sábado, 16 de abril de 2016

Preventive Effects of Cocoa and Cocoa Antioxidants in Colon Cancer



Currently, in a society where prevalence of cancer is on the top of illnesses, the rythm of life that society obbey us, forcing to have an inadecuate diet and a deficit of physical exercise that increase the risk of this disease.
I´ve chosen this article because it exposes the healing properties of natural products such as cocoa known
since ancient times.



Preventive Effects of Cocoa and Cocoa Antioxidants in Colon Cancer
María Angeles Martín, Luis Goya and Sonia Ramos *
Department of Metabolism and Nutrition, Institute of Food Science and Technology and Nutrition (ICTAN-CSIC) Madrid, Spain
22 January 2016

Abstract
 Colorectal cancer is one of the main causes of cancer-related mortality in the developed world. Carcinogenesis is a multistage process conventionally defined by the initiation, promotion and progression stages.
 Natural polyphenolic compounds can act as highly effective antioxidant and chemo-preventive agents able to interfere at the three stages of cancer. Cocoa has been demonstrated to counteract oxidative stress and to have a potential capacity to interact with multiple carcinogenic pathways involved in inflammation, proliferation and apoptosis of initiated and malignant cells. Therefore, restriction of oxidative stress and/or prevention or delayed progression of cancer stages by cocoa antioxidant compounds has gained interest as an effective approach in colorectal cancer prevention. 

  


Introduction
Cancer is a multistage process conventionally defined by three stages: initiation, promotion and progression. Development of colon cancer typically is initiated from normal epithelial cells via aberrant crypts and progressive adenoma stages to carcinomas in situ and then metastasis. Along this process, oxidative stress has the potential to affect numerous signaling pathways related to the proliferation of initiated cells and enhanced malignant transformation .In the initiation stage, the generation of reactive oxygen species (ROS) has been involved in DNA damage and in the development of aberrant crypt foci (ACF),the earliest identifiable precancerous lesions in colon cancer. Similarly, in the post-initiation/promotion stages, ROS also contribute to abnormal gene expression and modification of second-messenger systems in epithelial cells within the ACF.
 
 Aerobic organisms cannot avoid free radical and ROS generation, which are produced during normal oxygen metabolism or induced by exogenous damage. In a physiological situation, cells maintain the balance between the generation and counteraction of ROS through non-enzymatic processes (mainly glutathione (GSH)) and enzymatic defenses (catalase (CAT), glutathione peroxidase (GPx), glutathione reductase (GR), glutathione-S-transferase (GST) superoxide dismutase (SOD), etc.). However, when the cellular balance is altered and antioxidant defenses overwhelmed, cells can be damaged. All of these modifications might provoke errors during DNA replication and genetic alterations, modulate transcription of redox-regulated proteins, etc., leading to enhanced cell proliferation and tumor promotion/progression.

Therefore, inhibition of oxidative stress together with the modulation of signaling routes related to cell survival/proliferation exerted by natural antioxidant compounds seems to be an effective approach in preventing and slowing down the initiation and progression of colon cancer.

Cocoa and its flavonoids are strong antioxidant substances so they can prevent the DNA damage caused by free radicals or carcinogenic agents acting through the modulation of enzymes related to oxidative stress (CAT, GR, GPx, SOD, etc.) and the alteration of the procarcinogenic metabolism by inhibiting phase I drug-metabolizing enzymes (cytochrome P450) or activating phase II conjugating-enzymes (glucuronidation, sulfation, acetylation, methylation and conjugation).

Animal studies have proven that cocoa and its main flavanols would prevent and/or slow down the initiation promotion of colon cancer. However, amounts administrated are probably higher than what a person should normally consume and, despite these doses could be achievable through supplementation, more moderate quantities of cocoa would be desirable.

In summary, daily consumption of small amounts of flavanols and procyanidins from cocoa or chocolate, together with an ordinary dietary intake of flavonoids, would constitute a natural approach to potentially prevent colon cancer with minimal toxicity. Nevertheless, cocoa and its derivative products merit further investigations, since the molecular mechanisms of action are not completely elucidated. Additionally, extensive well-controlled and well-designed human epidemiological and intervention studies are needed to fully assess the potential of cocoa in terms of optimal dose, route of administration, cancer targets and preventive activities.

martes, 5 de abril de 2016

Progress Being Made at Understanding, Treating Complicated Grief

Columbia University’s M. Katherine Shear, M.D., has been leading the way in untangling when the normal grieving process goes awry and how to restore the balance with psychotherapy.
For a long time, the psychiatric community has had a mixed understanding of grief. The concept of grief as an important part of dealing with loss was well recognized, and a trained professional could easily identify someone going through the grieving process. But, as M. Katherine Shear, M.D., the Marion E. Kenworthy Professor of Psychiatry at Columbia University, pointed out, “What wasn’t covered during my training—and something that I think is still lacking—was a discussion of what grief itself actually entailed.”
Such questions were daunting, but ones that many medical professionals at the time did not focus on because they ascribed to the same mantra found among the general public: everyone grieves in his or her own way.“What sort of forms does [grief] take? How long do we expect it to last? And importantly, is there a point at which grief becomes problematic?” Shear continued.
Shear, however, was determined to come up with answers to her questions about grief. For the past two decades, she has been leading efforts to delineate the line between healthy and unhealthy grieving and develop a strategy to treat “complicated grief” (CG).
The efforts of Shear and her colleagues are beginning to pay off; complicated grief is now recognized in DSM-5 as a disorder in need of further study (tentatively named persistent complex bereavement disorder), and it is set to be described in the upcoming 11th edition of the International Classification of Diseases (as prolonged grief disorder). In addition, Shear developed a successful behavioral intervention—complicated grief therapy, or CGT.
“It’s impressive to see how far we’ve come,” said Charles Reynolds III, M.D., an endowed professor of geriatric psychiatry at the University of Pittsburgh Medical Center (UPMC). He has worked with Shear in this area since the early days. “We now recognize complicated grief as a serious condition that affects about 1 in 10 people who experience a loss; it does not go away by itself, and it is a risk factor for both suicidal ideation and cardiac disease.
“But we also now have a targeted therapy, an active body of ongoing research, and we have made progress in clarifying the diagnostic criteria,” Reynolds continued. “It wouldn’t surprise me to see complicated grief fully recognized in DSM-5.1.”
The diagnostic specifics are still being worked out, but at its core, complicated grief is characterized by intense grieving that is both persistent (currently 12 months or more for an adult or six months or more for youth) and impairs a person’s ability to function.
While previously viewed as a form of depression that stemmed from the loss and bereavement, these incidences of persistent and problematic grief also displayed signs of adjustment disorder and posttraumatic stress disorder (PTSD), Shear observed. So in devising a targeted therapeutic strategy, she reached out to several experts for help, such as Ellen Frank, Ph.D, who was using interpersonal therapy (IPT) to treat depression in the elderly, and the University of Pennsylvania’s Edna Foa, Ph.D., a leader in PTSD. Foa had developed a treatment known as prolonged exposure, which encourages patients to remember and engage with the traumatic events rather than avoid them.
The team infused elements of these different approaches to create a targeted intervention for complicated grief. While patients enrolled in pilot studies of CGT did report improvements in mood, the researchers discovered that many patients dropped out after the first few sessions.
“When we grieve, we are expressing a desire to be with our lost loved one,” she said. “And the thoughts that trigger the outward symptoms are often positive, not just negative.”After reflecting on these results, Shear had an epiphany—complicated grief was not about depression and loss; it was an expression of love.
Over time, the reactions aroused by those thoughts dissipate—but in the case of complicated grief, the stimulus remains strong. “That led me to consider the angle that complicated grief might be a form of craving bearing some resemblance to substance abuse,” Shear said.
Working with that notion, Shear sought out another UPMC colleague, Allan Zuckoff, Ph.D., a psychologist who was using motivational interviewing (MI) to help people with substance abuse problems commit to treatment.
The strategy for MI is to work collaboratively with patients to explore and resolve their ambivalence about changing their behavior—in the case of complicated grief, ambivalence is about acknowledging the finality of the loss.
“I had seen the potential of MI to resolve ambivalence for a variety of problems, and when Kathy approached me about joining her group, I was fascinated by the idea of engaging people to move on from loss,” Zuckoff told Psychiatric News.
People with CG worry that if their grief goes away, they might forget the person who died or that it reflects that they didn’t love the person as much as they believed, Zuckoff explained.
“An important aspect of the CGT process is affirming that we are not trying to extinguish the grief,” Zuckoff said. “We want people to be able to access memories of their loved one, but in a way that is more controlled and less dominated by pain.”
Shear and her colleagues have carried out three large, randomized clinical studies with CGT, and the results have been impressive so far. A 2005 trial involving 95 middle-aged adults (average age 49) found that CGT was nearly twice as effective as interpersonal therapy (IPT), with a 51 percent response rate compared with 28 percent, respectively.
This past November, a follow-up trial of 151 older adults (average age 66) found a similarly marked improvement, with CGT having a 70 percent response rate compared with 32 percent for IPT.
The recent work is critical. “CGT is gaining wide acceptance,” Shear noted, “but there are still some professionals who question why you would encourage people to revisit their traumatic loss, which can be a painful experience,” she said. “And there has been reluctance to try CGT in geriatric populations. These latest findings have been very positive in that regard.”
A few weeks after her study, researchers in Australia found that cognitive-behavioral therapy (CBT) coupled with prolonged exposure was more effective at treating complicated grief than CBT alone, validating that revisiting the loss of a loved one is a crucial part of the CG healing process.
As experts continue to examine the benefits of CGT, they continue to search for potential risk factors for CG. A number of studies have suggested higher rates of CG among people who have experienced sudden and violent deaths, such as military personnel, while a recent study in Palliative Medicine found that preexisting depression may increase the risk of CG in older adults.
Shear is currently leading a large, multicenter trial of over 400 participants to examine the efficacy of antidepressants alone or in combination with CGT.
While the trial keeps her busy, Shear is focusing most of her time in 2015 on dissemination. She recently penned a feature in the New England Journal of Medicine and is engaged in rolling out CGT to primary care clinics throughout New York state. “We need to make the public aware and get therapists trained,” she said. ■

lunes, 4 de abril de 2016

Flu Shot Might Cut Stillbirth Risk

A new Australian study has found that a simple seasonal flu shot may reduce a pregnant woman´s  risk of stillbirth.

The study was quite large where nearly 58,000 births were studied in which more than 5,000 women took the flu shot, during the 2012-2013 flu seasons.

They discovered that women who received the flu shot had 51% lower risk of stillbirth than those who didn’t. They added that similar results were found during the 2009 H1N1 pandemic.

The author said that further research was needed to confirm the possible association between stillbirths, but they were hopefull, since about 40% of pregnant women go unvaccinated, even when having the flu during pregnancy has been linked to fetal death and premature birth. However, many pregnant women don't get a flu shot because of concerns for the safety of the fetus.

According to the U.S. Centers for Disease Control and Prevention, everyone 6 months of age and older, including pregnant women during any trimester, should get an annual flu shot.

There are more than 3 million stillbirths worldwide each year. If a link between flu season and stillbirth is found, it could have a major impact on infant deaths, according to the study authors.

In my opinion this is an interesting article, where a simple flu shot can prevent such terrible things as premature births and stillbirths.

We can also appreciate the divergent opinions when it comes to the pregnant women to decide whether is it best to take the flu shot, afraid of what may happen to their baby, or risking a stillbirth.

Is the seasonal flu shot a good measure in reducing the number of stillbirths and premature births? Are people misinformed about the benefits of a seasonal flu shot during pregnancy? What do you guys think?

(If you want to see the articles visit: )
http://cid.oxfordjournals.org/content/early/2016/03/10/cid.ciw082.abstract
https://www.nlm.nih.gov/medlineplus/news/fullstory_158080.html

jueves, 31 de marzo de 2016

Artificial sweeteners may promote diabetes, claim scientists

Controversial research suggests artificial sweeteners may raise blood sugar levels by promoting growth of certain gut bacteria.

 Artificial sweeteners may contribute to soaring levels of diabetes, according to a controversial study that suggests the additives could exacerbate the problem they are meant to tackle.
Researchers in Israel found that artificial sweeteners used in diet drinks and other foods can disrupt healthy microbes that live in the gut, leading to higher blood sugar levels – an early sign of diabetes.
Sweeteners such as saccharin, aspartame and sucralose are widespread in western diets and are often used to cut calories or prevent tooth decay. The additives are so common that scientists behind the latest study called for a reassessment of the “massive usage” of the chemicals.

“Our findings suggest that non-caloric artificial sweeteners may have directly contributed to enhancing the exact epidemic that they themselves were intended to fight,” the authors write in the journal Nature.

Eran Elinav, a senior author on the study at the Weizmann Institute of Science in Rehovot, said that while the evidence against the sweeteners was too weak to change health policies, he had decided to give them up.

But the study has left many experts unconvinced. The findings draw largely on tests of just one sweetener in mice, raising doubts about their relevance for people, and to other sweeteners. Large studies in humans have found that sugar substitutes can help people maintain a healthy weight and protect against diabetes.

“This new report must be viewed very cautiously,” said Stephen O’Rahilly, director of the Metabolic Diseases Unit at Cambridge University, “as it mostly reports findings in mice, accompanied by human studies so small as to be difficult to interpret.”

Brian Ratcliffe, professor of nutrition at Robert Gordon University in Aberdeen, said: “Most of the effects that they report relate to saccharin with little or no effect of aspartame. Their paper ought to be limited to ‘saccharin’ in the title rather than attributing the effects to all artificial sweeteners.”

The UK is poised to fall in line with World Health Organisation recommendations to halve sugar intake to 5% of daily calories, a move expected to drive sales of diet drinks and low-calorie foods.
In the first of a series of experiments, the Israeli group found that mice fed on three artificial sweeteners – saccharin, aspartame and sucralose – developed high blood sugar levels. But when the mice were given antibiotics to kill off their gut microbes, the ill effects disappeared.

The scientists then focused on saccharin. They transferred gut microbes from mice fed on the sweetener to different mice that had no gut bacteria of their own. Soon after, the recipient mice developed high blood sugar levels themselves. Genetic analyses of the gut microbes from mice fed on saccharin found that as a group they behaved differently, breaking down more carbohydrate in the diet than normal.

The scientists ran tests on 400 people and found that those who consumed the most artificial sweeteners had different gut microbes than others, and on average were heavier and more glucose intolerant.

In their final set of experiments, the scientists gave seven people the maximum allowed daily dose of saccharin for a week. Each dose was enough to sweeten around 40 cans of diet cola. At the end of the week, four in seven had high blood sugar levels and their gut microbes mirrored the changes seen in mice fed on the additives.

To round off the study, the researchers transferred bugs from the people who developed high blood sugar after massive doses of artificial sweeteners into mice that had no gut bugs of their own. These mice went on to develop high blood sugar too.

According to Elinav, the study shows that artificial sweeteners may contribute to higher blood sugar in mice and some people. One possible explanation is that artificial sweeteners let some microbes thrive at the expense of others, leaving a population that extracts more energy from the diet than normal.

“This large body of work we’ve performed should be studied further because of the potentially harmful effects that could be happening from sweetener consumption to very large subsets of the population,” said Eran Segal, a co-author of the paper.

There are studies that report more diabetes among people who consume lots of diet drinks. But in many cases it is impossible to work out what is to blame. Lots of people are already fat and on course to develop diabetes when they turn to diet drinks to lose weight.

Nita Forouhi, head of nutritional epidemiology at Cambridge, said the study suggested artificial sweeteners were not the “innocent magic bullets” they were intended to be. “But it does not yet provide sufficient evidence to alter public health and clinical practice,” she said.

Christopher Corpe of King’s College London, who studies how the gut senses sugars, said that future work needed to draw on much larger numbers of healthy and obese or diabetic people who consume more realistic amounts of artificial sweeteners.

sábado, 12 de marzo de 2016

Poliomyelitis
Fact sheet N°114
Updated October 2015

Key facts
·                                 Polio (poliomyelitis) mainly affects children under 5 years of age.
·                                 One in 200 infections leads to irreversible paralysis. Among those paralysed, 5% to 10% die when their breathing muscles become immobilized.
·                                 Polio cases have decreased by over 99% since 1988, from an estimated 350 000 cases then, to 359 reported cases in 2014. The reduction is the result of the global effort to eradicate the disease.
·                                 Today, only 2 countries (Afghanistan and Pakistan) remain polio-endemic, down from more than 125 in 1988.
·                                 As long as a single child remains infected, children in all countries are at risk of contracting polio. Failure to eradicate polio from these last remaining strongholds could result in as many as 200 000 new cases every year, within 10 years, all over the world.
·                                 In most countries, the global effort has expanded capacities to tackle other infectious diseases by building effective surveillance and immunization systems.

Polio and its symptoms
Polio is a highly infectious disease caused by a virus. It invades the nervous system, and can cause total paralysis in a matter of hours. The virus is transmitted by person-to-person spread mainly through the faecal-oral route or, less frequently, by a common vehicle (e.g. contaminated water or food) and multiplies in the intestine. Initial symptoms are fever, fatigue, headache, vomiting, stiffness of the neck and pain in the limbs. One in 200 infections leads to irreversible paralysis (usually in the legs). Among those paralysed, 5% to 10% die when their breathing muscles become immobilized.
People most at risk
Polio mainly affects children under 5 years of age.
Prevention
There is no cure for polio, it can only be prevented. Polio vaccine, given multiple times, can protect a child for life.
Global caseload
Polio cases have decreased by over 99% since 1988, from an estimated 350 000 cases in more than 125 endemic countries then, to 359 reported cases in 2014.
Today, only 2 countries in the world remain endemic for the disease–the smallest geographic area in history. Of the 3 strains of wild poliovirus (type 1, type 2, and type 3), wild poliovirus type 2 was eradicated in 1999 and case numbers of wild poliovirus type 3 are down to the lowest-ever levels with the no cases reported since November 2012 from Nigeria.
The Global Polio Eradication Initiative
Launch
In 1988, the forty-first World Health Assembly adopted a resolution for the worldwide eradication of polio. It marked the launch of the Global Polio Eradication Initiative (GPEI), spearheaded by national governments, WHO, Rotary International, the US Centers for Disease Control and Prevention (CDC), UNICEF, and supported by key partners including the Bill and Melinda Gates Foundation. This followed the certification of the eradication of smallpox in 1980, progress during the 1980s towards elimination of the poliovirus in the Americas, and Rotary International’s commitment to raise funds to protect all children from the disease.
Progress
Overall, since the GPEI was launched, the number of cases has fallen by over 99%. Today, only 2 countries in the world remain polio-endemic: Pakistan and Afghanistan.
In 1994, the WHO Region of the Americas was certified polio-free, followed by the WHO Western Pacific Region in 2000 and the WHO European Region in June 2002. On 27 March 2014, the WHO South-East Asia Region was certified polio-free, meaning that transmission of wild poliovirus has been interrupted in this bloc of 11 countries stretching from Indonesia to India. This achievement marks a significant leap forward in global eradication, with 80% of the world’s population now living in certified polio-free regions.
Of the 3 types of wild poliovirus (type 1, type 2 and type 3), type 2 wild poliovirus transmission has been successfully stopped (since 1999).
More than 13 million people are able to walk today, who would otherwise have been paralysed. An estimated 1.5 million childhood deaths have been prevented, through the systematic administration of Vitamin A during polio immunization activities.
Opportunity and risks: an emergency approach
The strategies for polio eradication work when they are fully implemented. This is clearly demonstrated by India’s success in stopping polio in January 2011, in arguably the most technically-challenging place, and polio-free certification of the entire South-East Asia Region of the World Health Organization occurred in March 2014.
However, failure to implement strategic approaches leads to ongoing transmission of the virus. Endemic transmission is continuing in Pakistan and Afghanistan. Failure to stop polio in these last remaining areas could result in as many as 200 000 new cases every year, within 10 years, all over the world.
Recognizing both the epidemiological opportunity and the significant risks of potential failure, the new Polio Eradication and Endgame Strategic Plan 2013-2018 has been developed, in consultation with polio-affected countries, stakeholders, donors, partners and national and international advisory bodies. The new Plan was presented at a Global Vaccine Summit in Abu Dhabi, United Arab Emirates, at the end of April 2013. It is the first plan to eradicate all types of polio disease simultaneously – both due to wild poliovirus and due to vaccine-derived polioviruses.
Future benefits of polio eradication

Once polio is eradicated, the world can celebrate the delivery of a major global public good that will benefit all people equally, no matter where they live. Economic modelling has found that the eradication of polio would save at least US$ 40–50 billion over the next 20 years, mostly in low-income countries. Most importantly, success will mean that no child will ever again suffer the terrible effects of lifelong polio-paralysis.