Islamabad - A study suggests that another known risk factor for osteoarthritis is obesity. This is partly because of the excess stress put on joints when carrying around more weight, but the connection between excess weight and osteoarthritis may run a little deeper than that.

A team of researchers from the Queensland University of Technology and the University of Southern Queensland, both in Australia, recently investigated a connection between dietary fat and the onset of osteoarthritis. The group was led by professors Yin Xiao and Lindsay Brown.

This recently published study follows on from Prof Xiao’s earlier work, which found that antioxidants and anti-cholesterol drugs may slow the progression of the joint damage attributed to the fatty acids found in foods such as palm oil and butter.

In this research project, Prof Xiao looked specifically at the effects of a diet rich in saturated fatty acids and simple carbohydrates on osteoarthritis. These dietary components mirror the nutritional elements commonly found in junk food - high fats and high carbohydrates

The study demonstrates that osteoarthritis may be less to do with the general usage of our joints and more to do with what we eat on a regular basis. As Prof Xiao says, “Our findings suggest that it’s not wear and tear but diet that has a lot to do with the onset of osteoarthritis.”

According to their results, a diet containing 20 percent saturated fats and simple carbohydrates “produced osteoarthritis-like changes in the knee.”

Prof Yin Xiao said that “Saturated fatty acid deposits in the cartilage change its metabolism and weaken the cartilage, making it more prone to damage. This would, in turn, lead to osteoarthritis pain from the loss of the cushioning effect of cartilage. We also found changes in the bone under the cartilage on a diet rich in saturated fat.”

Meanwhile a new research finds that high levels of a certain protein may increase obesity by suppressing the energy-producing action of brown and beige fat.

White fat mainly stores energy in the form of triglycerides - a type of fat commonly found in the blood, which may trigger conditions such as heart disease and diabetes if abnormally high. Brown fat, on the other hand, specializes in expending that energy by creating heat during exposure to cold temperatures, in a process known as thermogenesis.

There are also structural differences between these types of fat. Brown and beige fat have more mitochondria, which are also known as the “powerhouses” of the cell because they turn food into energy. White fat, on the other hand, has fewer mitochondria and blood vessels.

Specifically, in high amounts, Id1 inhibits the activity of the key transcription factor, PGC1 alpha. This transcription factor regulates thermogenesis by controlling the unique protein Ucp1, which, in turn, makes brown fat cells burn energy for heat more efficiently.

Additionally, the researchers found that Id1 inhibits another transcription factor, Ebf2, which usually helps white fat turn into beige.


Ande and team also demonstrated that removing Id1 increases the expression of the beige gene and Ucp1 in the response of white fat to cold exposure.

Furthermore, removing the Id1 protein did not seem to suggest that it is needed for normal functioning - at least not in mice.

According to the researchers, the findings suggest that the Id1 protein is a risk factor for obesity and diabetes, and it could be a target for reversing these two conditions.

“If we can target Id1, we may able to prevent and ultimately reduce the risk of obesity and related disease.”