Posted on Diabetes

Do sex differences in how we respond to insulin explain why type 2 diabetes is more common in men?

“In insulin resistance, fat cells are less sensitive to insulin and so both of these processes are impaired. This can lead to more fat circulating in the bloodstream, which raises the risk of T2D.
“In insulin resistance, fat cells are less sensitive to insulin, so both processes are impaired. This can lead to more fat circulating in the bloodstream, which raises the risk of diabetes.

New research could help explain why type 2 diabetes is more common in men than in women.

“Previous studies have shown that men develop type 2 diabetes ( at a younger age and a lower weight than women and, overall, men appear to be at higher risk of the condition,” says lead researcher Dr Daniel P Andersson, at the Department of Endocrinology, Karolinska University Hospital Huddinge, Stockholm, Sweden. “One reason for this may be differences in how the sexes’ adipose tissue responds to insulin. 

“Adipose tissue is the main organ for the storage of excess energy, and this is done in lipids called triglycerides, which consist of free fatty acids. When there is excess energy, insulin decreases the breakdown of triglycerides (lipolysis) releases free fatty acids to the blood and increases energy storage as triglycerides (lipogenesis) in fat cells.

“If the insulin resistance of adipose cells is more pronounced, or severe, in men than in women, this could help explain why T2D is more common in men than women.”

To explore this further, Dr Andersson measured the adipose insulin resistance index (AdipolR, a measure of insulin sensitivity of fat cells, with higher values indicating more insulin resistance) in 2,344 women and 787 men, with an average age of 44 years and BMI of 35 kg/m2.

Men had higher AdipoIR values than women, but only when obesity (body mass index 30 kg/m² or more) was present. This was the case both for physically active and sedentary people, in those with and without cardiometabolic disease and in people using nicotine and not.

In a subgroup of 259 women and 54 men living with obesity, the researchers also took biopsies from the adipose tissue to study the effect of insulin on isolated fat cells.

This showed clear differences between the sexes. In men, compared to women, a 10-fold higher concentration of insulin was needed to block the breakdown of triglycerides to fatty acids, and the blockage was also less effective in men.

However, the storage capacity of the fat cells was similar for both sexes.

Dr Andersson explains: “In individuals who are living with obesity, you often have an excess of energy available in the body and insulin should decrease the release of fatty acids and increase the storage of lipids in adipose tissue to reduce the free fatty acids circulating in the blood.

“When looking at sex differences, we found that men who were living with obesity had increased adipose insulin resistance and higher levels of free fatty acids in the blood.

“The differences seen between men and women were mainly related to decreased ability of insulin to block the breakdown of fatty acids in fat cells from men rather than sex differences in storage capacity.

“Fatty acids in the bloodstream have effects in the liver, muscle and the pancreas and could lead to further local insulin resistance in these organs, creating a vicious circle that, over time, could lead to development of type 2 diabetes.”

The researchers conclude that in individuals who are living with obesity, adipose tissue insulin resistance is more severe in men than in women, which may partly explain why T2D is more common in men.

Posted on Fibromyalgia

Fibromyalgia and Long Covid : Why They Are Confusing Medicine Completely

In this video, we talk about Fibromyalgia and Long Covid ( residual symptoms after Covid infection) . Both diseases have confusing symptoms, what this means for patients’ lives, and how they function. After observing these conditions, we say there is a fair amount of overlap. We explain why this is the case. And provide resources for improved treatment /functioning.

Posted on Mental health

‘How I rewired my brain in six weeks’

There is growing evidence that simple, everyday changes can alter our brains and how they work.   So, how do we keep our brains healthy?   BBC journalist Melissa Hogenboom explores the latest scientific research and has her brain scanned and analysed, with intriguing results.

Posted on Multiple Sclerosis, Patient Talk

Interferon-beta regulates excessive alternative splicing in multiple sclerosis

Journal of Interferon & Cytokine Research (JICR)

The authoritative peer-reviewed source for research, analysis, and advances on the therapeutic role of cytokines and IFNs. CREDIT Mary Ann Liebert, Inc.

A new study found extensive alternative splicing of messenger RNA in the blood cells of untreated multiple sclerosis patients compared to healthy controls. The study, which showed that highly dysregulated alternative splicing was largely corrected by interferon-ß (IFN- ß) therapy, was published in the peer-reviewed Journal of Interferon & Cytokine Research (JICR). 

Anthony Reder and Xuan Feng, from the University of Chicago Department of Medicine, and coauthors reported that during long-term IFN- ß therapy, multiple sclerosis exacerbations were linked to more dysregulated alternative splicing. Furthermore, alternative splicing predicted future clinical exacerbations.

“Alternative splicing is a potential biomarker warning of disease activity and for predicting therapeutic response to IFN- ß treatment,” stated the investigators. “Alternative splicing in multiple sclerosis suggests new directions for investigation of disease mechanisms, therapeutic monitoring, and drug choices in multiple sclerosis and in autoimmune and viral diseases.”

“These novel findings demonstrate that measurement of alternatively spliced mRNA transcript levels in blood leukocytes from patients with multiple sclerosis may help to predict clinical responsiveness to IFN-b therapy,” says Journal of Interferon & Cytokine Research Executive Editor Raymond Donnelly, PhD.