Selenium

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Information on nutritional supplements people with ALS have been taking

Effects on ALS[edit]

"Multiple biological functions of selenium manifest themselves mainly via 25 selenoproteins that have selenocysteine at their active centre. Selenium is vital for the brain and seems to participate in the pathology of disorders such as Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis and epilepsy. Since selenium was shown to be involved in diverse functions of the central nervous system, such as motor performance, coordination, memory and cognition, a possible role of selenium and selenoproteins in brain signalling pathways may be assumed. The aim of the present review is to analyse possible relations between selenium and neurotransmission. Selenoproteins seem to be of special importance in the development and functioning of GABAergic (GABA, γ-aminobutyric acid) parvalbumin positive interneurons of the cerebral cortex and hippocampus. Dopamine pathway might be also selenium dependent as selenium shows neuroprotection in the nigrostriatal pathway and also exerts toxicity towards dopaminergic neurons under higher concentrations. Recent findings also point to acetylcholine neurotransmission involvement. The role of selenium and selenoproteins in neurotransmission might not only be limited to their antioxidant properties but also to inflammation, influencing protein phosphorylation and ion channels, alteration of calcium homeostasis and brain cholesterol metabolism. Moreover, a direct signalling function was proposed for selenoprotein P through interaction with post-synaptic apoliprotein E receptors 2 (ApoER2)."[1]

"Some trace metals may increase risk of amyotrophic lateral sclerosis (ALS), whereas others may be beneficial. Our goal was to examine associations of ALS with blood levels of selenium (Se), zinc (Zn), copper (Cu), and manganese (Mn). We conducted a case-control study of 163 neurologist confirmed patients from the National Registry of Veterans with ALS and 229 frequency-matched veteran controls. We measured metal levels in blood using inductively coupled plasma mass spectrometry and estimated odds ratios (ORs) and 95% confidence intervals (CIs) for associations between ALS and a doubling of metal levels using unconditional logistic regression, adjusting for age, gender, and race/ethnicity. ALS was inversely associated with both Se (OR=0.4, 95% CI: 0.2-0.8) and Zn (OR=0.4, 95% CI: 0.2-0.8). Inverse associations with Se were stronger in patients with bulbar compared to spinal onset, worse function, longer diagnostic delay, and longer collection delay; inverse associations with Zn were stronger for those with worse function and longer collection delay. In contrast, ALS was positively associated with Cu (OR=3.4, 95% CI: 1.5-7.9). For Mn, no linear trend was evident (OR=0.9, 95% CI: 0.6-1.3, Ptrend=0.51). Associations of Se, Zn, Cu, and Mn with ALS were independent of one another. Adjustment for lead levels attenuated the positive association of ALS with Cu but did not change associations with Se, Zn, or Mn. In conclusion, Se and Zn were inversely associated with ALS, particularly among those with worse function, suggesting that supplementation with these metals may benefit such patients, while Cu was positively associated with ALS. Deficiencies of Se and Zn and excess Cu may have a role in ALS etiology."[2]

CASE REPORT: In a 49-year-old male patient suffering from muscle weakness and fasciculations, progressive muscular atrophy, a variant of ALS, was diagnosed after extensive examinations ruling out other diseases. Due to supposed mercury exposure from residual amalgam, the patient's teeth were restored. Then, the patient received sodium 2,3-dimercaptopropanesulfate (DMPS; overall 86 × 250 mg in 3 years) in combination with α-lipoic acid and followed by selenium. In addition, he took vitamins and micronutrients and kept a vegetarian diet. The excretion of metals was monitored in the urine. The success of the therapy was followed by scoring muscle weakness and fasciculations and finally by electromyography (EMG) of the affected muscles. First improvements occurred after the dental restorations. Two months after starting therapy with DMPS, the mercury level in the urine was increased (248.4 µg/g creatinine). After 1.5 years, EMG confirmed the absence of typical signs of ALS. In the course of 3 years, the patient recovered completely. CONCLUSIONS: The therapy described here is a promising approach to treating some kinds of motor neuron disease and merits further evaluation in rigorous trials.[3]

Regulated pathways[edit]

Possible synergies[edit]

Cautions and risks[edit]

Selenium is toxic in its inorganic hexavalent form (selenate) and increases ALS risk, among several other diseases.[4]

Discussion threads on the ALSTDI forum[edit]

Where to get it[edit]

References[edit]

  1. Solovyev &: Importance of selenium and selenoprotein for brain function: From antioxidant protection to neuronal signalling. J. Inorg. Biochem. 2015;153:1-12. PMID: 26398431. DOI. Multiple biological functions of selenium manifest themselves mainly via 25 selenoproteins that have selenocysteine at their active centre. Selenium is vital for the brain and seems to participate in the pathology of disorders such as Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis and epilepsy. Since selenium was shown to be involved in diverse functions of the central nervous system, such as motor performance, coordination, memory and cognition, a possible role of selenium and selenoproteins in brain signalling pathways may be assumed. The aim of the present review is to analyse possible relations between selenium and neurotransmission. Selenoproteins seem to be of special importance in the development and functioning of GABAergic (GABA, γ-aminobutyric acid) parvalbumin positive interneurons of the cerebral cortex and hippocampus. Dopamine pathway might be also selenium dependent as selenium shows neuroprotection in the nigrostriatal pathway and also exerts toxicity towards dopaminergic neurons under higher concentrations. Recent findings also point to acetylcholine neurotransmission involvement. The role of selenium and selenoproteins in neurotransmission might not only be limited to their antioxidant properties but also to inflammation, influencing protein phosphorylation and ion channels, alteration of calcium homeostasis and brain cholesterol metabolism. Moreover, a direct signalling function was proposed for selenoprotein P through interaction with post-synaptic apoliprotein E receptors 2 (ApoER2).
  2. Peters et al.: Blood levels of trace metals and amyotrophic lateral sclerosis. Neurotoxicology 2016;54:119-26. PMID: 27085208. DOI. Some trace metals may increase risk of amyotrophic lateral sclerosis (ALS), whereas others may be beneficial. Our goal was to examine associations of ALS with blood levels of selenium (Se), zinc (Zn), copper (Cu), and manganese (Mn). We conducted a case-control study of 163 neurologist confirmed patients from the National Registry of Veterans with ALS and 229 frequency-matched veteran controls. We measured metal levels in blood using inductively coupled plasma mass spectrometry and estimated odds ratios (ORs) and 95% confidence intervals (CIs) for associations between ALS and a doubling of metal levels using unconditional logistic regression, adjusting for age, gender, and race/ethnicity. ALS was inversely associated with both Se (OR=0.4, 95% CI: 0.2-0.8) and Zn (OR=0.4, 95% CI: 0.2-0.8). Inverse associations with Se were stronger in patients with bulbar compared to spinal onset, worse function, longer diagnostic delay, and longer collection delay; inverse associations with Zn were stronger for those with worse function and longer collection delay. In contrast, ALS was positively associated with Cu (OR=3.4, 95% CI: 1.5-7.9). For Mn, no linear trend was evident (OR=0.9, 95% CI: 0.6-1.3, Ptrend=0.51). Associations of Se, Zn, Cu, and Mn with ALS were independent of one another. Adjustment for lead levels attenuated the positive association of ALS with Cu but did not change associations with Se, Zn, or Mn. In conclusion, Se and Zn were inversely associated with ALS, particularly among those with worse function, suggesting that supplementation with these metals may benefit such patients, while Cu was positively associated with ALS. Deficiencies of Se and Zn and excess Cu may have a role in ALS etiology.
  3. Mangelsdorf et al.: [Healing of Amyotrophic Lateral Sclerosis: A Case Report]. Complement Med Res 2017;24:175-181. PMID: 28641283. DOI. BACKGROUND: Amyotrophic lateral sclerosis (ALS) is a devastating disease leading to death within 3-5 years in most cases. New approaches to treating this disease are needed. Here, we report a successful therapy. CASE REPORT: In a 49-year-old male patient suffering from muscle weakness and fasciculations, progressive muscular atrophy, a variant of ALS, was diagnosed after extensive examinations ruling out other diseases. Due to supposed mercury exposure from residual amalgam, the patient's teeth were restored. Then, the patient received sodium 2,3-dimercaptopropanesulfate (DMPS; overall 86 × 250 mg in 3 years) in combination with α-lipoic acid and followed by selenium. In addition, he took vitamins and micronutrients and kept a vegetarian diet. The excretion of metals was monitored in the urine. The success of the therapy was followed by scoring muscle weakness and fasciculations and finally by electromyography (EMG) of the affected muscles. First improvements occurred after the dental restorations. Two months after starting therapy with DMPS, the mercury level in the urine was increased (248.4 µg/g creatinine). After 1.5 years, EMG confirmed the absence of typical signs of ALS. In the course of 3 years, the patient recovered completely. CONCLUSIONS: The therapy described here is a promising approach to treating some kinds of motor neuron disease and merits further evaluation in rigorous trials.
  4. Vinceti et al.: Long-term mortality patterns in a residential cohort exposed to inorganic selenium in drinking water. Environ. Res. 2016;150:348-56. PMID: 27344266. DOI. Selenium (Se) is a metalloid of considerable nutritional and toxicological importance in humans. To date, limited epidemiologic evidence exists about the health effects of exposure to this trace element in drinking water. We investigated the relationship between Se levels in water and mortality in the municipality of Reggio Emilia, Italy, where high levels of Se were previously observed in drinking water. From 1974 to 1985, 2065 residents consumed drinking water with Se levels close to the European standard of 10μg/l, in its inorganic hexavalent form (selenate). Follow-up was conducted for the years 1986-2012 in Reggio Emilia and a lesser exposed comparison group of around 100,000 municipal residents, with comparable socio-demographic characteristics. Overall mortality from all causes, cardiovascular disease and cancer showed little evidence of differences. However, excess rate ratios were seen for some site specific cancers such as neoplasms of buccal cavity and pharynx, urinary tract, lymphohematopoietic tissue, melanoma, and two neurodegenerative diseases, Parkinson's disease and amyotrophic lateral sclerosis. Excess mortality in the exposed cohort for specific outcomes was concentrated in the first period of follow-up (1986-1997), and waned starting 10 years after the high exposure ended. We also found lower mortality from breast cancer in females during the first period of follow-up. When we extended the analysis to include residents who had been consuming the high-selenium drinking water for a shorter period, mortality rate ratios were also increased, but to a lesser extent. Overall, we found that the mortality patterns related to long-term exposure to inorganic hexavalent selenium through drinking water were elevated for several site-specific cancers and neurodegenerative disease.