Iron Game
Veteran
Despite an ominous past, researchers have given an outlawed diet drug from the 1930s hope for resurrection. In addition to potentially reversing diabetes, 2,4 Dinitrophenol may also eliminate a fatty liver.
In general, drugs that cause more harm than good become banned substances – a consequence intended to protect humans from harm. Banning a drug typically relegates it to the grave, rendering it useless. Despite the good intentions of drug regulating agencies, a banned drug’s future disease-curing potential is seldom discovered.
About a Fatty Liver
Estimated to affect between 10 and 46 percent of American adults,*fatty liver disease*is the most common liver disorder in Western industrialized countries. A fatty liver (steatosis) is one of the most common reasons for abnormal liver blood tests. The liver is actively involved in processing fat. Normally, the liver alters the form of fat in the blood, manufactures fat and metabolizes fat. When any aspect of these fat-related jobs becomes unbalanced, fat droplets can accumulate in the liver.
Although steatosis rarely causes any major problems, about 10 to 20 percent of those affected go on to a more advanced form of fatty liver known as nonalcoholic steatohepatitis (NASH).*NASH*is a serious illness in which inflammation and scarring can provoke cancer and liver failure. Currently, there are no medications available to treat steatosis or NASH.
About 2,4 Dinitrophenol
Originally used as an industrial chemical and explosive, 2,4 Dinitrophenol (DNP) gained notoriety during World War I. This chemical was used excessively by French munitions workers during that time, and heavy exposure to DNP was linked to weight loss. A 1931 study released by Stanford University clearly stated DNP’s effects on shedding body fat, and drugmakers began including DNP into diet pills. It didn’t take long for DNP to reveal its hazards, which included cataracts and death. By 1938, the U.S. Food and Drug Administration (FDA) banned DNP because of the numerous fatalities it caused.
Scientists believe that DNP works by inhibiting ATP (adenosine triphosphate) molecule. ATP is used in transporting energy within the body’s cells. Your body:
converts adenosine diphosphate into ATPconverts ATP back to adenosine phosphate after it is used
2,4 Dinitrophenol inhibits this energy transportation process. The excess energy is expelled as heat – which burns up to 50 percent more calories than usual. The overall effect of DNP is that this chemical increases body temperature and metabolic rate – sometimes to a fatal level. However, new research breathes a second chance into this chemical that the U.S. government once branded “extremely dangerous and not fit for human consumption.”
Hope for DNP
Skipping over the obvious danger of overheating to the point of death, DNP demonstrates an extremely valuable ability. DNP alters the activity of mitochondria (the cellular component where ATP is manufactured), forcing the body to burn fat. In addition, this banned chemical has been found to boost insulin sensitivity. People with a fatty liver and/or diabetes often have insulin resistance, a condition where cells don’t respond normally to the hormone that controls blood sugar levels. By boosting insulin sensitivity, DNP improves blood sugar levels.
Researchers from Yale University decided to design a safer version of DNP that would retain its benefits. First, researchers tried to limit the effects of the drug by creating a version that is active mainly in the liver. As reported in a 2013 study, this version of the drug was about one-tenth as toxic as standard DNP while reducing fat in the liver and improving insulin sensitivity. Nonetheless, scientists yearned for even more encouraging results.
Then, a 2015 study published in the journalScience*documented the results of a slow-release version of DNP. Their work could be a turning point in the global battle against a fatty liver:
By reducing the amount of drug in the bloodstream at any one time, the slow-release DNP is safer than the original banned substance.When fed to rats that consume a fat-laden diet and develop their own version of a fatty liver, the slow-release drug slashed their liver fat levels by about 90 percent.Rodents that consumed the slow-release DNP also saw improvements in their insulin sensitivity and blood glucose quantities.In rats with NASH, the slow-release DNP reduced fibrosis, the scarring that can cause cirrhosis and liver failure.Slow-release DNP also reversed diabetes in affected rats.The researchers determined the slow-release version to be safer than the liver-targeted version of DNP.
Although there is a long way to go before DNP is resurrected and approved, the slow-release version represents an exciting possibility for the millions of people trying to restore a healthful balance of fat within their liver.
In general, drugs that cause more harm than good become banned substances – a consequence intended to protect humans from harm. Banning a drug typically relegates it to the grave, rendering it useless. Despite the good intentions of drug regulating agencies, a banned drug’s future disease-curing potential is seldom discovered.
About a Fatty Liver
Estimated to affect between 10 and 46 percent of American adults,*fatty liver disease*is the most common liver disorder in Western industrialized countries. A fatty liver (steatosis) is one of the most common reasons for abnormal liver blood tests. The liver is actively involved in processing fat. Normally, the liver alters the form of fat in the blood, manufactures fat and metabolizes fat. When any aspect of these fat-related jobs becomes unbalanced, fat droplets can accumulate in the liver.
Although steatosis rarely causes any major problems, about 10 to 20 percent of those affected go on to a more advanced form of fatty liver known as nonalcoholic steatohepatitis (NASH).*NASH*is a serious illness in which inflammation and scarring can provoke cancer and liver failure. Currently, there are no medications available to treat steatosis or NASH.
About 2,4 Dinitrophenol
Originally used as an industrial chemical and explosive, 2,4 Dinitrophenol (DNP) gained notoriety during World War I. This chemical was used excessively by French munitions workers during that time, and heavy exposure to DNP was linked to weight loss. A 1931 study released by Stanford University clearly stated DNP’s effects on shedding body fat, and drugmakers began including DNP into diet pills. It didn’t take long for DNP to reveal its hazards, which included cataracts and death. By 1938, the U.S. Food and Drug Administration (FDA) banned DNP because of the numerous fatalities it caused.
Scientists believe that DNP works by inhibiting ATP (adenosine triphosphate) molecule. ATP is used in transporting energy within the body’s cells. Your body:
converts adenosine diphosphate into ATPconverts ATP back to adenosine phosphate after it is used
2,4 Dinitrophenol inhibits this energy transportation process. The excess energy is expelled as heat – which burns up to 50 percent more calories than usual. The overall effect of DNP is that this chemical increases body temperature and metabolic rate – sometimes to a fatal level. However, new research breathes a second chance into this chemical that the U.S. government once branded “extremely dangerous and not fit for human consumption.”
Hope for DNP
Skipping over the obvious danger of overheating to the point of death, DNP demonstrates an extremely valuable ability. DNP alters the activity of mitochondria (the cellular component where ATP is manufactured), forcing the body to burn fat. In addition, this banned chemical has been found to boost insulin sensitivity. People with a fatty liver and/or diabetes often have insulin resistance, a condition where cells don’t respond normally to the hormone that controls blood sugar levels. By boosting insulin sensitivity, DNP improves blood sugar levels.
Researchers from Yale University decided to design a safer version of DNP that would retain its benefits. First, researchers tried to limit the effects of the drug by creating a version that is active mainly in the liver. As reported in a 2013 study, this version of the drug was about one-tenth as toxic as standard DNP while reducing fat in the liver and improving insulin sensitivity. Nonetheless, scientists yearned for even more encouraging results.
Then, a 2015 study published in the journalScience*documented the results of a slow-release version of DNP. Their work could be a turning point in the global battle against a fatty liver:
By reducing the amount of drug in the bloodstream at any one time, the slow-release DNP is safer than the original banned substance.When fed to rats that consume a fat-laden diet and develop their own version of a fatty liver, the slow-release drug slashed their liver fat levels by about 90 percent.Rodents that consumed the slow-release DNP also saw improvements in their insulin sensitivity and blood glucose quantities.In rats with NASH, the slow-release DNP reduced fibrosis, the scarring that can cause cirrhosis and liver failure.Slow-release DNP also reversed diabetes in affected rats.The researchers determined the slow-release version to be safer than the liver-targeted version of DNP.
Although there is a long way to go before DNP is resurrected and approved, the slow-release version represents an exciting possibility for the millions of people trying to restore a healthful balance of fat within their liver.
