Using an animal model, the study鈥檚 researchers found that the motor performance and muscle endurance of mice with ALS improved when they were given higher than normal doses of vitamin D.

鈥淲e are the only group in Canada that is looking at the connection between dietary interventions and the effects on the ALS model,鈥� says 91亚色 kinesiology Professor Mazen Hamadeh (left)聽of the University鈥檚 Muscle Health Research Centre in the Faculty of Health. Hamadeh supervised the research led by 91亚色 master of science degree students Jesse Solomon and Alexandro Gianforcaro in the School of Kinesiology & Health Science.

The researchers conducted three different studies looking at different amounts of vitamin D. The first looked at the effects of 10 times the adequate intake of vitamin D on the ALS animal model 鈥� the equivalent of 8,000 IU/day in humans. Results showed an improvement in both motor performance and endurance, but no change to disease outcomes, such as onset, progression or lifespan.

鈥淲e followed up with another study because we thought we didn鈥檛 give high enough amounts of vitamin D,鈥� says Hamadeh. In the second study, the amount of vitamin D was increased to 50 times the suggested adequate intake amount or the equivalent of 40,000 IU per day in humans. Again, there was definite improvement in functional outcomes, but not in disease outcomes, confirming the findings of the first study, he says.

The researchers then thought that perhaps the recommended adequate intake amount of vitamin D was set too high and there was already an overabundance of vitamin D being administered. That led to a third study where only one fortieth of the recommended adequate intake amount was administered using the animal model, which induced a vitamin D deficiency. This study was published in PLoS ONE, an international online peer-reviewed journal, on Dec. 27.

This third study produced some interesting results, says Hamadeh. When vitamin D deficiency was induced before disease onset, disease severity was reduced, but after disease onset, it was worse. 鈥淪o at very low levels there is something happening in the cell that is causing them to function better only for a little bit of time, only until disease onset, than they progress regularly,鈥� he says.

The key now is to find out what molecular changes are occurring in the muscle, spinal cord and brain when vitamin D is administered, and that is what Hamadeh and his students are currently working on.

鈥淎LS is the most common motor neuron disease and up until now there is no cure for it. It is also a fast-progressing disease. Between diagnosis and death, there are usually two to five years. We are trying to see whether by modulating the diet, by changing the diet, we can influence not only when the disease starts, but how fast it progresses and whether it can affect lifespan,鈥� says Hamadeh.

鈥淭o find a dietary intervention that could influence a fast-paced disease after diagnosis of the disease, meaning after some irreversible damage has happened, means this particular nutrient has to be very powerful to either halt or slow the pace of the disease.鈥�

The model Hamadeh works with suffers from heightened oxidative stress, a state of increased levels of free radicals or oxidants that are produced naturally inside the cell during normal functioning and metabolism. There is an association between oxidative stress and chronic, metabolic, autoimmune, neurodegenerative and neuromuscular diseases, including ALS, Type 1 and Type 2 diabetes, cardiovascular disease, obesity, hypertension, Alzheimer鈥檚, Parkinson鈥檚 and multiple sclerosis.

Hamadeh hopes his research and that of his students will help not only ALS, but many other similar diseases that share common mechanisms with ALS.

By Sandra McLean, YFile writer

Republished courtesy of YFile鈥� 91亚色鈥檚 daily e-bulletin.

The post High doses of vitamin D might affect Lou Gehrig's disease appeared first on Research & Innovation.

The research, which looked at the effects of caloric restriction in a mouse model of ALS, found that restricting caloric intake to 60 per cent of the usual mouse diet significantly hastened the onset and progression of ALS, as well as death. It is the first study to demonstrate that caloric restriction in animal models of ALS produces molecular-level changes that lead to cell death.

The study was published today by the open access peer reviewed journal Public Library of Science (). Former 91亚色 graduate student Barkha P. Patel, supervised by assistant professor Mazen J. Hamadeh (left), led the research at 91亚色鈥檚 Muscle Health Research Centre, in collaboration with researchers at McMaster University.

鈥淩esearch has shown that restricting calories can extend lifespan in animals, so we were surprised to find during an earlier study with the same animal model of ALS that it actually hastened the clinical onset of the disease,鈥� said Hamadeh, of the School of Kinesiology and Health Science in 91亚色鈥檚 . 鈥淚n this study, we set out to discover how caloric restriction actually led to changes at the molecular level.鈥�

ALS, also known as Lou Gehrig鈥檚 Disease, is characterized by degeneration of motor neurons in the brain and spinal cord and is associated with an increase in oxidative stress 鈥� the physiological stress on the body that is caused by damage from free radicals that are not neutralized by antioxidants.

The study sought to unravel the mechanism behind the acceleration of the clinical onset and progression of ALS when calories are restricted. It found that caloric restriction shortens lifespan through an increase in protein involved in lipid damage, inflammation and cell death.

If the results from the animal model of ALS are extrapolated to patients with the disease, caloric restriction would be contraindicated, Patel said.

For more information about nutrition research in ALS at 91亚色, visit Hamadeh's Web site.

By Janice Walls, media relations coordinator. Republished courtesy of 91亚色 Media Relations.

The post Cutting calories may accelerate ALS, 91亚色 researchers suggest appeared first on Research & Innovation.