Kyselina alfa lipoová - thioktová
The oral supplementation of LA can be a potential supplement in cancer treatment, as it improved survival [58] and reduced unwanted effects of chemotherapy [59]. LA is important in combating inflammation and pain. Positive data on rheumatoid arthritis [60], chronic pain [61], neuropathy [62], migraines [63], ulcerative colitis [64] were published.In various clinical trials which investigated the therapeutic potential of LA, it was concluded that moderate doses (up to 1800 mg/day) were considered safe. Meanwhile, high doses or intraperitoneally administered LA, at a dosage of 5 to 10 g/day, can elevate hydroperoxide levels in the blood [65].
?-Lipoic acid and Alzheimer’s disease, Parkinson’s disease, Huntington’s disease and Multiple Sclerosis
In an open clinical study, 600 mg LA was given daily to nine patients with AD (receiving a standard treatment with acetylcholinesterase inhibitors) to examine the influence of LA on the progression of AD. LA treatment stabilized cognitive functions in the patients, shown by constant scores in neuropsychological tests (mini-mental state examination, AD assessment scale and cognitive subscale) [196]. LA has the ability to intervene with pathogenic principles of AD, as it stimulates acetylcholine (ACh) production by activating choline acetyltransferase and elevating glucose uptake, as a result providing more acetyl-CoA for ACh production [197]. LA might represent a potential neuroprotective therapy for AD.In experimental models of PD, lipopolysaccharide (LPS) can be used to activate glial cells [200]. Nasal LPS-induced PD is completely inflammation-driven, and it effectively replicates the chronic, progressive PD pathology [201].
LA can block the LPS-induced inflammatory process [202]. LA administration ameliorated motor dysfunction, preserved dopaminergic neurons and reduced SN ?-synuclein accumulation. In M1 microglia LA blocked nuclear factor-?B activation and expression of pro-inflammatory molecules. Further neuroprotective action of LA was studied in an experimental model of PD, induced in male Wistar rats by intrastriatal injection of 6-OHDA. LA improved learning and memory performance and neuromuscular coordination. LA significantly reduced lipid peroxidation levels, and recovered catalase activity and dopamine levels that were damaged by 6-OHDA administration all which lead to a reduction of oxidative stress [203]. It can be concluded that LA displays significant antiparkinsonian effects.
In the 3-NP rat model of HD the neuroprotective effect of LA and acetyl-L-carnitine (ALCAR) on 3-NP-induced alterations in mitochondrial structure, lipid composition, and memory functions was investigated. The combined supplementation of LA + ALCAR improved mitochondrial lipid composition, blocked mitochondrial structural changes, and mitigated cognitive deficits in 3-NP-treated animals. Thus, a combined supplementation of LA + ALCAR can be a possible therapeutic strategy in HD management [206]. It was examined whether LA exerted neuroprotective effects in transgenic mouse models of HD. LA generated significant increases in survival in R6/2 and N171-82Q transgenic mouse models of HD. These results indicate that LA may have valuable effects in HD patients [207].
Studies investigating the effects of LA on demyelination and axonal damage in optic nerve, spinal cord, and brain reported that LA-treated EAE animals had reduced damage in the CNS, which was timing- and route of administration dependent [211,213,214]. LA administration by intraperitoneal (i.p.) injection seven days or directly after immunization protected axons from demyelination and damage [211,213]. Delayed LA administration also decreased damage to the optic nerve but not as profoundly as the immediate treatment [213]. Oral administration was only protective immediately, but not delayed after EAE immunization [211]. LA treatment lead to a reduced disease severity in EAE model animals [215].
The use of LA is desirable in numerous areas of health. LA has various beneficial effects on the aging process and neurological disorders. More evaluation is needed to instruct health professionals better on the safety of prescribing LA as a supplement.
ALA - Alpha Lipoic Acid
- May benefit healthy individuals who are at genetic risk of cancer
- Due to mutation of gene CDH1 over Soy Bean
VHL mutace
- Avoid nutritional supplements Alpha Lipoic Acid with mutation of gene VHL.
- VHL is one of the genes generally available in panels for cancer risk testing.
- VHL mutation causes biochemical pathways/processes like
- Endoplasmic Reticulum Stress and Hypoxia to get impacted.
- Direct or indirect drivers of cancer molecular endpoints.
- Alpha Lipoic Acid should not be taken when the genetic panel identifies mutation of VHL for Kidney Cancer.
- Alpha Lipoic Acid impacts pathways/processes like Endoplasmic Reticulum Stress and creates adverse conditions with VHL.
- addon.life/2022/11/15/for-which-cancer-types-should-i-avoid-alpha-lipoic-acid-supplement/
CDH1 Mutation
- CDH1 is one of the genes available in panels for cancer risk testing.
- CDH1 mutation causes biochemical pathways/processes like
- PI3K-AKT-MTOR Signaling,
- Adherens junction
- Epithelial to Mesenchymal Transition to get impacted.
- Direct or indirect drivers of cancer molecular endpoints
- Alpha Lipoic Acid supplements may be considered when the genetic panel identifies mutations in CDH1 for Gastric Cancer
- Alpha Lipoic Acid impacts pathways/processes like PI3K-AKT-MTOR Signaling and creates a canceling effect in those individuals with CDH1 mutation.
- addon.life/2022/11/15/for-which-cancer-types-should-i-avoid-alpha-lipoic-acid-supplement/