The Tennessee Titans and the broader NFL community received tragic news this week when former Titans running back Chris Johnson revealed his ALS diagnosis publicly. The announcement sent shockwaves through the community, and also raised some familiar questions about the long-term health risks facing football players after their careers end.

To better understand the disease, its connection to the sport, and where the science stands, I sat down with an expert. Dr. Jinsy Andrews, director of the ALS clinic and director of clinical trials at NYU Langone Health, was kind enough to join me to discuss ALS, CTE, and how we know about their connection to football.

What ALS is and why football players are at increased risk

ALS, or amyotrophic lateral sclerosis, is commonly known in the United States as Lou Gehrig’s disease. Dr. Andrews did not mince words about just how brutal it is.

“It’s a tough disease. Some say it’s even worse than cancer,” Andrews said. “It is something that causes progressive weakness of your arms, your legs. It takes away your speech and your swallowing function and even your breathing, and most people pass away from the lack of ability to breathe in 3 to 5 years from their symptom onset.”

There is no cure. The majority of cases (roughly 90%) are sporadic, meaning scientists cannot trace them to a specific genetic cause. But researchers are learning more about risk factors, and that’s where the connection to football gets concerning.

Andrews pointed to a 2021 study that examined NFL players who played from 1960 to 2019. That group was 4 times more likely to develop ALS than the general population. Players who developed ALS also tended to have longer NFL careers than those who did not.

The concussion connection and beyond

The instinct for football fans is to connect ALS risk (along with all other neurological issues) to concussions and repetitive head impacts, and there is reason for that. The same researchers behind the 2021 ALS study were involved in early investigations of chronic traumatic encephalopathy (CTE). But Andrews was careful to distinguish between them. CTE involves psychiatric symptoms like suicidality, mood swings, and memory loss that are not typically present in ALS alone. They aren’t the same, but they’re more connected than I realized.

The connection to physical trauma extends beyond football. Andrews noted that U.S. military veterans with 6 months of active duty face 2 times greater risk of developing ALS than the general population.

“Scientists are still trying to figure out what it is that’s specific to that activity that leads to motor nerve degeneration,” Andrews said. Theories range from overuse of cellular energy systems (mitochondria), to chemicals in playing surfaces,, to inflammation triggered by repeated impacts. Animal models have shown that physical impacts raise chemicals linked to the kind of inflammation that may lead to ALS.

For what it’s worth, the NFL’s concussion settlement explicitly includes ALS as a compensable condition with significant financial awards, a detail I was not aware of before researching for this conversation. So even the league acknowledges in one of their most public-facing policies, at least in part, that ALS is connected to football trauma.

Where the science stands today

I asked Andrews whether researchers understand the actual mechanical trigger in sporadic ALS cases. When you randomly develop the disease, what switch is actually being flipped? She compared the current state of knowledge to an incomplete puzzle.

“We know some of the switches that are not working in ALS,” she said. “The powerhouse of the cell, the mitochondria, we know that there’s abnormal proteins that are in those nerves that don’t belong there. And we’re trying to figure out how to target them to get them out of there so that nerves can survive longer.”

On the biomarker front, neurofilament has emerged as a leading indicator. It doesn’t diagnose ALS specifically, but it signals structural nerve damage and helps researchers evaluate whether experimental treatments are working. Andrews acknowledged that diagnostic delays (typically around a year) remain a significant challenge. Discovering you actually have ALS often comes many months after the disease takes hold.

One of the most encouraging developments has been in genetic forms of ALS. A therapy called tofersen was approved for a genetic form called SOD1, and Andrews cited the case of Chris Snow, who had a 1-year prognosis but lived significantly longer because of the treatment. Additional gene therapies are in the pipeline, and Andrews expressed a sense of genuine optimism that breakthroughs in genetic ALS could eventually unlock treatments for sporadic forms as well.

She described ALS as “not an incurable disease”, but rather a historically underfunded one. The funding problem traces back decades, as she noted that between the first approved therapy in the 1990s and the second in 2017, there was essentially no progress. The 2014 Ice Bucket Challenge provided a critical influx of funding that directly contributed to the SOD1 breakthrough.