Thursday 30 August 2012
Vitamin B3 'helps kill superbugs'????
Vitamin B3 (Niacin)
Vitamin B3 (Niacin)
Overview:
Dietary Sources:
Available Forms:
How to Take It:
- Infants birth - 6 months: 2 mg (adequate intake)
- Infants 7 months - 1 year: 4 mg (adequate intake)
- Children 1- 3 years: 6 mg (RDA)
- Children 4 - 8 years: 8 mg (RDA)
- Children 9 - 13 years: 12 mg (RDA)
- Boys 14 - 18 years: 16 mg (RDA)
- Girls 14 - 18 years: 14 mg (RDA)
- Men 19 years and older: 16 mg (RDA)
- Women 19 years and older: 14 mg (RDA)
- Pregnant women: 18 mg (RDA)
- Breastfeeding women: 17 mg (RDA)
Precautions:
Possible Interactions:
- Azathioprine (Imuran)
- Chloramphenicol (Chloromycetin)
- Cycloserine (Seromycin)
- Fluorouracil
- Levodopa and carbidopa
- Mercaptopurine (Purinethol)
Alternative Names:
- Reviewed last on: 8/31/2011
- A.D.A.M. Editorial Team: David Zieve, MD, MHA, and David R. Eltz. Previously reviewed by Steven D. Ehrlich, NMD, Solutions Acupuncture, a private practice specializing in complementary and alternative medicine, Phoenix, AZ. Review provided by VeriMed Healthcare Network (6/12/2011).
Supporting Research
AIM-HIGH Investigators. The role of niacin in raising high-density lipoprotein cholesterol to reduce cardiovascular events in patients with atherosclerotic cardiovascular disease and optimally treated low-density lipoprotein cholesterol Rationale and study design. The Atherothrombosis Intervention in Metabolic syndrome with low HDL/high triglycerides: Impact on Global Health outcomes (AIM-HIGH). Am Heart J. 2011 Mar;161(3):471-477.e2.Bissett DL, Oblong JE, Berge CA, et al. Niacinamide: A B vitamin that improves aging facial skin appearance. Dermatol Surg. 2005;31:860-865; discussion 865.
Brown BG, Zhao XQ, Chalt A, et al. Simvastatin and niacin, antioxidant vitamins, or the combination for the prevention of coronary disease. N Engl J Med. 2001;345(22):1583-1592.
Cumming RG, Mitchell P, Smith W. Diet and cataract: the Blue Mountains Eye Study. Ophthalmology. 2000;107(3):450-456.
Draelos ZD, Ertel K, Berge C, et al. Niacinamide-containing facial moisturizer improves skin barrier and benefits subjects with rosacea. Cutis. 2005;76:135-141.
Elam M, Hunninghake DB, Davis KB, et al. Effects of niacin on lipid and lipoprotein levels and glycemic control in patients with diabetes and peripheral arterial disease: the ADMIT study: a randomized trial. Arterial Disease Multiple Intervention Trial. JAMA. 2000;284:1263-1270.
Garcia-Closas R. et al. Food, nutrient and heterocyclic amine intake and the risk of bladder cancer. Eur J Cancer. 2007;43(11):1731-40.
Goldberg A, Alagona P, Capuzzi DM, et al. Multiple-dose efficacy and safety of an extended-release form of niacin in management of hyperlipidemia. Am J Cardiol. 2000;85:1100-1105.
Guyton JR. Niacin in cardiovascular prevention: mechanisms, efficacy, and safety. Curr Opin Lipidol. 2007 Aug;18(4):415-20.
Jacques PF, Chylack LT Jr, Hankinson SE, et al. Long-term nutrient intake and early age related nuclear lens opacities. Arch Ophthalmol. 2001;119(7):1009-1019.
Kuzniarz M, Mitchell P, Cumming RG, Flood VM. Use of vitamin supplements and cataract: the Blue Mountains Eye Study. Am J Ophthalmol. 2001;132(1):19-26.
Mittal MK, Florin T, Perrone J, Delgado JH, Osterhoudt KC. Toxicity from the use of niacin to beat urine drug screening. Ann Emerg Med. 2007;50(5):587-90.
Nutrients and Nutritional Agents. In: Kastrup EK, Hines Burnham T, Short RM, et al, eds. Drug Facts and Comparisons. St. Louis, Mo: Facts and Comparisons; 2000:4-5.
Raja R, Thomas JM, Greenhill-Hopper M, Ley SV, Almeida Paz FA. Facile, one-step production of niacin (vitamin B3) and other nitrogen-containing pharmaceutical chemicals with a single-site heterogeneous catalyst. Chemistry. 2008;14(8):2340-8.
Sanyal S, Karas RH, Kuvin JT. Present-day uses of niacin: effects on lipid and non-lipid parameters. Expert Opin Pharmacother. 2007 Aug;8(11):1711-7.
Torkos S. Drug-nutrient interactions: a focus on cholesterol-lowering agents. Int J Integrative Med. 2000;2(3):9-13.
Wolerton: Comprehensive Dermatalogic Drug Therapy, 2nd ed. Philadelphia, PA: Saunders Elsevier. 2007.
Zhao H, Yang X, Zhou R, Yang Y. Study on vitamin B1, vitamin B2 retention factors in vegetables. Wei Sheng Yan Jiu. 2008;37(1):92-6.
Read more: http://www.umm.edu/altmed/articles/vitamin-b3-000335.htm#ixzz2520UrkZZ
Wednesday 22 August 2012
MRSA and C. diff deaths falling
MRSA and C. diff deaths falling
Monday 22 August 2011
how the body stops C. diff from being toxic
Gut's hospital bug defence found
Related Stories
The way cells in the gut fight off toxins produced by a hospital bug has been discovered by US researchers.
Writing in Nature Medicine, they showed how a chemical - GSNO - deactivated a toxin from Clostridium difficile which causes inflammation and diarrhoea.
They hope to use their findings to develop a treatment for C. difficile.
A specialist in the bacterium said the discovery was "exciting", but any treatment was still a long way off.
C. difficile is one of many bacteria which can live in the human gut without causing health problems.
No competition“Start Quote
End Quote Dr Jonathan Stamler Case Western Reserve UniversityUnderstanding how this mechanism deactivates toxins provides a basis for developing new therapies that can target toxins directly”
A course of antibiotics, which wipes out other bacteria in the gut, can allow C. difficile to multiply and run rampant in the bowels.
They produce large numbers of toxins which enter the cells lining the bowel. This damages the cells resulting in inflammation, cramps, fever, diarrhoea and blood-stained stools.
It is particularly a problem in hospitals as the bacteria can spread, and many patients could be taking antibiotics or have a weakened immune system.
In hospitals in England there were 10,414 C. difficile infections during the financial year 2010-11, down from 33,442 in 2007-08.
Access deniedThe whole toxin is unable to penetrate cells so it needs to cleave off a smaller chunk.
Scientists have identified the chemical GSNO - S-nitrosoglutathione - which is produced by the bowels in response to inflammation. It can bind to the toxin, preventing cleavage, so the toxin cannot enter cells.
One of the researchers Dr Jonathan Stamler, from the Case Western Reserve University, said: "Understanding how this mechanism deactivates toxins provides a basis for developing new therapies that can target toxins directly and thereby keep bacterial infections, like C. diff, from spreading."
In experiments on mice, the study showed giving the chemical orally increased survival. Researchers now want to begin clinical trials.
The report's lead author Prof Tor Savidge, from the University of Texas, believes the technique could be used on other infections.
"Along with its potential to provide a much-needed new approach to treating Clostridium difficile infection, the discovery could be applied to developing new treatments for other forms of diarrhoea, as well as non-diarrheal diseases caused by bacteria," he said.
Prof Nigel Minton, from the Clostridia Research Group at the University of Nottingham, said: "This is an exciting discovery.
"Anything that can add to our scant arsenal of available treatments for combating this devastating disease is an important step forward.
"Having said that, one imagines that an actual therapeutic based on this discovery is some way off, either from being developed, and more importantly, from entering the clinic."
Related Stories
- Q&A: Clostridium difficile 19 OCTOBER 2007, HEALTH
- C. diff rise due to 'gene switch' 28 SEPTEMBER 2009, HEALTH
- C. diff testing 'is often wrong' 01 NOVEMBER 2008, HEALTH
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Monday 28 September 2009
Dramatic rise in C. diff deaths
Tackling hospital infections is a top government priority |
Between 2005 and 2006 the number of death certificates which mentioned the infection rose by 72% to 6,480, most of which were elderly people.
In over half of cases, it was listed as the underlying cause of death.
It is thought that some of the increase may be due to more complete reporting on death certificates.
Deaths involving C. difficile increased by 77% in men, and 66% in women between 2005 and 2006.
Since 2006 we have taken significant steps to tackle infections Professor Brian Duerden, Department of Health |
Rates in both sexes have gone up dramatically since 2001, when there were only 1,200 mentions of the infection on death certificates.
The ONS figures also showed deaths involving MRSA remained roughly the same between 2005 and 2006 - at around 1,650.
C. difficile usually affects the elderly, and can prove fatal if antibiotic treatment fails to kill all the spores in the gut, and they take hold again before the patient's own gut bacteria have had chance to mount a resistance.
It is also very difficult to eradicate from the ward environment, which means it is easy for other patients to become infected.
Professor Brian Duerden, chief microbiologist at the Department of Health, said in July 2005 they called for more accurate reporting of infections such as MRSA and C. difficile on death certificates.
"These statistics from 2006 show that this move has worked and our figures are now in line with other developed countries.
"Since 2006 we have taken significant steps to tackle infections.
"These include stringent hand-washing guidance for the NHS, a bare below the elbows dress code, putting matrons back in charge of cleanliness on their wards and an ongoing deep clean of every ward."
And he added hospital infection rates were now falling.
The Health Protection Agency reported in November 2007 that rates of C. difficile infection may be levelling off with the number of new cases down 7% to 13,660, while MRSA cases are falling.
Liberal Democrat health spokesman Norman Lamb said: "These figures beg the question of why it took so long for the government to realise the seriousness of deadly infections such as C. difficile.
"Recent successes in keeping infection rates down are down to the hard work of NHS staff, who are up against enormous pressure to hit targets while keeping their wards infection-free."
Shadow health secretary, Andrew Lansley, said: "Almost three times as many people are now killed by hospital infections as are killed on the roads each year.
"The overall scale of infection is unacceptable and the need for a comprehensive infection control strategy, including improved antibiotic prescribing and access to isolation facilities, hand hygiene and cleanliness is paramount."
He added: "An expert told the Department of Health last week that it was the government's failure to implement guidelines since as far back as 1994 that has contributed to the recent rise."
C. diff rise due to 'gene switch
C. diff rise due to 'gene switch'
Most deaths from C. difficile occur in the over 65s |
The rise in Clostridium difficile infections in recent years is due to genetic changes rather than dirty hospitals, say UK researchers.
Comparison of an historic strain and a strain from the outbreak at Stoke Mandeville hospital in 2003 found it had evolved to be more virulent.
It can spread more easily and cause more severe symptoms, the team reports in Genome Biology journal.
NHS trusts have a target to cut C. difficile infections by 30% by 2010/11.
The bacteria are present in the gut of as many as 3% of healthy adults and 66% of infants.
It rarely causes problems in healthy people but can lead to illness when the normal balance of bacteria in the gut is disrupted, for example with use of certain antibiotics, and it is the leading cause of hospital-acquired diarrhoea.
The deep clean programme was never going to work against this organism in the long term Professor Brendan Wren |
In the past five years, a new group of highly virulent C. difficile strains has emerged - PCR-ribotype 027 - which cause more severe diarrhoea and a higher rate of deaths.
Analysis of the full genome of the "hyper-virulent" strains and an older strain showed the bacteria have acquired genes which enable them to survive better in the environment, spread more easily and make patients more severely ill.
In all, five different genetic regions appear to have accumulated in the bacteria in past couple of decades, the team reported in Genome Biology.
Fighting back
The number of cases of C. difficile has risen dramatically since the 1990s, although latest figures show cases are now consistently falling.
Stoke Mandeville Hospital saw two major outbreaks of C. difficile between 2003 and 2006 that caused 35 deaths.
Study leader Professor Brendan Wren, from the London School of Hygiene and Tropical Medicine, said the study would help scientists understand how C. difficile became so aggressive.
"These strains came from nowhere and the sudden rise in C. difficile was due to their spread.
"The bugs are fighting back and the one clear thing that comes out of this study is it is not down to cleaning but that the strain has evolved with new chunks of DNA.
"The deep clean programme was never going to work against this organism in the long term."
Hygiene measures are still needed to keep the infection under control, he added.
A spokeswoman for the Health Protection Agency said it closely monitored the evolution of C. difficile strains.
"All strains of C. difficile require intervention and control - the intervention involved when dealing with the 027 strain is no different than how any other strain is treated.
"All C. difficile requires treatment and vigilant infection control procedures in order to reduce rates of infection."
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