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Ceffer
2018 Jul 19, 7:51pm
Ceffer
2018 Jul 19, 7:51pm
Stoopid Millenials can't even consume a healthy, longevity inducing substance without killing themselves.
2
anonymous
2019 Feb 1, 1:28am
Liver cirrhosis: Once thought to be irreversible, cirrhosis of the liver now seems treatable — and drug development is proceeding apace.
When people talk about scars, they often speak of indelible reminders of old wounds. For most of the twentieth century, liver cirrhosis — a condition defined by extensive scarring of the liver — was similarly thought to be irreversible.
However, researchers now know that this is not necessarily true. If the underlying disease process can be thwarted, mechanisms intrinsic to the liver can begin to resolve the scarring. Although a few studies had hinted at the liver’s resilience, only after the broad introduction of effective treatments for the viral liver infections hepatitis B and hepatitis C did clinicians become widely convinced.
Scientists have also gained a deeper understanding of the biology of scar formation (fibrosis) and regression, and numerous drug companies are redoubling efforts to find interventions that can help to halt scarring or even remove existing scars.
Biologists refer to scar formation as fibrosis because scar tissue is comprised mainly of collagen fibres rather than cells. Laying down these bundles of protein — a process known as fibrogenesis — is the body’s basic response to injury. But injury to the liver — induced by alcohol abuse, non-alcoholic fatty liver disease, the viruses that cause hepatitis and several other conditions — can lead to ongoing fibrogenesis.
Fibrosis is mediated by cells known as myofibroblasts. In the liver, most myofibroblasts are derived from hepatic stellate cells (HSCs) — enigmatic cells that store vitamin A. Drug companies are aiming both to prevent the activation of these HSCs, stopping them from becoming myofibroblasts, and to suppress the fibrogenic functions of activated cells.
No drug is yet approved for treating cirrhosis, but one approach involves blocking the activity of chemical messengers that initiate fibrogenesis. A drug that binds to receptors for signaling molecules called cytokines is in an advanced clinical trial. Frustratingly, however, many of the chemical messengers that instigate fibrosis have crucial functions beyond the liver — raising concerns about potential side effects. Another strategy, which involves blocking the intracellular signaling pathways that maintain HSC activation, is similarly prone to unwanted effects.
More Including short video: https://www.nature.com/articles/d41586-018-07759-2
When people talk about scars, they often speak of indelible reminders of old wounds. For most of the twentieth century, liver cirrhosis — a condition defined by extensive scarring of the liver — was similarly thought to be irreversible.
However, researchers now know that this is not necessarily true. If the underlying disease process can be thwarted, mechanisms intrinsic to the liver can begin to resolve the scarring. Although a few studies had hinted at the liver’s resilience, only after the broad introduction of effective treatments for the viral liver infections hepatitis B and hepatitis C did clinicians become widely convinced.
Scientists have also gained a deeper understanding of the biology of scar formation (fibrosis) and regression, and numerous drug companies are redoubling efforts to find interventions that can help to halt scarring or even remove existing scars.
Biologists refer to scar formation as fibrosis because scar tissue is comprised mainly of collagen fibres rather than cells. Laying down these bundles of protein — a process known as fibrogenesis — is the body’s basic response to injury. But injury to the liver — induced by alcohol abuse, non-alcoholic fatty liver disease, the viruses that cause hepatitis and several other conditions — can lead to ongoing fibrogenesis.
Fibrosis is mediated by cells known as myofibroblasts. In the liver, most myofibroblasts are derived from hepatic stellate cells (HSCs) — enigmatic cells that store vitamin A. Drug companies are aiming both to prevent the activation of these HSCs, stopping them from becoming myofibroblasts, and to suppress the fibrogenic functions of activated cells.
No drug is yet approved for treating cirrhosis, but one approach involves blocking the activity of chemical messengers that initiate fibrogenesis. A drug that binds to receptors for signaling molecules called cytokines is in an advanced clinical trial. Frustratingly, however, many of the chemical messengers that instigate fibrosis have crucial functions beyond the liver — raising concerns about potential side effects. Another strategy, which involves blocking the intracellular signaling pathways that maintain HSC activation, is similarly prone to unwanted effects.
More Including short video: https://www.nature.com/articles/d41586-018-07759-2
The authors noted a sharp spike in mortality starting in 2009. The reason for the spike is unclear, but Dr. Neehar Parikh, a liver specialist at the University of Michigan Medical School and Tapper's co-author, has a theory.
"It correlates with the global financial crisis," Parikh says. "We hypothesize that there may be a loss of opportunity, and the psychological burden that comes with that may have driven some of those patients to abusive drinking."
The increase among younger Americans is particularly troubling, because it kills people in the prime of their life.
"Each young patient that dies is a tragedy," says Parikh. "It's years of life lost."
The study is the latest to confirm that liver-related illnesses are becoming increasingly prevalent. A report published Tuesday by the CDC shows that the age-adjusted death rate from liver cancer has increased 43 percent since 2000. And a recent study of veterans found that cirrhosis cases nearly doubled between 2001 and 2013.
But Dr. Vijay Shah, who heads the Division of Gastroenterology and Hepatology at the Mayo Clinic and was not involved with this research, says that the study's emphasis on young Americans is new.
"Alcohol-related liver cirrhosis used to be considered a disease that would happen after 30 years of heavy alcohol consumption," Shah says. "But this study is showing that these problems are actually occurring in individuals in their 20s and 30s."
"There has been a shift in the kind of patient we're seeing," agrees Dr. Sumeet Asrani, a liver specialist practicing in Dallas who did not contribute to the study. "It fits with what we see in practice. We're seeing younger and younger patients with alcoholic liver disease."
Despite the recent increase, cirrhosis remains a relatively minor cause of death for young Americans, accounting for only 1.4 percent of total deaths in the 25-34 age range. But it's much more significant for young Native Americans, accounting for 6.3 percent of deaths.
Tapper thinks the problem is only going to get worse. Some conditions that cause liver trouble, like hepatitis C, have been falling. But other risk factors, including obesity, are on the rise. Alcohol consumption and obesity could interact to worsen liver disease, Tapper says.
Tapper says he thinks that policy could play a role in addressing the problem. For instance, strategic taxation of alcoholic beverages could deter consumption, just as raising the taxes on cigarettes has been shown to reduce smoking. He cites the example of Scotland, which recently set minimum prices for units of alcohol to deter binge drinking. He also points to public health interventions, such as counseling, that help people quit drinking.
The good news is that liver disease is often reversible. Many patients can recover if they stop drinking soon enough.
"I've had patients who came to me in a wheelchair," Tapper says. "Three months later, they're shoveling snow and their lab tests are normal. It's always because they made that choice to stop drinking."
https://www.npr.org/sections/health-shots/2018/07/18/630275042/a-spike-in-liver-disease-deaths-among-young-adults-fueled-by-alcohol