Constant Pain Can Lead to Diabetes, High Cholesterol and Heart Problems

/

By Dr. Forest Tennant, PNN Columnist

Intractable Pain Syndrome (IPS) is constant pain with cardiovascular, metabolic and hormonal complications. Constant pain is a severe stressor that causes the adrenal hormones cortisol and adrenalin to rise in the blood as the body attempts to reduce stress.

These hormonal elevations can lead to serious metabolic consequences that need to be well known to persons who have IPS, as well as their family and medical practitioners. High levels of adrenalin cause blood pressure and the pulse rate to rise. When cortisol is elevated, it causes the hormone insulin and blood sugar (glucose) to rise in the blood.

If blood sugar remains too high for too long, a person can develop diabetes or pre-diabetes, which is often called “insulin resistance.” Most persons believe that diabetes is a metabolic disease and is unrelated to hormones. The fact is that insulin, cortisol and adrenaline are hormones.

In addition to diabetes, a person with constant pain is also at high risk of developing or experiencing any or all of the following: 

  • Heart Attack

  • Heart Pain (Angina)

  • Stroke

  • Dementia

  • Arteriosclerosis

Some persons with IPS have died suddenly and unexpectedly, sometimes while asleep. Often these cases are falsely labelled as a drug overdose.

There are three reasons for sudden, unexpected death in persons with IPS who are undertreated and have cardiovascular, metabolic and hormonal complications.

  • Cardiac Arrythmia

  • Adrenal Failure          

  • Hypoglycemia (Excess Insulin)

Every person with IPS needs to be evaluated for diabetes, pre-diabetes, hypertension, tachycardia and excess cholesterol. Steps must be taken to eliminate or reduce any or all of these IPS complications. Consult your medical practitioner at your earliest opportunity for an evaluation of these complications. 

Forest Tennant, MD, DrPH, is retired from clinical practice but continues his research on intractable pain and arachnoiditis. This column is adapted from newsletters recently issued by the IPS Research and Education Project of the Tennant Foundation. Readers interested in subscribing to the newsletter can sign up by clicking here. The Tennant Foundation gives financial support to Pain News Network and sponsors PNN’s Patient Resources section.     

Genetic Variation Raises Risk of Post-Traumatic Pain

/

By Pat Anson, Editor

If you have chronic pain because of an accident, injury or assault, it could be because you have a genetic variation that makes you more likely to develop post-traumatic pain.

That’s the key finding behind a new study published in the Journal of Neuroscience. Researchers at the University of North Carolina studied over 1,500 people who were admitted to emergency rooms for trauma after a motor vehicle collision.

In addition to genotyping the patients, the researchers assessed their distress immediately after the accident, as well as their pain and post-traumatic stress symptoms six weeks later. Participants with a particular variant in the gene FKBP5 reported more severe pain and distress at follow up.

FKBP5 is a critical regulator of the stress response and affects how we respond to environmental stimuli. Previous studies have shown that certain variants of the gene play a role in the development of neuropsychiatric disorders such as post-traumatic stress disorder, depression, suicide risk and aggressive behavior.

UNC School of Medicine researchers were the first to show an association between FKBP5 and post-traumatic chronic pain. A 2013 study found that people with a particular variation of the gene are likely to experience more pain after exposure to trauma compared to people who don't have the variant.

The new study by the same research group builds on that discovery by showing that the variation inhibits the regulation of cortisol, a stress hormone that sensitizes peripheral nerves. People with high levels of cortisol are likely to experience more pain.

"In our current study, we showed that the reason this variant affects chronic pain outcomes is because it alters the ability of FKBP5 to be regulated by a microRNA called miR-320a," said lead author Sarah Linnstaedt, PhD, a professor of anesthesiology and an investigator in the UNC Institute for Trauma Recovery.

"In other words, it does not negatively regulate FKBP5, thus causing FKBP5 to be over-expressed. High levels of FKBP5 can be detrimental because it alters natural feedback mechanisms that control circulating cortisol levels."

Linnstaedt says the findings suggest there could be new therapeutic approaches to treating traumatic pain, such as medication that inhibits the activity of FKBP5 or gene editing that alters the variation.

Funding for the UNC study was provided by the National Institute of Arthritis, Musculoskeletal, and Skin Diseases, The Mayday Fund, a Future Leaders in Pain Grant from The American Pain Society, and the National Human Genome Research Institute.