Amyotrophic lateral sclerosis (ALS) is an incurable neurodegenerative disease resulting in progressive weakness and selective degeneration of the motor neurons, leading to death from respiratory failure within 3–4 years [1], though 10% of people with ALS will live ten years or longer. The onset of amyotrophic lateral sclerosis (ALS) is more common in adults over the age of 40 years. However, ALS may also occur in people in their 20s or 30s. Here is a short video explanation of ALS.
Viruses do not cause ALS, but may accelerate the disease in susceptible individuals.
Fatigue is a common symptom among individuals with ALS and may be present in all stages of the disease.
ALS patients present risk factors associated with an increased incidence of venous thromboembolic (VTE) such as age or reduced mobility.
BMAA, formaldehyde, mercury, manganese and zinc rank highest for ALS association in this systematic and state-of the science review of the role of environmental factors.
This systematic review and meta-analysis showed that environmental/occupational lead exposure was positively proportional to the risk of ALS.
This meta-analysis of 16 studies show that a variety of exercise regimens are safe and well-tolerated in people with ALS. Exercise may maintain or improve function for mild-moderate disease severity. Some studies suggest that it can slow decline in function. Exercise is also important to avoid disuse atrophy, or weakness, that results from not using muscles. Only those who had high levels of physical activity from their occupation—but not from leisure activities—had an increased risk of ALS. In general, exercise is not a risk factor for the development of ALS.
Here is another systematic review of clinical trials published in the last 5 years in which one of the interventions was therapeutic physical exercise in patients with ALS, using the ALSFRS-R as the main outcome variable. the participants showed significant improvements in functional abilities in the short, medium and long terms. The conclusion is that therapeutic physical exercise could contribute to slowing down the deterioration of the musculature of patients with ALS, thus facilitating their performance in activities of daily living, based on the significant differences shown by these individuals in the short, medium and long term both in subjective perception, measured with ALSFRS-R, and functional capacities.
Acetyl-L-carnitine (ALCAR) counteracts motor-neuron death induced by toxic agents or deprivation of trophic factors and slows disease progression in animal models [2,3,4]. The drug also ameliorates mitochondrial dysfunction [5], restores synaptic transmission [6] and exerts protective effects against neuroinflammation [7]. As a consequence, decreased levels of oxidative stress markers and pro-inflammatory cytokines have been detected [8, 9].
Impaired macroautophagy is frequently present in ALS. Mutations in genes that encode essential autophagy factors result in impaired autophagy and lead to neurodegenerative conditions such as amyotrophic lateral sclerosis (ALS). Increased autophagy may prevent neurodegeneration. Autophagy modulation can dramatically influence ALS-related neurodegeneration. Damaged activity of RNA-binding proteins (RBPs) associated with amyotrophic lateral sclerosis (ALS) can be alleviated by inducing autophagy, a process where cells degrade or recycle components that are damaged or no longer needed, a study says. This blog post on autophagy may be relevant.
Blackberries helped mice with ALS live longer.
Treatment with curcumin shows encouraging results indicating a slight slowdown in disease progression, improving aerobic metabolism and oxidative damage. Given the strong activity of curcumin as an antioxidant, it could have a crucial role in neuron degeneration. Curcumin works by many different mechanisms. Curcumin is fat-soluble. Too much curcumin can cause anemia. Consuming curcumin with piperine from black pepper can increase absorption up to 2000%. Curcumin + piperine with a fatty meal may be just as good as more expensive curcumin products.
Curcumin contains antioxidant properties and it appears ten times more powerful than vitamin E as a free radical scavenger [31]. Due to the ability of curcumin to cross the blood–brain barrier [32], it also decreases the ROS level [33], protects the brain from lipid peroxidation and reduces the neuron death induced by oxidative insults [34]. Supplementation with 600 mg/day of curcumin for 6 months improved stable disease scores.
Nanocurcumin is safe and might improve the probability of survival as an add-on treatment in patients with ALS, especially in those with existing bulbar symptoms.
A high-fiber diet may slow the progression of ALS.
People with amyotrophic lateral sclerosis (ALS) who eat more foods high in certain omega-3 fatty acids like flaxseed oil, walnuts, canola oil and pumpkin seeds may have a slower physical decline from the disease and may have a slightly extended survival. This longitudinal analyses based on 1,002,082 participants (479,114 women and 522,968 men) in 5 prospective cohorts found that consumption of foods high in ω-3 PUFAs may help prevent or delay the onset of ALS.
Diet may help minimize the severity of ALS and point to the role of oxidative stress in ALS severity. Antioxidant nutrients, foods high in carotenoids, fruits, and vegetable intake appear to be associated with better ALS function at baseline. ALS patients should eat foods high in antioxidants and carotenes, as well as high fiber grains, fish, and poultry. Fruit polyphenols, found in blueberries, might reverse progression to some degree. There is some evidence for the benefit of folic acid, Vitamin E, Coenzyme Q10, Alpha Lipoic Acid (ALA), and Ginkgo in reducing the effects of ALS. Overall nutritional status is extremely important for survival time after diagnosis. However, one study shows that hydration might be even more important than nutrient status.
Polyphenols from colorful fruits and veggies may benefit ALS patients. Several studies performed in ALS animal models demonstrated that polyphenols have a neuroprotective role [112].
The ALS medicine Edaravone works by relieving the effects of oxidative stress, which may be related to the death of motor neurons (nerve cells) in people with ALS. Keeping motor neurons healthy may help to preserve muscle function.
Milk and lunch meats were associated with lower measures of function, or more severe disease.
Eating on a strict schedule could improve quality of life for patients with neurodegenerative diseases for which there are no known cures.
Sleep disorders are observed in 70% of patients with ALS [8]. Sleep disorders impair the cell clearance of misfolded neurotoxin proteins and affect the immunological and redox system resulting in neuroinflammation and oxidative stress [9]. Prolonging sleep time and improving sleep structure may be helpful in the treatment of ALS. This blog post on sleep may be beneficial.
High-dose leucine (isoleucine) can reduce B12 putting one at risk of ALS. High-dose B12 may stabilize ALS.
TUDCA (tauroursodeoxycholic acid) is a small molecule that is being explored for its potential as a treatment for amyotrophic lateral sclerosis (ALS). Research has shown that TUDCA can decrease nerve cell death, a hallmark of ALS, through its ability to act as an antioxidant that prevents toxic reactive oxygen species from accumulating inside cells. The molecule also has the ability to control immune function. Preclinical studies indicate that TUDCA exerts its effects not only by regulating and inhibiting the apoptotic cascade, but also by reducing oxidative stress, protecting the mitochondria, producing an anti-neuroinflammatory action, and acting as a chemical chaperone to maintain the stability and correct folding of proteins. TUDCA capsules are available from DoubleWood Supplements.
Smoking can raise your risk of developing ALS. Studies suggest that the longer you smoke the more likely you are to develop ALS. So quitting smoking can help lower your risk of developing ALS.
In addition, factors that raise oxidative stress — a type of chemical imbalance in the body — can also worsen the risk for developing ALS. Eating a diet high in fruits, vegetables, and fish and low in processed foods can lower your risk of developing ALS.
Growing evidence (presented in this video) indicates that gut microbiome may actively contribute to ALS pathogenesis. ‘Microbiome’ includes all the microorganisms living (e.g., bacteria, virus, fungi) in the body. Increasing evidence suggests that ALS patients have inflammation in the gut and changes in the composition of gut microbes (the gut microbiome), with lower levels of beneficial bacteria. This blog post on gut health may be beneficial.
Catechins are polyphenolic flavonoids which possess strong antioxident properties and include, epigallocatechin, epicatechin, and epicatichin-3-gallate. Catechins are considered free radical scavengers found in high concentrations in some plants, fruits and vegetables. They are considered the health promoting constituent of green tea, blue berries, cocoa, prune juice, red wine, and Ginko Baloba to name a few. Studies have shown that catechins cross the blood brain barrier and are incorporated into brain tissue where they exert potent neuroprotective actions by modulating mitochondrial responses to oxidative insults.
Vitamin D participates in several distinct pathways that are potentially important in ALS physiopathology including calcium regulation and potentiation of protective neurotrophic factors (81). In a retrospective study of 74 ALS patients, risk of death was significantly increased in those with severe vitamin D deficiency (<25 nmol/L) compared to patients with normal vitamin D (82).
A high BMI has been shown to be beneficial in avoiding ALS and treating ALS. Several studies have reported that nutritional status is closely related to the survival time of ALS patients, and there exists a U-shaped association between patients’ body mass index (BMI) and mortality.[1,4]. ALS patients need more calories to improve functionality and to live longer.
Cannabis delayed ALS progression in mice. There is now good animal based evidence that that cannabinoids are capable of slowing disease progression of ALS in mice (93–96). The mechanisms are not entirely clear but it is likely this occurs partially by cannabinoids acting as anti-oxidants and neuromodulators, although other mechanisms are likely as well. In a survey of 131 patients with ALS, those who were able to obtain cannabis found it preferable to prescription medication in managing their symptoms (104). Patients with ALS previously have reported that cannabis is at least moderately effective at reducing symptoms of pain, spasticity, drooling, appetite loss, and depression (104).
Here is an ALS functional rating scale for keeping track of one’s decline. Here is a doctor talking about respiratory issues: how to avoid and how to treat.
This highly rated Wikipedia article is an excellent source of information beyond what is found in this blog. In that Wikipedia entry “Around half of people with ALS develop at least mild difficulties with thinking and behavior, and about 15% develop frontotemporal dementia.10 Exercise may help avoid this fate – see this blog post on exercise to keep one’s marbles.
This site may be of interest: https://www.everythingals.org/
Here is Dr. Bedlack on ALS stabilization and even (rarely) reversals. Here is a more detailed video on rare ALS reversals.
