An extract on #powerbuilding
Jouko is best known for winning both the 1997 and 1999 World's Strongest Man, and finishing second in 1998. Ahola also won the Europe's Strongest Man contest twice, in 1998 and 1999, and finished fourth in 1996. Jouko won the World's Strongest Team in 1997 and 1999, and was second in 1998.
Ahola set world records for the Hercules hold (45.7 sec, 197 kg) and Atlas Stones (215 kg).
He is one of only seven men to be a repeat champion in the World's Strongest Man competition.
Jouko was a very successful strongman competitor, at 6' 1" (1.85 m) and 275 lbs (125 kg), corresponding to a BMI of 35.8, which is low by WSM standards.
After his strongman career, Ahola has directed his focus towards films. So far, his most notable roles have been in Kingdom of Heaven, Bad Day to Go Fishing, War of the Dead and Invincible.
Ahola starred in Werner Herzog's 2001 film Invincible as early 20th century Jewish strongman Zishe Breitbart. Jouko played a former world wrestling champion in Alvaro Brechner's 2009 film Bad day to go fishing, (Mal da para pescar). The film premiered at Cannes Film Festival.
Jouko appeared in the music video for Robin's "Faija skitsoo" in 2012. He also made a cameo appearance on the second season of The Dudesons TV series, which aired worldwide in 2008.
Jouko also serves as a judge and event organizer for the World's Strongest Man contest.
In 2013 he appears in the new History Channel series Vikings.
The cause of IBM is unknown. IBM likely results from the interaction of a number of genetic and environmental factors.
There are two major theories about how sIBM is caused. One hypothesis suggests that the inflammation-immune reaction, caused by an unknown trigger likely an undiscovered virus or an autoimmune disorder is the primary cause of sIBM and that the degeneration of muscle fibers and protein abnormalities are secondary features. Despite the arguments "in favor of an adaptive immune response in sIBM, a purely autoimmune hypothesis for sIBM is untenable because of the disease's resistance to most immunotherapy."
The second school of thought advocates the theory that sIBM is a degenerative disorder related to aging of the muscle fibers and that abnormal, potentially pathogenic protein accumulations in myofibrils play a key causative role in sIBM (apparently before the immune system comes into play). This hypothesis emphasizes the abnormal intracellular accumulation of many proteins, protein aggregation and misfolding, proteosome inhibition, and endoplasmic reticulum (ER) stress.
One review discusses the "limitations in the beta-amyloid-mediated theory of IBM myofiber injury."
Dalakas (2006) suggested that a chain of events causes IBMsome sort of virus, likely a retrovirus, triggers the cloning of T cells. These T cells appear to be driven by specific antigens to invade muscle fibers. In people with sIBM, the muscle cells display flags telling the immune system that they are infected or damaged (the muscles ubiquitously express MHC class I antigens) and this immune process leads to the death of muscle cells. The chronic stimulation of these antigens also causes stress inside the muscle cell in the endoplasmic reticulum (ER) and this ER stress may be enough to cause a self-sustaining T cell response (even after a virus has dissipated). In addition, this ER stress may cause the misfolding of protein. The ER is in charge of processing and folding molecules carrying antigens. In IBM, muscle fibers are overloaded with these major histocompatibility complex (MHC) molecules that carry the antigen protein pieces, leading to more ER stress and more protein misfolding.
A self-sustaining T cell response would make sIBM a type of autoimmune disorder. When studied carefully, it has not been impossible to detect an ongoing viral infection in the muscles. One theory is that a chronic viral infection might be the initial triggering factor setting IBM in motion. There have been a handful of IBM casesapproximately 15that have shown clear evidence of a virus called HTLV-1. The HTLV-1 virus can cause leukemia, but in most cases lies dormant and most people end up being lifelong carriers of the virus. One review says that the best evidence points towards a connection with some type of retrovirus and that a retroviral infection combined with immune recognition of the retrovirus is enough to trigger the inflammation process.
The hypothesis that beta amyloid protein is key to IBM has been supported in a mouse model using an A vaccine that was found to be effective against inclusion body myositis in mouse models. Although this vaccine is likely not safe for human use, it still shows that attacking A has efficacy in mice against IBM.
Following up on earlier leads, the Greenberg group report finding that the protein TDP-43 is a very prominent and highly sensitive and specific feature of IBM. This protein is normally found within the nucleus but in IBM is found in the cytoplasm of the cell. This important advance should help develop a new screening technique for IBM and may provide clues in terms of a therapeutic approach