Coenzyme Q, CoQ10, ubiquinone
Roc did not take CoQ10. Previously, the literature strongly condemned it as a supplement, except for when experiencing leg pain while taking statins to control cholesterol, both under a doctor’s supervision. Below is one article from 2009.
Oct 2009 – Coenzyme Q (CoQ10) supplements provide no benefits and may impair brain function – Coenzyme Q10 (CoQ10) is widely consumed as a dietary supplement to enhance bioenergetic capacity and to ameliorate the debilitative effects of the aging process or certain pathological conditions. Our main purpose in this study was to determine whether CoQ10 intake does indeed attenuate the age-associated losses in motor, sensory, and cognitive functions or decrease the rate of mortality in mice…Our results suggest that prolonged intake of CoQ10 in low amounts has no discernable impact on cognitive and motor functions whereas intake at higher amounts exacerbates cognitive and sensory impairments encountered in old mice. These findings do not support the notion that CoQ10 is a fitness-enhancing or an “antiaging” substance under normal physiological conditions.
However, now the literature has changed substantially.
CoQ10 (posted May 26, 2023)
The following articles make clear the benefits of getting adequate amounts of zinc, selenium and CoQ10. Three Brazil nuts, 270mcg, appears frequently as a good dosage. CoQ10 is safe up to 1200mg. 60 to 500 mg/day for periods from one week to four months significantly decreased production of inflammatory cytokines.
It says 3 Brazil nuts have 270mcg of selenium (385% of the daily need).
Selenium + CoQ10, a powerhouse of antioxidantsThe SeQ10 group had a significant increase in SIRT1 concentration, while the placebo group had a decrease.
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Coenzyme Q10 supplementation – In ageing and disease. See numbers 5 to the conclusion and it clearly states that COQ10 is beneficial for heart issues and inflammation. Ageing and use of statins may result in coenzyme Q10 deficiency and supplementation may alleviate cardiovascular disease and inflammation.
Clinical trials with bioavailable coenzyme Q10 of longer duration to assess benefits for diseases associated with ageing are needed. Clinical trials, systematic reviews, and meta-analyses have examined the safety and efficacy of CoQ10 in the treatment of human diseases. With regards to safety, the highest dose for long-term CoQ10 supplementation is 1200 mg daily. Clinical trials, systematic reviews, and meta-analyses have examined the safety and efficacy of CoQ10 in the treatment of human diseases. With regards to safety, the highest dose for long-term CoQ10 supplementation is 1200 mg daily. A 2-year treatment with CoQ10 (300 mg/day) as adjuvant therapy in a randomized, controlled multicenter trial on 420 patients suffering from heart failure demonstrated a reduction in major cardiovascular events (Mortensen et al., 2014). . A recent meta-analysis explored the efficacy of CoQ10 on the plasma concentrations of C-reactive protein (CRP), interleukin 6 (IL-6) and tumor necrosis factor alpha (TNF-α) in patients with various diseases with significant inflammation as a common factor and concluded that CoQ10 in doses ranging from . 60 to 500 mg/day for periods from one week to four months significantly decreased production of inflammatory cytokines (Fan et al., 2017). Alleviation of symptoms of chronic fatigue syndrome or myalgic encephalopathy has also been reported after supplementation with CoQ10 combined with a niacin derivative (Campagnolo et al., 2017). , a screening for oxidative stress markers in patients with Parkinson’s disease reported lower levels of CoQ10 and higher levels of lipoprotein oxidation in the plasma, cerebrospinal fluid, and the cortex region of the brain compared with non-affected individuals (Buhmann et al., 2004; Hargreaves et al., 2008). there is no evidence to indicate that CoQ10 supplementation can delay the progression of Huntington’s disease (McGarry et al., 2017) or of Alzheimer’s disease (Galasko et al., 2012). A poor transport of CoQ10 across the blood-brain barrier may explain the latter results (Wainwright, 2018; Wainwright et al., 2020).
Selenium and Coenzyme Q10 Intervention Prevents Telomere Attrition, with Association to Reduced Cardiovascular Mortality. Source: https://www.mdpi.com/2072-6643/14/16/3346
and https://pubmed.ncbi.nlm.nih.gov/32417634/
Does a role for selenium in DNA damage repair explain apparent controversies in its use in chemoprevention? Considerable experimental evidence indicates that one possible mechanism by which selenium supplementation may exert its benefits is by enhancing the DNA damage repair response, and this includes data obtained using cultured cells, animal models as well as in human clinical studies. In these studies, selenium supplementation has been shown to be beneficial in reducing the frequency of DNA adducts and chromosome breaks, consequentially reducing the likelihood of detrimental mutations that ultimately contribute to carcinogenesis.
Effect of the Interaction Between Selenium and Zinc on DNA Repair in Association With Cancer Prevention. Aside from its antioxidant activity, selenium may also exhibit protection against DNA damage by increasing the activity of DNA repair enzymes, such as DNA glycosylases, and repair pathways that involve members, such as p53 and BRCA1 [28].
Selenium Compounds Regulate p53 by Common and Distinctive Mechanisms
Selenium 200mcg –- Selenium reduces side effects of radiotherapy. 10 After reviewing six studies, researchers found that selenium intake (300-500 mcg/day for 10 days to 6 months) reduced the side effects of radiotherapy without reducing effectiveness. Researchers recommended that cancer patients who are deficient in selenium consider supplementation
When researchers studied a population of people 90 years old and above, they found that the OLDEST inhabitants— those over 100 years old—all had something in common: They had the highest levels of the trace mineral selenium. 1 There’s a reason selenium levels are connected to longevity. SeleniumɸMW
[study][mice]: “Selenium mediates exercise-induced adult neurogenesis and reverses learning deficits induced by hippocampal injury and aging”Selenium reverses cognitive decline in aging and in hippocampal injury. Although the neurogenesis-enhancing effects of exercise have been extensively studied, the molecular mechanisms underlying this response remain unclear. Here, we propose that this is mediated by the exercise-induced systemic release of the antioxidant selenium transport protein, selenoprotein P (SEPP1). Using knockout mouse models, we confirmed that SEPP1 and its receptor low-density lipoprotein receptor-related protein 8 (LRP8) are required for the exercise-induced increase in adult hippocampal neurogenesis. In vivo selenium infusion increased hippocampal neural precursor cell (NPC) proliferation and adult neurogenesis. Mimicking the effect of exercise through dietary selenium supplementation restored neurogenesis and reversed the cognitive decline associated with aging and hippocampal injury, suggesting potential therapeutic relevance. These results provide a molecular mechanism linking exercise-induced changes in the systemic environment to the activation of quiescent hippocampal NPCs and their subsequent recruitment into the neurogenic trajectory
3-2021 – Methionine restriction (MR) dramatically extends the healthspan of several organisms. Methionine-restricted rodents have less age-related pathology and increased longevity as compared with controls, and recent studies suggest that humans might benefit similarly. Mechanistically, it is likely that the decreased IGF-1 signaling that results from MR underlies the benefits of this regimen. Thus, we hypothesized that interventions that decrease IGF-1 signaling would also produce MR-like healthspan benefits. Selenium supplementation inhibits IGF-1 signaling in rats and has been studied for its putative healthspan benefits. Indeed, we show that feeding mice a diet supplemented with sodium selenite results in an MR-like phenotype, marked by protection against diet-induced obesity, as well as altered plasma levels of IGF-1, FGF-21, adiponectin, and leptin. Selenomethionine supplementation results in a similar, albeit less robust response, and also extends budding yeast lifespan. Our results indicate that selenium supplementation is sufficient to produce MR-like healthspan benefits for yeast and mammals.
Sweden indicates that combining selenium with CoQ10 has been found to dramatically slash the risk of death from cardiovascular disease.
The following articles make clear the benefits of getting adequate amounts of zinc, selenium and CoQ10. Three Brazil nuts, 270mcg, appears frequently as a good dosage. CoQ10 is safe up to 1200mg. 60 to 500 mg/day for periods from one week to four months significantly decreased production of inflammatory cytokines.
Selenium + CoQ10, a powerhouse of antioxidantsThe SeQ10 group had a significant increase in SIRT1 concentration, while the placebo group had a decrease.
|
Coenzyme Q10 supplementation – In ageing and disease. See numbers 5 to the conclusion and it clearly states that COQ10 is beneficial for heart issues and inflammation. Ageing and use of statins may result in coenzyme Q10 deficiency and supplementation may alleviate cardiovascular disease and inflammation.
Clinical trials with bioavailable coenzyme Q10 of longer duration to assess benefits for diseases associated with ageing are needed. Clinical trials, systematic reviews, and meta-analyses have examined the safety and efficacy of CoQ10 in the treatment of human diseases. With regards to safety, the highest dose for long-term CoQ10 supplementation is 1200 mg daily. Clinical trials, systematic reviews, and meta-analyses have examined the safety and efficacy of CoQ10 in the treatment of human diseases. With regards to safety, the highest dose for long-term CoQ10 supplementation is 1200 mg daily. A 2-year treatment with CoQ10 (300 mg/day) as adjuvant therapy in a randomized, controlled multicenter trial on 420 patients suffering from heart failure demonstrated a reduction in major cardiovascular events (Mortensen et al., 2014). . A recent meta-analysis explored the efficacy of CoQ10 on the plasma concentrations of C-reactive protein (CRP), interleukin 6 (IL-6) and tumor necrosis factor alpha (TNF-α) in patients with various diseases with significant inflammation as a common factor and concluded that CoQ10 in doses ranging from . 60 to 500 mg/day for periods from one week to four months significantly decreased production of inflammatory cytokines (Fan et al., 2017). Alleviation of symptoms of chronic fatigue syndrome or myalgic encephalopathy has also been reported after supplementation with CoQ10 combined with a niacin derivative (Campagnolo et al., 2017). , a screening for oxidative stress markers in patients with Parkinson’s disease reported lower levels of CoQ10 and higher levels of lipoprotein oxidation in the plasma, cerebrospinal fluid, and the cortex region of the brain compared with non-affected individuals (Buhmann et al., 2004; Hargreaves et al., 2008). there is no evidence to indicate that CoQ10 supplementation can delay the progression of Huntington’s disease (McGarry et al., 2017) or of Alzheimer’s disease (Galasko et al., 2012). A poor transport of CoQ10 across the blood-brain barrier may explain the latter results (Wainwright, 2018; Wainwright et al., 2020).
Selenium and Coenzyme Q10 Intervention Prevents Telomere Attrition, with Association to Reduced Cardiovascular Mortality. Source: https://www.mdpi.com/2072-6643/14/16/3346
and https://pubmed.ncbi.nlm.nih.gov/32417634/
Does a role for selenium in DNA damage repair explain apparent controversies in its use in chemoprevention? Considerable experimental evidence indicates that one possible mechanism by which selenium supplementation may exert its benefits is by enhancing the DNA damage repair response, and this includes data obtained using cultured cells, animal models as well as in human clinical studies. In these studies, selenium supplementation has been shown to be beneficial in reducing the frequency of DNA adducts and chromosome breaks, consequentially reducing the likelihood of detrimental mutations that ultimately contribute to carcinogenesis.
Effect of the Interaction Between Selenium and Zinc on DNA Repair in Association With Cancer Prevention. Aside from its antioxidant activity, selenium may also exhibit protection against DNA damage by increasing the activity of DNA repair enzymes, such as DNA glycosylases, and repair pathways that involve members, such as p53 and BRCA1 [28].
Selenium Compounds Regulate p53 by Common and Distinctive Mechanisms
Selenium 200mcg –- Selenium reduces side effects of radiotherapy. 10 After reviewing six studies, researchers found that selenium intake (300-500 mcg/day for 10 days to 6 months) reduced the side effects of radiotherapy without reducing effectiveness. Researchers recommended that cancer patients who are deficient in selenium consider supplementation
When researchers studied a population of people 90 years old and above, they found that the OLDEST inhabitants— those over 100 years old—all had something in common: They had the highest levels of the trace mineral selenium. 1 There’s a reason selenium levels are connected to longevity. SeleniumɸMW
[study][mice]: “Selenium mediates exercise-induced adult neurogenesis and reverses learning deficits induced by hippocampal injury and aging”Selenium reverses cognitive decline in aging and in hippocampal injury.
Although the neurogenesis-enhancing effects of exercise have been extensively studied, the molecular mechanisms underlying this response remain unclear. Here, we propose that this is mediated by the exercise-induced systemic release of the antioxidant selenium transport protein, selenoprotein P (SEPP1). Using knockout mouse models, we confirmed that SEPP1 and its receptor low-density lipoprotein receptor-related protein 8 (LRP8) are required for the exercise-induced increase in adult hippocampal neurogenesis. In vivo selenium infusion increased hippocampal neural precursor cell (NPC) proliferation and adult neurogenesis. Mimicking the effect of exercise through dietary selenium supplementation restored neurogenesis and reversed the cognitive decline associated with aging and hippocampal injury, suggesting potential therapeutic relevance. These results provide a molecular mechanism linking exercise-induced changes in the systemic environment to the activation of quiescent hippocampal NPCs and their subsequent recruitment into the neurogenic trajectory
Methionine restriction (MR) dramatically extends the healthspan of several organisms. Methionine-restricted rodents have less age-related pathology and increased longevity as compared with controls, and recent studies suggest that humans might benefit similarly. Mechanistically, it is likely that the decreased IGF-1 signaling that results from MR underlies the benefits of this regimen. Thus, we hypothesized that interventions that decrease IGF-1 signaling would also produce MR-like healthspan benefits. Selenium supplementation inhibits IGF-1 signaling in rats and has been studied for its putative healthspan benefits. Indeed, we show that feeding mice a diet supplemented with sodium selenite results in an MR-like phenotype, marked by protection against diet-induced obesity, as well as altered plasma levels of IGF-1, FGF-21, adiponectin, and leptin. Selenomethionine supplementation results in a similar, albeit less robust response, and also extends budding yeast lifespan. Our results indicate that selenium supplementation is sufficient to produce MR-like healthspan benefits for yeast and mammals.
Sweden indicates that combining selenium with CoQ10 has been found to dramatically slash the risk of death from cardiovascular disease.
