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jussipussi
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Viestejä52986

Mielenkiintoista seurata tuleeko näistä uusista alsutavista löydöksistä mitään merkittävämpää.

"Vitamin C uncouples the Warburg metabolic switch in KRAS mutant colon cancer.

Abstract

KRAS mutation is often present in many hard-to-treat tumors such as colon and pancreatic cancer and it is tightly linked to serious alterations in the normal cell metabolism and clinical resistance to chemotherapy.In 1931, the Nobel Prize in Medicine Otto Warburg stated that cancer was primarily caused by altered metabolism interfering with energy processing in the normal cell. Increased cell glycolytic rates even in the presence of oxygen is fully recognized as a hallmark in cancer and known as the Warburg effect.In the late 1970's, Linus Pauling and Ewan Cameron reported that vitamin C may have positive effects in cancer treatment, although deep mechanistic knowledge about this activity is still scarce.We describe a novel antitumoral mechanism of vitamin C in KRAS mutant colorectal cancer that involves the Warburg metabolic disruption through downregulation of key metabolic checkpoints in KRAS mutant cancer cells and tumors without killing human immortalized colonocytes.Vitamin C induces RAS detachment from the cell membrane inhibiting ERK 1/2 and PKM2 phosphorylation. As a consequence of this activity, strong downregulation of the glucose transporter (GLUT-1) and pyruvate kinase M2 (PKM2)-PTB dependent protein expression are observed causing a major blockage of the Warburg effect and therefore energetic stress.

We propose a combination of conventional chemotherapy with metabolic strategies, including vitamin C and/or other molecules targeting pivotal key players involved in the Warburg effect which may constitute a new horizon in anti-cancer therapies."

http://www.ncbi.nlm.nih.gov/pubmed/27323830

"Warburg effect

In oncology, the Warburg effect is the observation that most cancer cells predominantly produce energy by a high rate of glycolysis followed bylactic acid fermentation in the cytosol,[4] rather than by a comparatively low rate of glycolysis followed by oxidation of pyruvate in mitochondria as in most normal cells.[5][6][7] The latter process is aerobic (uses oxygen). Malignant, rapidly growing tumor cells typically have glycolytic rates up to 200 times higher than those of their normal tissues of origin; this occurs even if oxygen is plentiful.

Otto Warburg postulated this change in metabolism is the fundamental cause of cancer,[8] a claim now known as the Warburg hypothesis. Today,mutations in oncogenes and tumor suppressor genes are thought to be responsible for malignant transformation, and the Warburg effect is considered to be a result of these mutations rather than a cause.[9][10]"

https://en.wikipedia.org/wiki/Warburg_effect

jussipussi
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Viestejä52986

Assosiaatio.

https://www.ncbi.nlm.nih.gov/pubmed/27685994

Dietary Vitamin C Intake Reduces the Risk of Type 2 Diabetes in Chinese Adults: HOMA-IR and T-AOC as Potential Mediators.

Abstract

Despite growing interest in the protective role that dietary antioxidant vitamins may have in the development of type 2 diabetes (T2D), little epidemiological evidence is available in non-Western populations especially about the possible mediators underlying in this role. The present study aimed to investigate the association of vitamin C and vitamin E intakes with T2D risk in Chinese adults and examine the potential mediators. 178 incident T2D cases among 3483 participants in the Harbin People Health Study (HPHS), and 522 newly diagnosed T2D among 7595 participants in the Harbin Cohort Study on Diet, Nutrition and Chronic Non-communicable Diseases (HDNNCDS) were studied. In the multivariable-adjusted logistics regression model, the relative risks (RRs) were 1.00, 0.75, and 0.76 (Ptrend = 0.003) across tertiles of vitamin C intake in the HDNNCDS, and this association was validated in the HPHS with RRs of 1.00, 0.47, and 0.46 (Ptrend = 0.002). The RRs were 1.00, 0.72, and 0.76 (Ptrend = 0.039) when T2D diagnosed by haemoglobin A1c in the HDNNCDS. The mediation analysis discovered that insulin resistance (indicated by homeostasis model assessment) and oxidative stress (indicated by plasma total antioxidative capacity) partly mediated this association. But no association was evident between vitamin E intake and T2D.

In conclusion, our research adds further support to the role of vitamin C intake in reducing the development of T2D in the broader population studied. The results also suggested that this association was partly mediated by inhibiting or ameliorating oxidative stress and insulin resistance."

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Yläpään toiminnasta Ja ApoE4 Genotyypistä.

https://www.ncbi.nlm.nih.gov/pubmed/27709233

"Vitamin C Supplementation, ApoE4 Genotype and Cognitive Functioning in a Rural-Dwelling Cohort.

Abstract

OBJECTIVE:

Apolipoprotein E4 (APOE4) genotype has been implicated as a moderating factor in cognitive function studies. Although prior studies have suggested that vitamin C is associated with better cognitive function in elders, link between the two has been mixed. Limited data exist as to whether the APOE4 genotype influences these associations. Therefore, this study sought to determine whether the association between vitamin C and cognition in a rural community dwelling cohort differs by the APOE4 genotype.

DESIGN AND PARTICIPANTS:

Data were analyzed on 582 participants (n=183 men; n=399 women) from a rural community-based cohort. Cognition was assessed using the Repeatable Battery for the Assessment of Neuropsychological Status and The Executive Interview. APOE genotyping was ascertained by standard methods. The relation between vitamin C supplementation and cognition were analyzed first with ANOVA and then ANCOVA with age, gender, education as covariates. Analyses were initially run in the full sample and then split by APOE4 presence (yes/no).

RESULTS:

Overall, Vitamin C supplementation was associated with significantly better immediate memory (p=0.04), visuospatial skills (p=0.002), language (p=0.01), and global cognitive functioning (p=0.006). Among APOE4 non-carriers, vitamin C supplementation was positively associated with immediate memory (F[1,392] =6.7, p=0.01), visuospatial skills (F[1,391]=10.6, p=0.001), language (F[1,392]=13.0, p<0.001), attention (F[1,386]=7.9, p=0.005, and global cognition (F[1,382]=11.0, p=0.001. However, there was no significant link between vitamin C supplementation and cognition among APOE4 carriers.

CONCLUSION:

Vitamin C supplementation was found to be positively associated with cognition among this rural-dwelling community-based sample; however, the associations appeared to differ by APOE4 status. These data may suggest that targeted genotype-specific cognitive enhancement studies are needed to clarify the potential benefits of vitamin C supplementation."

jussipussi
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Viestejä52986

"Use of Vitamin E and C Supplements for the Prevention of Cognitive Decline.

Abstract

BACKGROUND:

There are few studies of the association between the use of antioxidant vitamin supplements and the risk of Alzheimer's disease (AD). Cognitive decline is generally viewed as part of the continuum between normal aging and AD.

OBJECTIVE:

To evaluate whether the use of vitamin E and C supplements is associated with reduced risks of cognitive impairment, not dementia (CIND), AD, or all-cause dementia in a representative sample of older persons ≥65 years old.

METHODS:

Data from the Canadian Study of Health and Aging (1991-2002), a cohort study of dementia including 3 evaluation waves at 5-yearly intervals, were used. Exposure to vitamins E and C was self-reported at baseline in a risk factor questionnaire and/or in a clinical examination.

RESULTS:

The data set included 5269 individuals. Compared with those not taking vitamin supplements, the age-, sex-, and education-adjusted hazard ratios of CIND, AD, and all-cause dementia were, respectively, 0.77 (95% CI = 0.60-0.98), 0.60 (95% CI = 0.42-0.86), and 0.62 (95% CI = 0.46-0.83) for those taking vitamin E and/or C supplements. Results remained significant in fully adjusted models except for CIND. Similar results were observed when vitamins were analyzed separately.

CONCLUSIONS:

This analysis suggests that the use of vitamin E and C supplements is associated with a reduced risk of cognitive decline. Further investigations are needed to determine their value as a primary prevention strategy."

https://www.ncbi.nlm.nih.gov/pubmed/27708183 .

käyttäjä-3779
Seuraa 
Viestejä1782

https://www.sciencedaily.com/releases/2016/10/161012132810.htm

Vitamins A and C aren't just good for your health, they affect your DNA too. Researchers at the Babraham Institute and their international collaborators have discovered how vitamins A and C act to modify the epigenetic 'memory' held by cells; insight which is significant for regenerative medicine and our ability to reprogramme cells from one identity to another. The research is published today in Proceedings of the National Academy of Sciences (PNAS).

A ja C -vitamiinit vaikuttavat DNA:han muuntaen solujen epigeneettistä "muistia", mikä mahdollistaa muun muassa solun geneettisen siirtymisen solulinjasta toiseen (kun uusi geenijoukko aktivoituu).

Keijona
Seuraa 
Viestejä15467

Jos c-aiheuttaa eräänlaista soludementiaa, niin se onko se hyvä vai huono asia riippuu siitä onko olemassaoleva solurakenne muistamisen arvoista. Tosinsanoen onko järkevää  rakennelmaa korjata vai olisiko kokonaan uusi rakennus parempi  vaihtoehto.

Rikkaalla riittävästi, köyhä haluaa lisää.

jussipussi
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Assosiaatio. C vitamiini vaikutus kollageenisynteesiin yksi mahdollinen selitys. C vitamiini assosioituu myös pienempään kivun tunteeseen erillisissa tutkimuksissa.

"Serum vitamin C and spinal pain: a nationwide study.

Abstract

Back pain brings about one of the heaviest burden of disease. Despite much research, this condition remains poorly understood, and effective treatments are frustratingly elusive. Thus, researchers in the field need to consider new hypotheses. Vitamin C (ascorbic acid) is an essential cofactor for collagen crosslinks, a key determinant of ligament, tendon, and bone quality. Recent studies have reported high frequency of hypovitaminosis C in the general population. We hypothesized that lack of vitamin C contributes to poor collagen properties and back pain. We conducted this study to examine the associations between serum concentration of vitamin C and the prevalence of spinal pain and related functional limitations in the adult general population. This study used nationwide cross-sectional data from the U.S. National Health and Nutrition Examination Survey (NHANES) 2003-2004. Data were available for 4742 individuals aged ≥20 years. Suboptimal serum vitamin C concentrations were associated with the prevalence of neck pain (adjusted odds ratio [aOR]: 1.5; 95% confidence interval [CI]: 1.2-2.0), low back pain (aOR: 1.3; 95% CI: 1.0-1.6), and low back pain with pain below knee (aOR: 1.3; 95% CI: 1.0-1.9) in the past 3 months, self-reported diagnosis of arthritis/rheumatism (aOR: 1.4; 95% CI: 1.2-1.7), and related functional limitations' score (adjusted difference of means [aB]: 0.03; 95% CI: 0.00-0.05).

The prevalence of hypovitaminosis C in the general population is high. Our study shows associations between vitamin C and spinal pain that warrant further investigation to determine the possible importance of vitamin C in the treatment of back pain patients."

https://www.ncbi.nlm.nih.gov/pubmed/27434504 .

jussipussi
Seuraa 
Viestejä52986

Viinan perkele.

Acute Ethanol Intake Induces NAD(P)H Oxidase Activation and Rhoa Translocation in Resistance Arteries.

Abstract

BACKGROUND::

The mechanism underlying the vascular dysfunction induced by ethanol is not totally understood. Identification of biochemical/molecular mechanisms that could explain such effects is warranted.

OBJECTIVE::

To investigate whether acute ethanol intake activates the vascular RhoA/Rho kinase pathway in resistance arteries and the role of NAD(P)H oxidase-derived reactive oxygen species (ROS) on such response. We also evaluated the requirement of p47phox translocation for ethanol-induced NAD(P)H oxidase activation.

METHODS::

Male Wistar rats were orally treated with ethanol (1g/kg, p.o. gavage) or water (control). Some rats were treated with vitamin C (250 mg/kg, p.o. gavage, 5 days) before administration of water or ethanol. The mesenteric arterial bed (MAB) was collected 30 min after ethanol administration.

RESULTS::

Vitamin C prevented ethanol-induced increase in superoxide anion (O2-) generation and lipoperoxidation in the MAB. Catalase and superoxide dismutase activities and the reduced glutathione, nitrate and hydrogen peroxide (H2O2) levels were not affected by ethanol. 

Vitamin C and 4-methylpyrazole prevented the increase on O2- generation induced by ethanol in cultured MAB vascular smooth muscle cells.

Ethanol had no effect on phosphorylation levels of protein kinase B (Akt) and eNOS (Ser1177 or Thr495 residues) or MAB vascular reactivity. 

Vitamin C prevented ethanol-induced increase in the membrane: cytosol fraction ratio of p47phox and RhoA expression in the rat MAB.

CONCLUSION::

Acute ethanol intake induces activation of the RhoA/Rho kinase pathway by a mechanism that involves ROS generation. In resistance arteries, ethanol activates NAD(P)H oxidase by inducing p47phox translocation by a redox-sensitive mechanism."

https://www.ncbi.nlm.nih.gov/pubmed/27812679 .

jussipussi
Seuraa 
Viestejä52986

Meta-analyysi.

"Meta-analysis of ascorbic acid for prevention of postoperative atrial fibrillation after cardiac surgery.

Abstract

PURPOSE:

Results of a systematic review and meta-analysis of published data on use of ascorbic acid to prevent postoperative atrial fibrillation (POAF) after cardiac surgery are presented.

METHODS:

MEDLINE and other sources were searched for reports on trials evaluating the effects of preoperative and/or postoperative use of ascorbic acid in patients undergoing cardiac surgery. For each study selected for meta-analysis, an assessment for risks of methodological bias was performed. Data on POAF frequency and length of stay (LOS) outcomes were pooled and analyzed via random-effects modeling.

RESULTS:

The 11 identified studies involved patients receiving coronary artery bypass grafts with or without valve replacement; both i.v. and oral ascorbic acid formulations were used. Analysis of pooled outcomes data on treatment and control groups indicated that ascorbic acid prophylaxis was associated with reductions in POAF frequency (odds ratio, 0.44; 95% confidence interval [CI], 0.32 to 0.61), intensive care unit (ICU) LOS (difference in means, -0.24 day; 95% CI, -0.45 to -0.03 day), and total hospital LOS (difference in means, -0.94 day; 95% CI, -1.65 to -0.23 day). Significant statistical, methodological, and clinical heterogeneity were observed.

CONCLUSION:

A meta-analysis revealed that, compared with use of a placebo or a non placebo control, perioperative administration of ascorbic acid to patients undergoing cardiac surgery was associated with a reduced frequency of POAF and a shorter ICU LOS and total hospital LOS."

https://www.ncbi.nlm.nih.gov/pubmed/27806938 .

jussipussi
Seuraa 
Viestejä52986

Yksi tupakoinnin riskeistä.

"Smokers under the age of 50 are more than eight times as likely as non-smokers to have a major heart attack, making them the most vulnerable of any age group of smokers, reveals research published online in the journal Heart."

http://medicalxpress.com/news/2016-11-eight-fold-higher-major-heart-50s....

Sydämen ohitusleikkauksessa tupakoinnin lopettaminen ennen leikkausta ja vaikutukset veren C-vitamiinpitoisuuteen.

Levels of vitamin C In the blood plasma patients treated with coronary artery bypass grafting increases significantly after surgery.

Abstract

One strong risk factor of coronary artery disease (CAD), which affects the levels of vitamin C in the blood is cigarette smoking. The supplementary effects of coronary artery bypass grafting (CABG) is smoking cessation by patients. Therefore, the aim of this study was to examine the level of vitamin C in the blood plasma one day before and one month after CABG. Human blood were collected from 20 patients (men); 1day before and 1 month after CABG. All patients were smoker and after CABG they declared their not smoking. The concentration of vitamin C in the blood plasma was assayed by FIA method with spectrophotometric detection. The mean value of the vitamin C concentration 1day before CABG was 12.36±2.84μmol/L (mean±SD), 1 month after CABG 40.07±10.95μmol/L (mean±SD). The average increase in the concentration of vitamin C was 3.27±0.73 times (mean±SD) and showed significant positive correlations (Pearson r=0.657, p=0.002).

It should be consider incorporating the recommendations of preoperative smoking cessation for at least one month prior to CABG and/or additional supplementation. In addition it would be relevant to monitor the level of vitamin C in the patients' blood in the preoperative period."

https://www.ncbi.nlm.nih.gov/pubmed/27890433 .

Ko C-vitamiinitasoilla 12.36±2.84μmol/L (mean±SD) ennen leikkausta voidaan spekuloida myös mahdollisella keripukilla.

"Scurvy, the classic disease of severe vitamin C deficiency, is characterized by symptoms related to connective tissue defects. Scurvy usually occurs at a plasma concentration of less than 11 µmol/L (0.2 mg/dL)."

https://www.ncbi.nlm.nih.gov/books/NBK225480/ .

"Jo hävinneeksi luultu keripukki on palannut Australiaan, kertoivat terveysviranomaiset tiistaina. Tauti oli purjelaivojen aikakaudella etenkin merimiesten riesana, koska nämä joutuivat olemaan kuukausikaupalla ilman tuoreita vihanneksia ja hedelmiä.

Viranomaisten mukaan keripukin paluu johtuu surkeista ruokailutottumuksista ja väärästä ruuan valmistamisesta."

http://www.ksml.fi/ulkomaat/Jo-h%C3%A4vinneeksi-luultua-keripukkia-l%C3%...

Tupakoijat kannattaisi mielestäni tutkia ihan erikseen veren C-vitamiinitasojen suhteen. Erityisesti leikkauksiin joutuvat.

jussipussi
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Viestejä52986

Sama alhaisten veren C-vitamiinpitoisuuksien (Osalla mahdolisesti keripukin, "suggesting severe vitamin C deficiency") ja tupakoinnin yhteys löytyi jo aikoinaan Pohjois-Karjalan tutkimuksissa.

"Plasma ascorbic acid concentrations in the Republic of Karelia, Russia and in NorthKarelia, Finland.

OBJECTIVES:

To determine the plasma ascorbic acid concentrations among men in North Karelia (Finland) and in Pitkäranta (Republic of Karelia) and to test how a short intervention would affect the plasma concentrations.

DESIGN:

The baseline survey was done as a cross-sectional population survey. A subsample was selected to the intervention study and randomised to treatment and control groups.

SETTING:

North Karelia province in Finland and the Pitkäranta area in the Republic of Karelia.

SUBJECTS:

In the cross-section population survey the stratified random sample of men between 25 and 64 years of age was 1000 in North Karelia and 500 in Pitkäranta. Participation rates were 68% and 77%, respectively. Plasma ascorbic acid measurements were made in one-third of the sample. In Pitkäranta 60 men, having very low plasma ascorbic acid concentrations, were invited to the intervention study.

INTERVENTIONS:

A controlled intervention study was made with blackcurrant-strawberry nectar in which vitamin C content was approximately 70 mg/100 g. The treatment group drank two times daily 200 ml nectar for 4-5 weeks. After intervention plasma ascorbic acid concentration was measured from both treatment and control groups.

RESULTS:

Plasma ascorbic acid concentrations were very different in the two areas. In Pitkäranta 93% of the men and in North Karelia only 2% of the men had plasma levels suggesting severe vitamin C deficiency. After intervention 46% of the men in the experimental group compared with 5% in the control group had plasma ascorbic acid concentrations exceeding 23 mumol/l (4.0 mg/l).

CONCLUSIONS:

In addition to a high smoking prevalence the very low ascorbic acid concentration among men in the Republic Karelia can have an effect on the high cardiovascular disease mortality."

https://www.ncbi.nlm.nih.gov/pubmed/?term=vitamin+c%2C+puska%2C+north+ka... .

.

Tältä vuodelta.

"Tobacco Control: From North Karelia to the National Level.

Abstract

After World War II, smoking among men was very common in Finland, and especially in North Karelia, contributing to the high rates of cardiovascular diseases and cancer. Thus, the North Karelia Project, from its very start in 1972, took reduction in smoking as one of its main targets. After 1977, the project actively contributed to national tobacco control work, including comprehensive legislation and many other activities. Smoking in North Karelia declined initially much more than in the rest of Finland, but thereafter there has been a steady national decline, resulting in a prevalence of daily smoking among adults of approximately 15% and contributing to the big reduction in the rates of heart disease and tobacco-related cancers, especially among men."

https://www.ncbi.nlm.nih.gov/pubmed/27242085 .

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Viestejä52986

Otsikko olisi ollut mielestäni totuudellisempi näin:

Why high-dose intravenous vitamin C kills cancer cells. (Suonensisäisesti)

"Why high-dose vitamin C kills cancer cells

Vitamin C has a patchy history as a cancer therapy, but researchers at the University of Iowa believe that is because it has often been used in a way that guarantees failure.

Most vitamin C therapies involve taking the substance orally. However, the UI scientists have shown that giving vitamin C intravenously—and bypassing normal gut metabolism and excretion pathways—creates blood levels that are 100 - 500 times higher than levels seen with oral ingestion. It is this super-high concentration in the blood that is crucial to vitamin C's ability to attack cancer cells.

Earlier work by UI redox biology expert Garry Buettner found that at these extremely high levels (in the millimolar range), vitamin C selectively kills cancer cells but not normal cells in the test tube and in mice. Physicians at UI Hospitals and Clinics are now testing the approach in clinical trials for pancreatic cancer and lung cancer that combine high-dose, intravenous vitamin C with standard chemotherapy or radiation. Earlier phase 1 trials indicated this treatment is safe and well-tolerated and hinted that the therapy improves patient outcomes. The current, larger trials aim to determine if the treatment improves survival.

In a new study, published recently in the December issue of the journal Redox Biology, Buettner and his colleagues have homed in on the biological details of how high-dose vitamin C (also known as ascorbate) kills cancer cells.

The study shows that vitamin C breaks down easily, generating hydrogen peroxide, a so-called reactive oxygen species that can damage tissue and DNA. The study also shows that tumor cells are much less capable of removing the damaging hydrogen peroxide than normal cells.

"In this paper we demonstrate that cancer cells are much less efficient in removing hydrogen peroxide than normal cells. Thus, cancer cells are much more prone to damage and death from a high amount of hydrogen peroxide," says Buettner, a professor of radiation oncology and a member of Holden Comprehensive Cancer Center at the University of Iowa. "This explains how the very, very high levels of vitamin C used in our clinical trials do not affect normal tissue, but can be damaging to tumor tissue."

"Our results suggest that cancers with low levels of catalase are likely to be the most responsive to high-dose vitamin C therapy, whereas cancers with relatively high levels of catalase may be the least responsive," he explains.

A future goal of the research is to develop methods to measure catalase levels in tumors.

http://medicalxpress.com/news/2017-01-high-dose-vitamin-cancer-cells.html .

"Tumor cells have decreased ability to metabolize H2O2: Implications for pharmacological ascorbate in cancer therapy

Highlights

• Ascorbate oxidizes in cell culture medium to generate a flux of H2O2.

• The rate constants for removal of extracellular H2O2 are on average 2-fold higher in normal cells than in cancer cells.

• The ED50 of high-dose ascorbate correlated with the ability of tumor cells to remove extracellular H2O2.

• The response to pharmacological ascorbate in murine-models of pancreatic cancer paralleled the in vitro results."

http://www.sciencedirect.com/science/article/pii/S2213231716302634 .

Vetyperoksidin muodostuminen ei ole ainoa mahdollinen mekanismi miten C-vitamiini mahdollisesti vaikuttaa syöpäsoluhin.

jussipussi
Seuraa 
Viestejä52986

"Vitamin C down-regulate apo(a) expression via Tet2-dependent DNA demethylation in HepG2 cells.

Abstract

Lipoprotein(a)[Lp(a)] is a risk factor for coronary heart diseases. However, the metabolism of this protein remains poorly understood. Efficient and specific drugs that can decrease high plasma levels of Lp(a) have not been developed yet. Vitamin C is responsible for maintaining the catalytic activity of a group of iron and 2-oxoglutarate (2OG)-dependent dioxygenases and induces the generation of 5-hydroxymethylcytosine (5hmC) via Ten-eleven translocation (Tet) dioxygenases. In addition,

It has been reported vitamin C deficiency induces atherosclerosis and increases Lp(a) and apo(a) plasma levels in Lp(a)+ mice. However, the mechanism is still unclear.

In this study, we investigated the effects of vitamin C on apo(a) expression and the possible molecular mechanism of vitamin C that influences apolipoprotein(a) [apo(a)] biosynthesis in HepG2 cells. Results showed that vitamin C significantly inhibited the expression and secretion levels of apo(a). Vitamin C can also increase ELK1 expression and hydroxymethylation of ELK1 promoter and the globle DNA in HepG2 cells. In addition, the effects of vitamin C inhibiting the apo(a) expression were attenuated by ELK1siRNA and Tet2siRNA. These results suggested vitamin C down-regulate apo(a) expression via Tet2-dependent DNA demethylation in HepG2 cells.

https://www.ncbi.nlm.nih.gov/pubmed/28192139

"Lipoprotein(a) (also called Lp(a) or LPA) is a lipoprotein subclass. Genetic studies and numerous epidemiologic studies have identified Lp(a) as a risk factor for atherosclerotic diseases such as coronary heart disease and stroke.[3][4][5][6][7]

---

However, individuals without Lp(a) or with very low Lp(a) levels seem to be healthy.[31] Thus, plasma Lp(a) is not vital, at least under normal environmental conditions. Since apo(a)/Lp(a) derived rather recently in mammalian evolution - only old world monkeys and humans have been shown to harbour Lp(a) - its function might not be vital but just evolutionarily advantageous under certain environmental conditions, e.g. in case of exposure to certain infectious diseases.

Another possibility, suggested by Linus Pauling, is that Lp(a) is a primate adaptation to L-gulonolactone oxidase (GULO) deficiency, found only in certain lines of mammals. GULO is required for converting glucose to ascorbic acid (vitamin C), which is needed to repair arteries; following the loss of GULO, those primates that adopted diets less abundant in vitamin C may have used Lp(a) as an ascorbic-acid surrogate to repair arterial walls.[32]"

https://en.wikipedia.org/wiki/Lipoprotein(a)  .

jussipussi
Seuraa 
Viestejä52986

"Ascorbic acid ameliorates behavioural deficits and neuropathological alterations in rat model of Alzheimer's disease.

Abstract

Exploring the links between neural pathobiology and behavioural deficits in Alzheimer's disease (AD), and investigating substances with known therapeutic advantages over subcellular mechanisms underlying these dysfunctions could advance the development of potent therapeutic molecules for AD treatment. Here we investigated the efficacy of ascorbic acid (AA) in reversing aluminium chloride (AlCl3)-induced behavioural deficits and neurotoxic cascades within prefrontal cortex (PFC) and hippocampus of rats. A group of rats administered oral AlCl3 (100mg/kg) daily for 15days showed degenerative changes characterised by significant weight loss, reduced exploratory/working memory, frontal-dependent motor deficits, cognitive decline, memory dysfunction and anxiety during behavioural assessments compared to control. Subsequent analysis showed that oxidative impairment-indicated by depleted superoxide dismutase and lipid peroxidation (related to glutathione-S-transferase activity), cholinergic deficits seen by increased neural acetylcholinesterase (AChE) expression and elevated lactate dehydrogenase underlie behavioural alterations. Furthermore, evidences of proteolysis were seen by reduced Nissl profiles in neuronal axons and dendrites which correspond to apoptotic changes observed in H&E staining of PFC and hippocampal sections. Interestingly, AA (100mg/kg daily for 15days) significantly attenuated behavioural deficits in rats through inhibition of molecular and cellular stressor proteins activated by AlCl3. 

Our results showed that the primary mechanisms underlying AA therapeutic advantages relates closely with its abilities to scavenge free radicals, prevent membrane lipid peroxidation, modulate neuronal bioenergetics, act as AChE inhibitor and through its anti-proteolytic properties.

These findings suggest that supplementing endogenous AA capacity through its pharmacological intake may inhibit progression of AD-related neurodegenerative processes and behavioural alterations."

https://www.ncbi.nlm.nih.gov/pubmed/28192749 .

jussipussi
Seuraa 
Viestejä52986

"Vitamin C may decrease risk of atrial fibrillation after cardiac surgery

Date: February 1, 2017

Source: University of Helsinki

Summary:

Vitamin C decreased the incidence of post-operative atrial fibrillation (AF) by 44% in cardiac surgery patients in nine randomized trials that were conducted outside of the USA according to a meta-analysis.

https://www.sciencedaily.com/releases/2017/02/170201141939.htm .

jussipussi
Seuraa 
Viestejä52986

jussipussi kirjoitti:
Sama alhaisten veren C-vitamiinpitoisuuksien (Osalla mahdolisesti keripukin, "suggesting severe vitamin C deficiency") ja tupakoinnin yhteys löytyi jo aikoinaan Pohjois-Karjalan tutkimuksissa.

Pohjois-Karjalan löydöksiä voisi tarkastella maallikon mielestäni yliyksinkertaistaen tupakointi, alhaiset C-vitamiinitasot veressä(käytännössä keripukkia)valtimoiden suonenseinämän vammautuminen/tulehdus ja näistä edellisistä johtuvat korkeat Lipoproteiini (a) tasot.

jussipussi
Seuraa 
Viestejä52986

"Obesity, cardiovascular disease, and role of vitamin C on inflammation: a review of facts and underlying mechanisms.

Abstract

Obesity means the accumulation of excessive fat that may interfere with the maintenance of optimal state of health. Obesity causes cardiac and vascular disease through well-known mediators such as hypertension, type-2 diabetes mellitus, and dyslipidemia, but there are evidences for other mediators such as chronic inflammation, oxidative stress, and thrombosis. The decreased levels of antioxidants factors and nitric oxide predispose to further cardiovascular adverse events. To reduce the risks, antioxidants can help by neutralizing the free radicals and protecting from damage by donating electrons.

Having the capacity, vitamin C protects from oxidative stress, prevention of non-enzymatic glycosylation of proteins, and enhances arterial dilation through its effect on nitric oxide release. It also decreases lipid peroxidation, and alleviates inflammation. The anti-inflammatory property of vitamin C could be attributed to ability to modulate the NF-kB DNA binding activity and down-regulation in the hepatic mRNA expression for the interleukins and tumor factors."

https://www.ncbi.nlm.nih.gov/pubmed/28168552 .

Vierailija

Voiko olla että c-vitamiinin puutos aiheuttaisi verisuoniin pieniä halkeiluja (niinkuin keripukissa) ja näitä sitten keho paikkailee jollain kolesteroli tms lipoproteiinijutuilla mitä lie? (sori tieteellisesti epämääräinen ulosantini) Tämä ilmenisi sitten ateroskleroosina jne. Eikös tupakka ja sokeri olleet c-vitamiinille ilkeitä.. 

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