Accidental Heat Therapy Saves Man Predicted to Develop Alzheimer’s Disease

An American man, Doug Whitney, whose genetics indicated a high likelihood of developing early-onset Alzheimer’s disease, has surprisingly managed to evade its effects. This remarkable outcome may be linked to unintentional heat exposure he experienced while working in a ship’s engine room, aligning with emerging evidence that suggests heat therapy could play a role in preventing symptoms of Alzheimer’s.

Whitney’s family carries the Presenilin 2 genetic variant, a mutation traced back to a small village in Volga, Germany, during the 18th century. Individuals with this mutation are typically predisposed to Alzheimer’s in their late 40s or early 50s.

“My family has been devastated by this disease,” Whitney remarked in a press statement. “My mother had 13 siblings, and 10 of them died before the age of 60. It was an epidemic.”

Despite sharing the same mutation, Whitney has reached his late 70s without experiencing significant memory loss or other Alzheimer’s symptoms, making him the only known mutation carrier to avoid the condition long after it was expected to manifest.

Dr. Jeffrey Kane from the French National Center for Scientific Research, became intrigued by Whitney’s case after discussing it with Dr. Randall Bateman, who has been studying Whitney for years.

At a conference, Kane presented research on the supportive effects of hyperthermia on mouse brains. A Finnish study found that frequent sauna users are 65% less likely to develop Alzheimer’s. Kane and colleague Emmanuel Planel from Université Laval in Quebec initiated a study to explore the underlying mechanisms.

The findings were compelling since Bateman knew of Whitney’s two-decade-long work in the extremely hot engine rooms of steam-powered naval vessels starting at age 18. Bateman discussed these circumstances with Kane and Planel, leading them to investigate further.

Engine room temperatures could soar up to 50°C (122°F), where Whitney would remain for extended periods, often needing to be hosed down to prevent overheating.

This prolonged heat exposure may have led to elevated levels of heat shock proteins in Whitney’s cerebrospinal fluid. These proteins are produced in response to heat and facilitate the repair and refolding of other proteins damaged by increased temperatures.

These heightened levels of heat shock proteins may have helped regulate tau, a crucial brain protein involved in Alzheimer’s disease. In affected individuals, tau misfolds and aggregates, which correlates with cognitive decline. Brain imaging studies reveal that Whitney’s brain holds negligible amounts of abnormal tau, likely explaining his absence of symptoms. Although his brain contains misfolded amyloid proteins associated with Alzheimer’s, symptoms remain unpredictable as evidenced in studies.

Support for their hypothesis emerged when Kane and Planel discovered that exposing mice to heat helped maintain the tau protein structure and facilitated increased clearance from the brain. Moreover, tau clearance was found to be more efficient in awake older adults compared to when they sleep, likely due to the natural elevation of body temperature during wakefulness.

Dr. Rebecca Nisbet from Australia’s Florey Brain Research Center notes that Whitney’s occupational heat exposure may elucidate his resistance to Alzheimer’s, yet genetic factors likely contribute as well. Whitney may carry a specific protective gene absent in affected family members, highlighting the complexity surrounding Alzheimer’s disease.

Nisbet has personally begun using saunas, inspired by this new evidence of their cognitive benefits. “I believe this is a harmless activity that can mitigate dementia risk,” she asserts.

Interestingly, regions with the lowest rates of cognitive impairment and Alzheimer’s in individuals over 60 tend to be located in very hot climates, such as Ballabgarh, India and the Bolivian Amazon. “While high temperatures alone can’t explain everything, they may be a significant contributing factor,” reflects Canet.

On the contrary, cold exposure could heighten Alzheimer’s risk. For instance, tau exhibits dysregulation in bears during hibernation, according to Nisbet. “The tau in a hibernating bear appears abnormal, yet normalizes promptly upon waking and warming up,” she explains.

Research has shown that general anesthesia, which lowers body temperature, can contribute to short-term cognitive issues reminiscent of Alzheimer’s disease, potentially due to its effects on tau. “Caution is advised in mouse studies, as prolonged anesthesia can lead to tau dysregulation,” warns Nisbet.