Woman, 60, is lucky to be alive after surgeons removed 35kg tumours

Woman, 60, is lucky to be alive after surgeons remove two giant ovarian tumours weighing 78lbs – the same as a fully-grown LABRADOR

  • Ms Adhikary was taken to hospital with bloating and severe abdominal pain
  • Doctors’ scans revealed she had two tumours weighing a total of 35kg (78lbs)
  • The massive growths were taking up 80 per cent of her abdomen
  • A team of six surgical staff removed the tumours in a delicate two-hour op 

A 60-year-old woman is lucky to be alive after surgeons removed  two giant ovarian tumours weighing 78lbs (35kg) which were taking up 80 per cent of her abdomen.     

Arati Adhikary was taken to hospital 10 days ago with a bloated stomach and severe abdominal pain, when doctors found tumours on both her ovaries.

The shocking growths – which together weighed the same as a big Labrador – had to be cut out in an operation lasting several hours.

Ms Adhikary had been struggling to walk because of the size of the lumps, which were so large and had grown so far from her ovaries they were pressing on her liver.

The surgeon who performed the operation said he does not know of any other surgery on such large tumours in India’s recent history.

And tests have not yet confirmed the cause of Ms Adhikary’s condition – though the lumps could be cancerous tumours or cysts.

Ms Adhikary is now recovering in hospital after the operation on Saturday and is expected to be discharged within the next week.

Arati Adhikary (pictured recovering in a hospital bed) went to hospital in severe pain and with a bloated stomach difficulty breathing, where doctors realised she had ovarian tumours taking up 80 per cent of her abdomen

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Arati Adhikary, from Kanchrapara in the Indian state of West Bengal, approximately 31 miles (51km) from Kolkata, was admitted to hospital several days ago in July.

She was suffering from severe pain in her upper body, she was not able to walk independently and had a bloated belly.

Doctors did several tests and an ultrasound scan, which revealed she had tumours growing out of both of her ovaries.

Tumours took up 80 per cent of her abdomen 

The tumours were so large they took up 80 per cent of Ms Adhikary’s abdomen, pushing her other internal organs out of the way.

The growths had expanded so far they were pressing on her intestines, liver, and diaphragm, making it difficult for her to breathe.

This means the huge lumps of tissue stretched from her pelvis, where they started in the ovaries, to her ribcage, which encases the liver and diaphragm, filling most of the space in between.   

Medical staff removed two ovarian tumours from Arati Adhikary, and found they weighed a combined 35kg – the same as a fully grown Labrador

Dr Mriganka Mouli Saha, assistant professor and gynaecological surgeon at the College of Medicine & JNM Hospital in West Bengal, led a team of six doctors during the operation.

He said: ‘The patient had a huge abdominal swelling and was in lot of pain. 

Tumours so big patient could not walk or breathe 

‘She could not walk without any support and had respiratory problems as well.

‘Two tumours were removed from her ovaries in a two-hour long operation. 

Ms Adhikary’s surgery took over two hours to complete and her surgeon described the procedure as ‘very risky’, saying he did not know of any others this size being operated on in recent Indian history

‘One was over 20kg and the other was around 15kg. The total weight of the tumours was 35.4kg (78lbs). 

‘It was a very risky operation. The patient could have collapsed during the surgery.

‘No such big ovarian tumour has been operated successfully in the country in the recent past.’      

Ms Adhikary is stable and expected to remain under observation for two days, and to be discharged within a week.

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Being overweight may change young adults’ heart structure, function

Even as a young adult, being overweight may cause higher blood pressure and thicken heart muscle, setting the stage for heart disease later in life, according to new research in the American Heart Association’s journal Circulation.

The study is the first to explore if higher body mass index (BMI) – a weight-for-height index – results in adverse effects on the cardiovascular system in young adults.

While observational studies can suggest associations between risk factors or lifestyle behaviors and heart disease, they cannot prove cause-and-effect. Here, investigators triangulated findings from three different types of genetic analysis to uncover evidence that BMI causes specific differences in cardiovascular measurements.

“Our results support efforts to reduce body mass index to within a normal, healthy range from a young age to prevent later heart disease,” said Kaitlin H. Wade, B.Sc., Ph.D., lead author of the study and a research associate at the Medical Research Council Integrative Epidemiology Unit at the University of Bristol Medical School in the United Kingdom.

Researchers used data on several thousand healthy 17-year-olds and 21-year-olds who have participated in the ongoing Children of the 90s study (also known as the Avon Longitudinal Study of Parents and Children) since they were born in the Bristol area of the United Kingdom.

The researchers’ findings suggest that higher BMI:

  • caused higher systolic (top number) and diastolic (bottom number) blood pressure; and
  • caused enlargement of the left ventricle, the heart’s main pumping chamber.

“Thickening of vessel walls is widely considered to be the first sign of atherosclerosis, a disease in which fatty plaques build up within the arteries and lead to heart disease. However, our findings suggest that higher BMIs cause changes in the heart structure of the young that may precede changes in blood vessels,” Wade said.

Two of the analyses used in the study (Mendelian randomization and recall-by-genotype) take advantage of the properties of genetic variation. Recall-by-genotype is novel and exploits the random allocation of genes at conception.

“At a population level, this provides a natural experiment analogous to a randomized trial where we can compare differences in an outcome (such as heart structure and function) with differences in BMI, without the relationship being skewed by other lifestyle and behavioral factors,” Wade said.

Most participants in the longitudinal studies were white, limiting the generalizability of the findings to other ethnic groups.

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Limit low-calorie sodas and drinks, and stick to water instead, researchers advise

People are drinking fewer diet drinks these days, and a panel of health experts agrees that’s a good idea.

A science advisory from the American Heart Association published Monday in the journal Circulation counsels against regular and long-term consumption of diet beverages, particularly in children. Instead, the group of leading nutritionists, doctors and researchers urged people to replace sugary and diet drinks with plain, carbonated or unsweetened flavored water.

The committee spent two years combing through dozens of studies – some of which brought up associations between low-calorie sweetened drinks and weight gain, dementia, stroke and other health problems – and concluded that the science was still too fuzzy to draw hard-and-fast conclusions about the health effects of diet drinks.

“There’s not a huge body of literature, either observational or clinical trials,” said the writing group’s chair, Rachel K. Johnson, a professor emeritus of nutrition at the University of Vermont. “Based on the evidence available at this time, this is the best advice we have.”

The advisory acknowledges the reality that many people might use diet drinks to wean off sugar-loaded drinks if they feel they can’t make the wholesale leap to water. “This approach may be particularly helpful for individuals who are habituated to a sweet-tasting beverage and for whom water, at least initially, is not a desirable option,” the report said.

Encouragingly, the writers pointed to federal data based on self-reported surveys showing adults and young people already are drinking less of both sugary and diet drinks.

In 2006, adults drank an average of about 5.6 ounces of low-calorie drinks a day. By 2014, that fell to 3.8 ounces a day, the federal data shows. Consumption for kids and teens declined during that time, too, in the range of less than an ounce a day. A serving size is about a cup, or 8 ounces. A can of soda is usually 12 ounces, although some come in 8-ounce sizes, too. Sports drinks come in a variety of bottle sizes, from 12 ounces to 32 ounces.

When it came to sugar-laden drinks, adults in 2000 drank about 16.2 ounces a day, according to the data. That declined to 8.4 ounces a day by 2014. Kids reported drinking 17.9 ounces each day in 2000, and 8.1 ounces a day in 2014. In 2016, the AHA issued its first scientific statement warning about added sugars intake for kids, saying children and teens should consume no more than 8 ounces of sugary beverages a week.

“We want to make crystal clear it’s important to maintain that [downward] trend,” said Alice H. Lichtenstein, vice chair of the writing group and director of the Cardiovascular Nutrition Laboratory at Tufts University in Boston.

“We hear a lot about potential adverse effects of low-calorie sweeteners, but much of it is speculation. We have to go with the available evidence,” said Lichtenstein, the Gershoff Professor of Nutrition Science and Policy at Tufts. “The best advice we can give at this time is to ramp down intake and avoid excess consumption.”

The advisory was more cautious in its advice for children because there is “virtually no data” on the long-term effects of low-calorie drinks, said writing group member Dr. Frank Hu, chair of the nutrition department at Harvard University and professor of nutrition and epidemiology.

“One question we discussed is whether for children who are obese and who drink regular soda on a regular basis, is it OK for them to drink diet soda instead?” Hu said. “The consensus is that for short-term weight control, it’s OK. Certainly, it’s not the best alternative … because we all know there are more healthy alternatives, such as water, low-fat and fat-free milk.”

The report included an exception for one specific population: children with diabetes. The authors say those children who eat a balanced diet and who are closely monitoring their blood sugar may help keep their levels in check by substituting low-calorie drinks for sugary ones when needed.

In 2012, the AHA and the American Diabetes Association issued a scientific statement saying artificial sweeteners used “judiciously” in foods and beverages could help people lower added sugars intake, maintain a healthy weight, and lower the risk of heart disease and Type 2 diabetes. But it warned the science was “limited and inconclusive” about that strategy.

The new science advisory included eight low-calorie sweeteners – six currently approved by the Food and Drug Administration and two extracts from plants.

AHA science advisories typically review and analyze recent research on topics related to heart and brain health, as a way to educate the public and synthesize the latest information.

While this new advisory pointed out the dearth of clear evidence from diet drink studies, nutrition researcher Christopher Gardner feels there is plenty that is clear.

“Artificial soda, there’s nothing good about it,” said Gardner, who was not an author on the latest advisory. He was lead author on the 2012 scientific statement and is director of Nutrition Studies at the Stanford Prevention Research Center. “There’s nothing health-promoting about it. The only health-related role it has is as a transition beverage, replacing or displacing sugar-sweetened beverages.”

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A brain injury diagnosed with a single drop of blood

Every year in Europe, 3 million people are admitted into hospitals for suspected mild traumatic brain injury (mTBI) cases. Yet 90 percent of these patients detect no trauma. Today, the only reliable diagnosis is the CT scan, which is only available in some hospitals.

Researchers from the University of Geneva (UNIGE), in collaboration with the Hospitals of Barcelona, Madrid and Seville, have developed a small device – the Point-of-Care Test (POCT)—that analyses the level of proteins in a single drop of blood to diagnose the possibility of a mild traumatic brain injury. This innovation, described in PLOS One, will not only relieve emergency departments, free patients from often long waits, but also save on costly medical examinations.

Head injury can cause symptoms such as blurred vision, vomiting, loss of consciousness or memory for about 30 minutes. There is then a risk of mild cerebral trauma, which represents more than 90 percent of brain injuries admitted to hospitals. But is there really a brain lesion? Or are these symptoms merely the consequence of the violence of the shock, of which will ultimately only leave a bump behind?

Today, the injured patients have to go to the emergency rooms of hospitals equipped with a CT scanner, an expensive examination that detects the presence or absence of brain trauma via X-rays. It often takes a long time for the majority of patients to return home without risk of sequelae, except for bad memories.

Find biomarkers for light traumas

“We wondered if it was possible to isolate certain proteins whose presence in the blood increases in the event of mild traumatic brain injury,” explains Jean-Charles Sanchez, professor at the Department of Internal Medicine of Specialties and the Biomarkers Centre of the Faculty of Medicine of the UNIGE. “Our idea was to find a way to do a quick examination that would allow us to determine whether an athlete can return to the field or if his condition requires hospitalization,” he adds.

During a shock to the head, brain cells are damaged and release proteins, increasing their level in the blood. Scientists at UNIGE and Spanish hospitals compared the blood of patients admitted for mild traumatic brain injury but diagnosed as negative with that of patients actually suffering from a brain lesion. Using proteomic analyses, which can quantify thousands of proteins simultaneously and observe variations in their levels in the blood, the researchers gradually isolated four molecules indicating the presence of a brain injury: H-FABP, Interleukin-10, S100B and GFAP. “We have noticed that the H-FABP level alone makes it possible to confirm that there is no risk of trauma in one third of patients admitted after a shock,” says Jean-Charles Sanchez. The rest of the patients will have to undergo a CT scan to confirm the diagnosis.

It was still necessary to develop a device that could be used everywhere, quickly and simply, and that could be available in pharmacies or sports halls. “When a person has an accident on a mountain, few clinics can do a CT scan,” notes the Geneva researcher. His team has developed a rapid diagnostic test called TBIcheck, inspired by the principle of pregnancy testing. By placing a single drop of blood on the well of a small plastic case, the patient knows within 10 minutes whether there is a risk of mild trauma, namely whether or not his H-FABP level is higher than 2.5 nanograms per millilitre of blood. “If a line appears, the injured person must go to a hospital for a CT scan, if there is nothing, he can go home safely,” Jean-Charles Sanchez says. In case of doubt, a small reader can be installed on TBIcheck. It will display the word “positive” or “negative” and send the result to the patient’s or caregiver’s smartphone via Bluetooth.

Commercialization planned for beginning 2019

These results, patented by UNIGE and awarded the Prix de l’Innovation Academy in December 2017, will be marketed from 2019 by ABCDx, a start-up founded four years ago by Jean-Charles Sanchez of UNIGE and Joan Montaner of Vall d’Hebron Hospital in Barcelona, co-authors of this study.

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Genetic study of familial leukemia solves 30-year medical mystery

A decades-old medical mystery has been solved by researchers at UC San Francisco and St. Jude Children’s Research Hospital in Tennessee, who have discovered a pair of inherited genetic mutations underlying a familial blood disorder that sometimes leads to leukemia.

The research, based on analysis of the DNA of 16 siblings in five families, reported that some children with these mutations recover spontaneously, and pointed to additional genetic markers that may help physicians avoid invasive and dangerous bone marrow transplants for patients with milder forms of the disease.

The puzzle surrounding the disorder dates back more than 30 years to when UCSF oncologist Kevin Shannon, MD, was a research fellow in the lab of renowned UCSF geneticist Yuet Wai Kan, MD, FRS. Shannon and colleagues encountered several families in which multiple children can develop low blood cell counts (myelodysplasic syndrome, or MDS) and a form of acute myeloid leukemia (AML), a severe and often deadly blood cancer. These patients also had one rather than the usual two copies of chromosome 7, a condition known as monosomy 7.

In 1989, using then-cutting-edge techniques, Shannon successfully narrowed down the region of chromosome 7 that was responsible for the condition, called familial monosomy 7 syndrome. Efforts to identify the specific genes involved were unsuccessful at the time, but Shannon and his colleagues started collecting and banking blood samples from other families with a similar medical history.

The current study, published July 26, 2018, in JCI Insight, was spearheaded by Shannon lab researcher Jasmine Wong, PhD, who had read Shannon’s 1989 paper before joining his lab, and has spent the past 10 years trying to understand the genetics that drive the disease.

“Reading that paper, I thought about what it must be like for parents to have more than one child get this really severe form of leukemia,” Wong said. “Maybe you’re trying to find out whether your second child could be a potential bone marrow donor for your first child, and then it turns out they both have the same condition. It’s heart-breaking, and also a really puzzling scientific mystery.”

Wong began by assembling the scores of blood samples Shannon had collected from familial monosomy 7 syndrome patients over the years into genetic family trees, or pedigrees, as well as identifying new patients with the help of UCSF pediatric oncologist Mignon Loh, MD, also an author on the new paper.

As often happens, the breakthrough ultimately came through a collaboration, between Wong and the St. Jude lab of co-senior author Jeffrey Klco, MD, PhD, in which he and co-first author Victoria Bryant, PhD, performed deep genetic sequencing of inherited DNA mutations in tissue samples from five of the families Wong had identified.

The data revealed that mutations in the genes SAMD9 and SAMD9L, which are located on chromosome 7, are strongly associated with monosomy 7 syndrome, but that a number of healthy siblings and parents of patients also carry these mutations without experiencing any symptoms.

The researchers showed that patients who did develop symptoms of MDS and AML also had a specific constellation of secondary genetic mutations that appear to have driven their more severe disease, while those without these additional mutations often never experienced any symptoms, or else began to experience low blood counts and then spontaneously recovered without treatment.

The findings could also be relevant to other blood disorders, the authors said. “Genetic alterations on chromosome 7 are very frequent in AML and MDS patients, and malignancies with monosomy 7 are associated with an unfavorable prognosis and respond poorly to existing therapies,” Wong said. “Since there are over 860 genes on chromosome 7, it would be interesting to understand what role SAMD9 and SAMD99L play in nonfamilial forms of MDS and AML, and how they interact with other genes on chromosome 7 and with cancer genes located on other chromosomes.”

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Checking phones in lectures can cost students half a grade in exams

Students perform less well in end-of-term exams if they are allowed access to an electronic device, such as a phone or tablet, for non-academic purposes in lectures, a new study in Educational Psychology finds.

Students who don’t use such devices themselves but attend lectures where their use is permitted also do worse, suggesting that phone/tablet use damages the group learning environment.

Researchers from Rutgers University in the US performed an in-class experiment to test whether dividing attention between electronic devices and the lecturer during the class affected students’ performance in within-lecture tests and an end-of-term exam.

118 cognitive psychology students at Rutgers University participated in the experiment during one term of their course. Laptops, phones and tablets were banned in half of the lectures and permitted in the other half. When devices were allowed, students were asked to record whether they had used them for non-academic purposes during the lecture.

The study found that having a device didn’t lower students’ scores in comprehension tests within lectures, but it did lower scores in the end-of-term exam by at least 5%, or half a grade. This finding shows for the first time that the main effect of divided attention in the classroom is on long-term retention, with fewer targets of a study task later remembered.

In addition, when the use of electronic devices was allowed in class, performance was also poorer for students who did not use devices as well as for those who did.

The study’s lead author, Professor Arnold Glass, added: “These findings should alert the many dedicated students and instructors that dividing attention is having an insidious effect that is impairing their exam performance and final grade.

“To help manage the use of devices in the classroom, teachers should explain to students the damaging effect of distractions on retention — not only for themselves, but for the whole class.”

This is the first-ever study in an actual classroom showing a causal relationship between distraction from an electronic device and subsequent exam performance.

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Protein affected by rare Parkinson’s mutation may lurk behind many cases of the disease: NIH-funded study could lead researchers to rethink how to treat the disorder

Mutations in the gene LRRK2 have been linked to about three percent of Parkinson’s disease cases. Researchers have now found evidence that the activity of LRRK2 protein might be affected in many more patients with Parkinson’s disease, even when the LRRK2 gene itself is not mutated. The study was published in Science Translational Medicine and was supported in part by the National Institute of Neurological Disorders and Stroke (NINDS), a part of the National Institutes of Health (NIH).

“This is a striking finding that shows how normal LRRK2 may contribute to the development of Parkinson’s disease,” said Beth-Anne Sieber, Ph.D., program director at NINDS. “This study also identifies LRRK2 as an integral protein in the neurobiological pathways affected by the disease.”

More than 10 years ago, researchers linked mutations in the LRRK2 gene with an increased risk for developing Parkinson’s disease. Those mutations produce a version of LRRK2 protein that behaves abnormally and is much more active than it would be normally.

Despite its importance in Parkinson’s disease, the very small amount of normal LRRK2 protein in nerve cells has made it difficult to study. In the current study, the authors developed a new method for observing LRRK2 cells that makes them glow fluorescently only when LRRK2 is in its activated state. They have also used detection of fluorescent signals to demonstrate loss of binding of an inhibitor protein to LRRK2 when LRRK2 is activated. The researchers looked first at postmortem brain tissue from Parkinson’s disease patients who did not have mutations in LRRK2. Compared to healthy individuals of similar ages, there was a striking increase in LRRK2 activity in the dopamine-containing neurons of the substantia nigra, the area of the brain most affected in Parkinson’s disease. This suggested that increased LRRK2 activity could be a common feature of the disease.

“This finding provided strong evidence that something is causing LRRK2 activity to increase in Parkinson’s disease patients, specifically in the area of the brain we would expect based on what we know of the disease,” said J. Timothy Greenamyre, M.D., Ph.D., Love Family Professor of Neurology in the University of Pittsburgh’s School of Medicine, director of the Pittsburgh Institute for Neurodegenerative Diseases (PIND), and senior author of this study.

To get a closer look at how LRRK2 activity is related to Parkinson’s disease. the researchers next turned to rodent models of the disorder. The sensitivity of their new technique allowed for the direct study of LRRK2 activity, which until now could not be done.

“Much of what we have known previously about LRRK2 comes from overexpression studies, where cells are forced to make much more of the protein than they would normally,” said Dr. Greenamyre “Our fluorescent assay reveals where LRRK2 is active in the brain and the relative level of activity without potential side effects from overexpression.”

By injecting rodents with the environmental toxin rotenone and studying the effect on LRRK2, the researchers linked increased LRRK2 activity with the accumulation of alpha-synuclein, a process that leads to the formation of Lewy bodies in the brain, a hallmark of Parkinson’s disease. In another model of the disease, where synuclein was present in much higher amounts than normal, LRRK2 activity was increased. In contrast, when the animals were treated with a drug that blocks LRRK2 activity, the accumulation of alpha-synuclein and Lewy body formation were both prevented.

Finally, additional links were found between LRRK2 activity and the potentially damaging consequences of Parkinson’s disease. Reactive oxygen species (ROS) are compounds that can interact and affect other components within cells, and ROS were increased in the brains of both rodent models. ROS were seen to increase the activity of LRRK2, and when ROS production was blocked, LRRK2 activation was not observed.

“Our findings suggest that both genetic and environmental causes of Parkinson’s disease can be tied back to the activity of LRRK2 protein,” said Dr. Greenamyre. “This is important, because it suggests that the drugs being developed for patients with the LRRK2 mutation, which represent a very small percentage of the affected population, could benefit a much greater number of people with the disease.”

Dr. Greenamyre and his research team plan to further study whether the neurodegeneration that occurs due to LRRK2 overactivity can be prevented and to identify the mechanisms that connect environmental stressors to LRRK2 activation.

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An In-Depth Look At Beauty DNA Test Kits

Beauty DNA kits are gaining popularity, but are they any good?

Beauty DNA test kits are gaining popularity. However, the accuracy of these at-home test kits is being questioned by those in the scientific community. Beauty DNA test kits examine patients’ genetic makeup to determine the health of their skin and hair. Kelsey Castanon from PopSugar tested a few beauty DNA kits and shared her results. Based on the article she wrote, these kits can be quite pricey, and the results can vary in range, depending on the test one takes.

The first two beauty DNA kits Castanon tested were from Orig3n, which costs $99 and Vitagene’s Skin Report, which costs $79. The results of both tests mainly focused on Castanon’s skin health. Based on her results, Orig3n and Vitagene recommended specific practices or certain ingredients to look for in beauty products to maintain or improve her skin’s health. Meanwhile, the third kit–HomeDNA Skin Care kit–gave the PopSugar reporter an extensive 11-page report on her skin health. Unlike the other two tests, however, the $99 DNA kit recommended specific products for Castanon to buy and use.

Scientists and professional medical providers seem to have a growing concern about the recommendations for at-home genetic tests like the HomeDNA Skin Care kit make to their patients. For this reason, Ambry Genetics tested the accuracy of at-home DNA tests. The study did not focus on beauty concerns, but diagnoses or medical predispositions patients had toward a particular illness or disease. The researchers concluded that up to 40 percent of raw data collected by the kits yielded false positives. In other words, the DNA kits are not that accurate in determining future medical risks, reported Fortune.

Hadley King, a dermatologist, talked about beauty DNA kits and their accuracy, as per Huffington Post. King’s thoughts on these home beauty tests seem to reflect the findings of Ambry Genetics’ study.

“At this stage right now, I think this is mostly a gimmick. Some of the products are great because they contain important ingredients like retinol and vitamin C, but we really don’t need to check DNA to recommend these ingredients. The future of medicine is definitely headed in a DNA-specific direction, but we are not yet at the stage where we can effectively harness this information for beauty products,” King said.

The study also observed that the recommendations at-home DNA kits made were not specific to a patient’s results, but were true for the general population, reported Nature. Both the study and King recommend talking to a medical provider when determining health care needs. Researchers believe the results from at-home DNA kits should be shared with a medical professional before treatment.

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FSSAI to notify claim regulations on health supplements and nutraceuticals

The government is in the process of notifying claim regulations on health supplements and nutraceuticals — a mix of nutritional and pharmaceutical products — keeping in mind global practices.

According to country’s apex food regulator, Food Safety and Standards Authority of India, health supplements and nutraceutical industry is a rapidly growing market in India, poised to be worth ~10 billion by 2025.

A mere combination of vitamins and minerals formulated into tablets, capsules or syrup is not food unless vitamins and minerals are added to an article of food. “As this sector grows, we have to put stringent regulatory mechanism in place as people tend to manufacture and sell just anything in the name of health supplements,” said Pawan Agarwal, chief executive officer, FSSAI.

In 2016, the regulator began the process of reigning in the sale of these products by way of rules under eight categories of foods.

The categories involved were health supplements, nutraceuticals, foods for special dietary use, food for special medical purpose, speciality food containing plants or botanicals, foods containing probiotics, foods containing prebiotics and the novel foods.

These foods are not permitted to contain hormones, steroids or psychotropic ingredients but may use approved colours and additives as permitted under the Food Safety and Standards (Food Product Standards and Food Additives) Regulations, 2011.

The quantity of nutrients add- ed to the articles of food shall not exceed the recommended daily allowance as specified by the Ind- ian Council of Medical Research and accepted by the FSSAI. The rules came into effect from January 1, 2018. With the market growing, the regulations have been reworked based on what other countries are following.

The FSSAI roped in The Confederation of Indian Industry (CII), to establish a ‘Resource Centre for Health Supplements and Nutraceuticals (ReCHaN) in partnership with International Alliance of Dietary/Food Supplement Associations (IADSA).

“Health supplement sector is very important for the country not only from the industry growth perspective but also from public health point of view… The new regulations will help the industry to grow further while at the same time safeguard consumer interest,” said Agarwal.

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How Close Are We, Really, to Curing Cancer with CRISPR?

Followers of science and health news, particularly those with a terminal illness, may get the impression that the dawn of a new, disease-free era is upon us — and nowhere is this idea more evident than in the latest buzzword in the health sciences, CRISPR.

With this tool, a form of genetic engineering, scientists can edit a genome — that is, alter a set of genes among the tens of thousands contained in an organism's DNA. With CRISPR, scientists may have the ability to remove or correct disease-causing genes or insert new ones that could theoretically cure disease, including cancer.

But the technology comes with both potential benefits and risks. [10 Amazing Things Scientists Just Did with CRISPR]

Two important CRISPR studies published this month underscore the promise and concerns. The first, from a multi-institute team led by researchers at the University of California, San Francisco (UCSF) and published in the journal Nature, revealed a new, more efficient way of making changes in the genome using CRISPR. This method, which uses electrical fields, drew widespread praise from the biomedical research establishment, as relayed in numerous news reports.

The second study, from the laboratory of Allan Bradley at Wellcome Sanger Institute in England, published a few days later in the journal Nature Biotechnology, suggested that CRISPR gene editing may be doing more damage than scientists thought.

So, what's going on? And how close are scientists to actually using CRISPR to effectively treat cancer?

CRISPR getting crisper

CRISPR is one tool among many in the 40-year-old field of genetic engineering, storming onto the scene in 2012. The technology offers unprecedented precision in editing the genome — that is, opening up a strand of DNA and correcting an error typed into the genetic code. CRISPR is not the first method for editing genes, but it seems to be the most precise so far.

Here's how it works: CRISPRs, short for clustered regularly interspaced short palindromic repeats (don't worry — most scientists can't remember this), are stretches of DNA found in bacteria and other microbes. These microorganisms use CRISPRs to find and remove viral DNA that has invaded their genomes. It's a host defense system. The CRISPRs and associated proteins, such as Cas9, essentially snip out the viral DNA and patch things up.

The technology is just now entering the realm of clinical application, with still only a handful of patients receiving the treatment, all starting in 2017. However, CRISPR is used now — broadly and remarkably successfully — in creating laboratory animals and cell lines with key genetic characteristics that help scientists better study human diseases.

In this regard, part of the CRISPR promise has already been realized in terms of "really advancing the landscape of research in biomedicine in a way nobody thought possible," said Fyodor Urnov, deputy director of the Altius Institute for Biomedical Sciences in Seattle, who uses CRISPR and other methods to edit human genes in the lab. [7 Diseases You Can Learn About from a Genetic Test]

And as for the other promise, clinical application, "There's really good news on the horizon," Urnov told Live Science.

CRISPR advances — and pitfalls

For CRISPR to work, the short strands first need to get into the nucleus of a cell, where DNA is found. To transport CRISPRs there, scientists use modified viruses, a decades-old delivery method. These harmless viruses invade the cell, as they are wont to do, and deposit the package. But manufacturing these viruses in significant numbers for clinical use can take months or a year, and critically ill patients usually don't have that long to wait.

That's why the new Nature article elicited such excitement and praise. In that work, scientists used electrical stimulation, not viruses, to ferry genetic material into the cell nucleus. This is called "electroporation," and it shortens the process to a few weeks. The method could greatly speed research efforts.

But the other new study, though it didn't reference the research on electrical stimulation, warned that CRISPR remains rife with danger. The technique can alter more parts of the DNA than scientists realized, including those parts located farther away from the region targeted by CRISPR, the researchers said.

In short, CRISPR can snip too much, and depending on what's snipped, this inaccuracy could spell trouble, the researchers wrote. Scientists using CRISPR might inadvertently cut out a cancer-suppression gene, for example.

And these errors could occur regardless of the ferry mechanism used, whether electroporation or viral vector, lead study author Michael Kosicki, a graduate student at the Wellcome Sanger Institute in England, told Live Science.

But Urnov, who wasn't involved in either study, said that he cautioned against drawing broad conclusions from the second paper. That study used mouse cells, not clinic-grade human cells, and did not use a CRISPR-Cas9 strain engineered for clinical use, he said. You can't compare the off-target cleavage seen in the mouse DNA to what might happen in the human studies, he added.

In the U.S. and Europe, no clinical trial would begin without passing through "rigorous safety review," Urnov said.

There are two primary safety concerns: 1) making sure the genetic change was made correctly, without snipping other regions, a danger that the second study highlighted and 2) ensuring the genetic change of interest, even if done correctly, is safe and that its alteration or removal has no unforeseen ramifications.

What cancer patients need to know

CRISPR has the potential to revolutionize cancer therapy, chiefly in the realm of immunotherapy. In cancer immunotherapy, the treatment genetically engineers immune cells called T cells to find and kill cancer cells, as if they were a cold virus. In 2017, the U.S. Food and Drug Administration approved two drugs for a type of immunotherapy called chimeric antigen receptor (CAR-T) immunotherapy. Neither treatment involved CRISPR, though.

But doctors worldwide are using both traditional immunotherapy and new CRISPR techniques to increase the number of cancer types that they can treat reliably, albeit all at the preliminary experimental level.

If you are cancer patient, the first thing you need to realize is that you don't necessarily want to be in need of these experimental therapies. If you do need one, that means the conventional treatments — chemotherapy, radiation and surgery — have failed. [7 Side Effects of Cancer Treatment, and How to Cope with Them]

The second thing that cancer patients must understand is that experimental CRISPR treatments are, well, experimental and not available to many. These treatments are offered primarily at research hospitals, and they don't work for the majority of patients. Doctors in those settings are trying to figure out if and how these therapies work, or how they need to be tweaked, so these physicians need to recruit patient-volunteers who have well-defined cancer types.

So, this is the key question: How close are we, really, to curing cancer with CRISPR? Of course, no expert can say for sure. Urnov said that he is confident that CRISPR technology will bring about more and more cures to a broad range of diseases, including certain cancer types, in the next few years.

Dr. Alexander Marson of UCSF, senior author on the electroporation study, suggested that we may get an answer about CRISPR's cancer applications rather soon. His team hopes to treat siblings who have an autoimmune disease so rare that it lacks a name. These patients' T cells have already been corrected using the non-viral gene-targeting method in the lab. The goal is to transfer corrected cells back into the children to treat their disease. Important  work remains ahead to develop clinical-grade corrected cells, test their safety and seek regulatory approval, Marson told Live Science.

Marson and other members of this team also are partnering with the Parker Institute for Cancer Immunotherapy in San Francisco to engineer cells to treat a variety of cancers, now that CRISPR-mediated immune cell reprogramming can be done so effectively without relying on viruses.

This, hypothetically, would quicken the pace of CRISPR's entry into clinical studies and arrival as a mainstream treatment.

Follow Christopher Wanjek @wanjek for daily tweets on health and science with a humorous edge. Wanjek is the author of "Food at Work" and "Bad Medicine." His column, Bad Medicine, appears regularly on Live Science.

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