This text presents a compelling theory on its underlying cause and a potentially simple treatment. The author describes their research into ALS, including two published papers focusing on the disease’s cause and treatment. Their theory centers around an impairment in calcium channels, which are critical for various cellular processes, and its connection to insulin dysfunction.

The idea of calcium channel dysfunction in ALS is not entirely new; it has been explored for decades. However, prior research was inconclusive due to contradictory data, leading scientists to abandon the direction. The author identifies a specific protein within the calcium channel complex as the likely culprit, which previous studies failed to investigate adequately.

The connection between calcium channel dysfunction and insulin production is a key element of the theory. Impaired calcium channels can affect pancreatic beta cells, which synthesize insulin. This dysfunction can lead to muscle degeneration, a hallmark of ALS. Intriguingly, historical research over the last 60 years supports this notion: more than 20 studies have shown impaired insulin function in ALS patients. Yet, this connection has not been widely recognized due to the way glucose regulation compensates.

The author argues that ALS symptoms emerge when insulin function deteriorates so severely that even the hyperactive calcium system cannot compensate. This insight leads to the proposal of a simple diagnostic test: the glucose challenge test, commonly used in pregnancy. By analyzing blood insulin levels within 30 minutes of a sugar load, doctors could detect impaired insulin function in ALS patients. This test is inexpensive, widely available, and non-invasive.

If the theory is correct, the treatment for ALS could be remarkably straightforward: insulin therapy. Administering insulin to ALS patients with detected deficiencies could not only delay disease progression but potentially improve symptoms. Importantly, the author notes that clinical trials may not even be necessary for this approach, as the glucose challenge test itself would confirm insulin impairment. Patients diagnosed with both ALS and diabetes would legally qualify for insulin treatment, bypassing lengthy trials.

Despite the promise of this theory, it has struggled to gain traction. Emails and papers sent to over 30 researchers and clinicians have elicited little response. The author laments this lack of attention, especially given the dire prognosis of ALS and the simplicity of the proposed diagnostic and treatment methods. They issue a call to action for ALS patients and their caregivers to advocate for the glucose challenge test and insulin treatment.

The stakes are high: if the theory is correct, a readily available remedy exists that could save lives immediately. The author acknowledges the possibility of being wrong but emphasizes the potential cost of inaction if they are right. They urge ALS patients and clinicians to explore this approach and bring it to light, as each year of delay results in unnecessary suffering and loss of life.