, there may still be a significant proportion of these populations experiencing subclinical niacin deficiency .
Niacin and riboflavin were supplemented in one of the treatment arms of the Linxian trials in China . The duration of the study was probably too short to examine the role of niacin during cancer initiation. In addition, the high esophageal cancer incidence in this population is associated with heavy contamination by fumonisin mycotoxins , which appear to promote carcinogenesis by a rather unique mechanism that may not be responsive to niacin status .
Studies on the impact of these treatments on cancer incidence are few in number, cover relatively short periods of time and represent late stages in the carcinogenic process. However, nicotinic acid therapy did not seem to cause the small increase in cancer incidence observed in populations using a variety of other non-statin drugs to lower blood cholesterol .
Interestingly, nicotinic acid use for 6 years by patients with cardiovascular disease led to a decrease in all-cause mortality measured 8 years after the drug use was discontinued . Epidemiological studies about niacin status and human cancer incidence often find significant associations, but interpretation of these is also difficult. In a variety of countries, including Iran, Africa, Italy, Switzerland and the United States, maize corn consumption which causes niacin deficiency , or low levels of estimated niacin intake, have been associated with an increased frequency of gastric, colon, oral, or esophageal cancers .
This is interesting from the perspective that niacin deficiency may target the gastrointestinal tract, as evidenced by diarrhea during pellagra, likely caused by the rapid cell turnover of these tissues. Niacin deficiency also causes inflammation and hyperplasia in the esophagus , which would also promote cancer at this site. No work has been done on the epidemiology of niacin deficiency and skin cancer, although animal models of niacin deficiency  and human familial DNA repair defects that mimic the sun sensitivity of pellagra  are associated with an increase in skin cancer risk .
Impaired conversion of coproporphyrinogen III into protoporphyrin IX results in higher coproporphyrin excretion in urine. Moreover, it impairs ribonucleic acid metabolism in erythrocytes; damage to erythrocyte membrane through the inhibition of membrane ATPase leads to reduced blood cell survival and hemolysis. In the gastrointestinal tract, lead may damage the autonomic system, causing peristalsis abnormalities. The neurological toxicity of lead stems from the fact that it is highly lipid-soluble; poisoning results in degenerative changes in the cerebral cortex, the cerebellum and subcortical nuclei, and the hypothalamus autonomic centers as well as segmental demyelination of peripheral nerve fibers.
After the absorption of a large amount of tetraethyl lead, patients present with acute poisoning; typically, there is a latent period, which may last between several hours and a few days and is followed by headache and dizziness, loss of appetite, insomnia and considerable weakness.
A physical examination reveals decreased blood pressure and heart rate values. Patients show signs and symptoms of nervous system damage, such as paresthesia in the limbs, nystagmus and euphoria. Next, they develop mental disorders such as delirium, delusions, and sometimes schizophrenic syndrome. A period of agitation is followed by obtundation and sometimes death . Toluene is a colorless liquid and has an odor similar to benzene.
It may be absorbed by the lungs and skin. Toluene is metabolized to benzoic acid by methyl group oxidation and is excreted in urine within 15 h of the end of exposure. Symptoms of acute toluene poisoning include irritated mucous membranes, headache and dizziness, somnolence, and, rarely, loss of consciousness.
Chronic poisoning is associated with pseudoneurotic disorders and possibly liver and kidney damage. This colorless, water-soluble solid is a derivative of pyridine, with a carboxyl group COOH at the 3-position.
Other forms of vitamin B3 include the corresponding amide nicotinamide, where the carboxyl group has been replaced by a carboxamide group CONH2 , as well as more complex amides and a variety of esters. Nicotinic acid and niacinamide are convertible to each other with steady world demand rising from 8, tons per year in the s to 40, in recent years .
Niacin cannot be directly converted to nicotinamide, but both compounds are precursors of the coenzymes nicotinamide adenine dinucleotide NAD and nicotinamide adenine dinucleotide phosphate NADP in vivo . NAD is important in catabolism of fat, carbohydrate, protein and alcohol, as well as cell signaling and DNA repair and NADP mostly in anabolism reactions such as fatty acid and cholesterol synthesis .
High energy requirements brain or high turnover rate gut, skin organs are usually the most susceptible to their deficiency. In animal models and in vitro, niacin produces marked anti-inflammatory effects in a variety of tissues-including the brain, gastrointestinal tract, skin and vascular tissue through the activation of NIACR1 .
Niacin has been shown to attenuate neuro-inflammation and may have efficacy in treating neuro-immune disorders such as multiple sclerosis and Parkinson's disease.
Niacin deficiency may target the gastrointestinal tract, as evidenced by diarrhea during pellagra, likely caused by the rapid cell turnover of these tissues. Niacin deficiency also causes inflammation and hyperplasia in the esophagus which would also promote cancer at this site. No work has been done on the epidemiology of niacin deficiency and skin cancer, although animal models of niacin deficiency and human familial DNA repair defects that mimic the sun sensitivity of pellagra are associated with an increase in skin cancer risk.
Maize consumption which causes niacin deficiency, have been associated with an increased frequency of gastric, colon, oral, or esophageal cancers. The biochemistry of vitamin B3 shows that high doses of Niacin increase the blood sugar levels in human and animals which can cause problems in cancer patients since cancer cells need glucose for respiration.
For the treatment, it is better to use nicotinamide and niacin for the prevention of cancer. Krutmann J, Humbert P Nutrition for healthy skin: Strategies for clinical and cosmetic practice. Springer Science Business Media. Diabetologia Zaminpira S, Niknamian S How butterfly effect or deterministic chaos theory in theoretical physics explains the main cause of cancer.
EC Cancer 2. J Natl Cancer Inst Int J Cancer Cancer Detect Prev Br J Cancer Environ Health Perspect Ann Oncol J Am Coll Nutr J of Parenteral and Enteral Nutrition Postgraduate Medicine British J of Dermatology Mutagenesis Felix CA Secondary leukemias induced by topoisomerase targeted drugs. Biochim Biophys Acta Kirkland JB Niacin and carcinogenesis.
Nutr Cancer Toth B Lack of carcinogenicity of nicotinamide and isonicotinamide following lifelong administration to mice. Oncology Cancer Res Front Biosci 1. Bryan GT The influence of niacin and nicotinamide on in vivo carcinogenesis.
Adv Exp Med Biol Free Radic Biol Med J Nutr Spronck JC, Kirkland JB Niacin deficiency increases spontaneous and etoposide-induced chromosomal instability in rat bone marrow cells in vivo.
Cancer prevention and screening: the next step in the era of precision medicine
Please review our updated policies, procedures, and information here. Read Advisory. The information below will discuss how this myth got started, what we know today, and identify what you can do to incorporate cancer-fighting foods within your routine. Berthelot would take various food substances i. When this ash was mixed with water, Berthelot was able to check the pH of each item. What he discovered was that items with a higher pH more alkaline were plant-based items such fruits and vegetables, while those with a lower pH more acidic were meats.
The Warburg effect may be the result of damage to the mitochondria in cancer, or an adaptation to low-oxygen environments within tumors, or a result of cancer.
What Causes Cancer?
The highest rates of oral cancer occur in the most disadvantaged sections of the population. Oral cavity, pharyngeal, and laryngeal cancer prevention approaches include avoiding or reducing risk factors like smoking, alcohol, and oral HPV infection. We appreciate your participation as it is critical to the success of this project.
Nicotinamide is a water-soluble amide form of niacin nicotinic acid or vitamin B3.