I was asked to the recent International Polio Conference to speak about our carnitine research here in WA. I have been meaning to simplify for the newsletter, what we have learnt since we started looking at blood levels of carnitine back in 1996 – so here’s 12-years worth of our carnitine journey. We couldn’t have done it without all of you – our members who have gone and had those blood tests done! There is also a 2016 update available.
Carnitine is an amino acid ie part of protein, and is found in our diet primarily in red meat. Avocado is the only reasonable plant source. The redder the meat the better – pork has only half and chicken only one tenth of the carnitine in red meat! We should get 75% of our needs from our diet and our bodies can make 25% – but only if the other nutrients needed are present in the body and you have muscles to store it!
How it really works. Carnitine transports protein fats into the cell so they can be broken down to produce energy to run the body. More energy is produced this way than using carbohydrate foods. Insulin is needed for energy from blood glucose – carbohydrate foods (yield is 36 ATP) but carnitine is needed to get energy from protein fat (energy yield this way is 129 ATP ie longer energy).
We have 2 types of muscles – Type 1 muscles use protein fats as fuel and Type 2 muscles use glucose. There are corresponding nerve types that make these muscles work. Swedish polio research by Borg & Grimby in Post Polio Syndrome by Halsteadi & Grimby Mosby USA 1995 showed that in muscle biopsies on polio muscle there were more Type 1 muscles and that some were abnormal Type 1 that were not as efficient.
This correlates with research documented in Human Physiology by D Moffett Mosby USA 1993 where switching of nerve type changes muscle type and fuel needed. This is in line with the accepted theory of ”sprouting” of remaining nerve endings to enable recovery of muscles affected by polio at the time of acute polio. The rest of this article can be seen here.