If the findings of a latest study undertaken by scientists at the University of Southern California and University of Oxford are to be believed, consuming foods with high-fructose corn syrup may help to contribute to a type 2 diabetes epidemic. The findings show that diabetes is higher by 20% in countries that use this sweetener in high amounts in comparison to those that don't. Besides, the findings also tell that the connection between notably enhanced occurrence of diabetes and HFCS (high-fructose corn syrup) is regardless of the total sugar use and obesity levels.
According to the University of Oxford's Institute of Social and Cultural Anthropology director and co-author of the study, Stanley Ulijaszek, their study reveals an ecological link suggesting potential risks of consuming elevated amounts of high-fructose corn syrup. In fact, HFCS, which is sweeter and is used as an additive in processed foods to enhance their appearance, contains more fructose compared to common table sugar.
Ulijaszek's team examined data concerning availability of HFCS in 42 countries and found that 8% people in countries using this food sweetener in high amounts suffer from type 2 diabetes in comparison to just 6.7% in those that don't. The study found that the use of HFCS is highest in the US, with each individual taking 29 kg of the food sweetener on average annually, while Hungary with 16 kg per head is second. Canada, Mexico, Argentina, Belgium, Bulgaria, Slovakia, Japan and Korea also have high HFCS use, while the consumption is below 0.5 kg per head in the UK.
Dismissing the belief that fructose is a natural sugar obtained from fruits as a myth, Ulijaszek says that natural fructose from fruits is excellent in low amounts since it is released slowly, but metabolically fructose and sucrose differ. However, it has been found that our huge quantities of fructose not having origin in fruits are difficult to metabolize and can enhance chances of developing type 2 diabetes - the most common cause of death worldwide.
Lead author and USC's Keck School of Medicine professor Michael Goran says that their study confirms that HFCS consumption may cause negative health conditions that are different from using natural sugar.
The study found that despite the fact that our body is unable to metabolize HFCS ingested in large amounts, it has been found that majority of people consume sweet foods containing this sweetener voraciously. This has reached such a point that by the end of 20th century, almost 40 per cent of entire caloric sweeteners in the US were HFCS - making the country the largest consumer of this food sweetener.
The study suggests that the best way to restrict the use of high-fructose corn syrup is to properly label the amount of HFCS and fructose in all sweet foods, including eatables and beverages.
The findings of another study reported in the International Journal of Obesity suggest that consumption of HFCS is not related to the obesity epidemic.
Infection control specialists are worried over the recent outbreaks of a dangerous new form of superbug in two hospitals in Toronto region. Findings of a recent study reported in medical journals have detailed the spread of the superbug and the way hospitals succeeded in stopping its spread in Canada.
However, they only report the initial outbreak of the bacteria having supposed NDM-1 enzyme, stating that anyway in both incidents, one of the victims carrying the bacteria appears to have been infected in Canada. The earlier cases of NDM-I infection in Canada included individuals who had acquired the bacteria from outside the country - mostly India and some in the USA.
While NDM-I, wherein ND represents New Delhi, is a positive bacteria detected in Canada first in 2010, worldwide this superbug was detected in a Swedish national, who visited India for treatment, in 2008. When this was reported in Lancet, it sounded an alarm globally as this signified a new means of drug resistance. In fact, NDM-1 has been there for a long time and has actually flourished with the increased use of antibiotics during the latter half of 2101 making pharmaceuticals scramble to develop medicaments to treat drug-resistant bacteria.
Interestingly, NDM-1 is not a bacterium, but an enzyme made by a few bacteria that inactivates an assortment of antibiotics. However, some drug can cure NDM-1 infection, but they are barely used antibiotics, including colistin, which is extremely toxic, but eventually NDM-1 becomes resistant to this drug also, says senior author of one study Dr. Andrew Simor, adding, while the term superbug has been around for several years threatening a situation where infections wouldn't be treated owing to hazards of drug resistance, now, with the existence of NDM-I, this threat seems to have become a reality.
What is more disturbing is that NDM-1 is produced by an unrestrained gene that moves from one bacterium to another and each time increasing the drug resistance of this enzyme, leaving few options for physicians. One patient mentioned in one study was affected by E. coli and Klebsiella pneumonia containing NDM-1, which led physicians to deduce that it transmits from one microbe to another in a patient.
Talking about NDM-1 and other similar drug-resistant enzymes, Toronto Mount Sinai Hospital's infection control head and author of one paper, Allison McGeer says five patients were involved in the outbreak at Brampton and all carried Klebsiella pneumonia. It was found that bacteria from each of them were related. Interestingly, none of them had been to countries having NDM-1 as an endemic. While the bacteria spread from these people to others, the researchers are yet to ascertain how they acquired it.
Simor suggests that the best way to stop the outbreak is for infection control teams at hospitals to ensure the prevention of its spread. The teams do take the hospitalized patient's rectal swabs for inspection; the samples are usually negative till three weeks after exposure. However, McGreer says that though the hospital staffs in Canada are careful about this issue, she is not certain if adequate attention is being paid to the danger.
The findings of recent study suggests that incorporating the anti-cholesterol drug lovastatin in traditional malarial treatment may to lessen neuro-inflammation plus ward off cerebral damage. A research report published in PLOS Pathogens on December 27, 2012 says that while this lab discovery may differ in the case of cerebral malaria and also the disease in humans, henceforth, scientists may consider using statin in clinical trials involving cerebral malaria - a major contagious ailment globally.
Stating that more than 500,000 children in sub-Saharan Africa develop malaria, an infection attributable to a parasitic Plasmodium falciparum that passes on to humans through females of Anopheles mosquito, associate chair (research) at the University of Utah's Department of Medicine and the research co-author, Dr. Guy Zimmerman emphasizes on the pressing need as well as unmet medical requirement for remedies to cure or put off cognitive injury in cerebral malaria. Such cognitive discrepancy may include poor ability to remember, learn, speak and/ or do arithmetic in children.
Besides lowering blood cholesterol, statins are also known to modulate various responses of the immune system. In a study undertaken on mice, Zimmerman and his colleagues from Brazil examined the outcome of using statins in cerebral malaria. They discovered that using lovastatin along with conventional anti-malarial treatment put off cognitive malfunctioning in rats affected by cerebral malaria. It was found that lovastatin not only reduces white blood cells build-up and seepage in the brain's blood vessels, it also lessens the manufacture of harmful molecules containing oxygen and additional issues that advance inflammation.
According to Zimmerman, though the means by which cerebral malaria is induced and ensuing cognitive failure are yet to be ascertained, treatment with statins lessen harmful inflammation of the blood vessels and cognitive malfunctioning, which indicate that inflammatory and vascular triggers result in cerebral pathology plus intellectual deficiencies.
Describing the findings as 'exciting', Zimmerman feels that the clinical inferences not only pertain to cerebral malaria, but also to additional serious general inflammatory syndromes that become complex owing to the involvement of the brain. His team believes that their observations are the earliest investigational proof that endorses the prospects of using statins to diminish cognitive damage in people with severe cerebral malaria.
Zimmerman and his Brazilian teammates also undertook a research using lovastatin in a trial model involving bacterial sepsis - a severe condition wherein the entire body becomes inflamed often resulting in cognitive impairment and found that this anti-cholesterol drug also puts off cognitive damage after bacterial sepsis.
Considering that epilepsy strikes over two million people in the United States, there is an urgent need to develop new treatment approaches helpful in putting off the occurrence of this neurological disorder, incapacitating the sufferers. Fortunately, latest findings from studies conducted by Mark S. Shapiro at the San Antonio-based University of Texas Health Science Center neuroscience laboratory and published in Neuron, a popular scientific journal, on December 20, 2012 shows some hope in this regard.
A professor of physiology associated with the School of Medicine, Dr. (Ph. D.) Shapiro says that most epilepsy victims are unable to take medications to treat their condition or the medications available are not effective enough. Consequently, most sufferers turn to surgery to amputate the hippocampus, the brain segment that stores memories and the centre where attacks are often constrained - limiting the choice for them.
Significantly, these studies discovered that particular genes are triggered during and following an epileptic attack, thereby transmitting a multitude of signals to lessen the wild discharge of nerve cells. Hence, a medication that exaggerates this reaction following the initial seizure may perhaps avert the occurrence of epilepsy and reappearance of seizures.
An epileptic seizure is basically a result of a hysterical electrical action of 'ion channels' or dedicated proteins that generate electricity in the brain. In fact, one in every 10 people has the chance of enduring a seizure, attributable to various reasons - stroke, traumatic brain injury and even an overdose of drugs during his/ her lifetime.
While some seizures cause full-scale epilepsy, others do not - some of them activating alteration in the brain that increases the risks of epilepsy. According to Dr. Shapiro, 'M-channel', an 'ion channel', works like a strong 'brake' to the brain's extreme reaction to stimulus, a condition called 'hyper-excitability', while AKAP79, a different protein working like an air-traffic controller, invites additional M-channels that form an element of neuro-protective response mechanism.
Dr. Shapiro said using medications in appropriate measure following a brain injury may effectively augment the functioning of AKAP79 which might stimulate this neuro-protective system to thwart a seizure from developing into epilepsy. He added that it is possible to effectively control the random electrical discharge of nerve cells within the brain.
The team at Shapiro laboratory documents the electrical currents and undertakes imaging in live cells to gauge their M-channel activity and also studied seizures in healthy rats. It was found that following a seizure there was a 10 times increase in M-channels' gene expression within the hippocampus in 24 hours. However, this outcome was not noticed in mice deficient in the AKAP79 gene's mouse version.
Besides, the findings also point to suggestions regarding respite from persistent pains, mental disorders and cardiovascular ailments. According to Dr. Shapiro, even chronic pains like migraines, hypertension and mood problems involve too much firing of nerve cell. Hence, enhancing signals of M-channel to lessen its firing of nerve cells may possibly be useful in treating these conditions.
Since November 1996, this report is the second research paper from the San Antonio-based University of Texas Health Science Center brought out by Neuron.
