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<br /> Ever thought how winter <keyword id="878748" type="UNKNOWN" weightage="100" keywordseo="shivering">shivering</keyword> can help you lose weight and <keyword id="964472" type="UNKNOWN" weightage="100" keywordseo="stay-healthy">stay healthy</keyword>? Yes, it is official – a new study suggests that shivering is as good as bouts of <keyword id="25289" type="UNKNOWN" weightage="100" keywordseo="moderate-exercise">moderate exercise</keyword> when it comes to doing away with energy-storing <keyword id="2066477" type="UNKNOWN" weightage="100" keywordseo="White-fat">white fat</keyword> in your body. In fact, it can trigger the conversion of white fat into energy-burning <keyword id="504723" type="UNKNOWN" weightage="100" keywordseo="Brown-fat">brown fat</keyword>, according to <keyword id="818302" type="UNKNOWN" weightage="100" keywordseo="endocrinologist">endocrinologist</keyword> <keyword id="2066479" type="UNKNOWN" weightage="100" keywordseo="Dr-Paul-Lee">Dr Paul Lee</keyword> from <keyword id="5629" type="COMPANY" weightage="100" keywordseo="Sydney">Sydney</keyword>’s <keyword id="561931" type="ORGANIZATION" weightage="100" keywordseo="Garvan-Institute-of-Medical-Research">Garvan Institute of Medical Research</keyword>. He recently undertook the study at the National Institutes of Health (<keyword id="204101" type="ORGANIZATION" weightage="100" keywordseo="NIH">NIH</keyword>) in <keyword id="6354998" type="COMPANY" weightage="80" keywordseo="Washington">Washington</keyword>.<br />
<br /> In case you still find it a bit difficult to digest, let’s get into the heart of the matter. Lee’s work has decoded how fat and muscle communicate with each other through specific <keyword id="6456241" type="UNKNOWN" weightage="100" keywordseo="Hormones">hormones</keyword> and turn white fat cells into brown ones to protect us from cold. Around 50g of white fat can store more than 300 kilocalories of energy while the same amount of brown fat can burn up to 300 kilocalories a day.<br />
<br />
The study, now published in <em>Cell Metabolism</em><em>, </em>shows that during cold exposure and exercise, levels of the hormone <keyword id="2066488" type="UNKNOWN" weightage="100" keywordseo="Irisin">irisin</keyword> (produced by muscle) and <keyword id="2066489" type="UNKNOWN" weightage="100" keywordseo="FGF21">FGF21</keyword> (produced by brown fat) rise. In fact, around 10-15 minutes of shivering stimulates <keyword id="2066495" type="UNKNOWN" weightage="100" keywordseo="Irisin-secretion-in-humans">irisin secretion in humans</keyword> to a point that can only be reached after exercising for an hour on a bicycle at a moderate level. In the laboratory, irisin and FGF21 turn human white fat cells into brown fat cells over a period of six days.<br />
<br /> A team from <keyword id="97117" type="ORGANIZATION" weightage="80" keywordseo="Harvard-University">Harvard University</keyword> discovered irisin in 2012 through an NIH-funded research project. Irisin has been identified as a muscle hormone stimulated by exercise and it turns white fat in animals into brown fat.<br />
<br />
Interestingly, researchers now think that exercise could be a shivering mimic as there is muscle contraction in both processes and exercise-stimulated irisin could have evolved from shivering in the cold.<br />
<br /> “Excitement in the brown fat field has risen significantly over the past few years because its energy-burning nature makes it a potential therapeutic target against <keyword id="6364492" type="UNKNOWN" weightage="100" keywordseo="Obesity">obesity</keyword> and <keyword id="6359018" type="UNKNOWN" weightage="100" keywordseo="diabetes">diabetes</keyword>,” Dr Lee told the media. “White fat transformation into brown fat could protect animals against diabetes, obesity and <keyword id="6691344" type="UNKNOWN" weightage="100" keywordseo="fatty-liver">fatty liver</keyword>. Also, glucose levels are lower in humans with more brown fat.”<br />
<br /> All humans are born with brown fat around their necks – a natural protective layer that keeps us warm as infants. Earlier, scientists believed that brown fat would disappear after early infancy, but the notion has now changed. It has been found that most adults carry brown fat and the more you have, the slimmer you are likely to stay. Well, that’s not surprising as more brown fat means higher rate of white fat conversion within your body and more <keyword id="2066500" type="UNKNOWN" weightage="100" keywordseo="Calorie-burning">calorie burning</keyword>.<br />
<br /> Although it is known that <keyword id="523425" type="UNKNOWN" weightage="100" keywordseo="cold-temperature">cold temperature</keyword> stimulates <keyword id="2066503" type="UNKNOWN" weightage="100" keywordseo="Brown-fat-formation">brown fat formation</keyword>, Dr Lee has undertaken the current study to pinpoint how the body signals that message to its cells and how the activation of brown fat happens.<br />
<br />
The body can sense and relay environmental changes to different organs via nerves and hormones. Being an endocrinologist, Dr Lee has investigated the hormones that are stimulated by cold environments.<br />
<br /> “We identified two hormones that are stimulated by cold – irisin and FGF21 – released from shivering muscle and brown fat, respectively. These hormones fired up the energy-burning rate in the laboratory, and the treated fat cells began to emit heat – a hallmark of <keyword id="2066513" type="UNKNOWN" weightage="100" keywordseo="Brown-fat-function">brown fat function</keyword>,” he stated.<br />
<br /> According to the <keyword id="14962" type="POSITION" weightage="100" keywordseo="researcher">researcher</keyword>, when we are cold, we first activate our brown fat because it burns energy and releases heat to protect us. When that energy is insufficient, muscles contract mechanically or <keyword id="204100" type="PERSON" weightage="100" keywordseo="Shiver">shiver</keyword>, helping raise the hormone level. This, in turn, triggers white fat conversion into brown fat and the calories locked there burn to generate more heat. From a clinical point of view, irisin and FGF21 represent a cold-stimulated hormone system and could be further explored to <keyword id="1899546" type="UNKNOWN" weightage="100" keywordseo="fight-obesity">fight obesity</keyword> through <keyword id="2066504" type="UNKNOWN" weightage="100" keywordseo="Brown-fat-activation">brown fat activation</keyword>.<br />
<br />
<strong>Input: </strong><keyword id="295418" type="ORGANIZATION" weightage="100" keywordseo="Garvan-Institute">Garvan Institute</keyword> and <em>Cell Metabolism</em><br />
<strong>Image: </strong>Thinkstock Photos/Getty Images

Shivering Through A
Severe Winter? It Can Make You Slim

Scientists have found that <keyword id="6354493" type="General" weightage="20" keywordseo="Children" source="Orion">children</keyword>'s immune systems, unlike those of adults, do not remember the virus and do not adapt, and so when exposed to SARS-CoV-2 again, their body still treats it as a new threat, risking reinfection.<br /><br />According to the study, children have largely avoided severe COVID-19 symptoms because they have a strong initial 'innate' immune reaction that quickly defeats the virus.<br /><br />And now, researchers led by scientists at the Garvan Institute of Medical Research, Australia, have uncovered what this might mean for the immune system, the study published in the journal Clinical Immunology said.<br /><br />"The price that children pay for being so good at getting rid of the virus in the first place is that they don't have the opportunity to develop 'adaptive' memory to protect them the second time they are exposed to the virus," said lead author Tri Phan, Co-Lead of the Precision Immunology Program at Garvan.<br /><br />"Because children haven't been exposed to many viruses, their immune system is still 'naive'. And because they don't develop memory T cells, they are at risk of getting sick when they become reinfected.<br /><br />"With each new infectious episode as they get older, there is a risk of their T cells becoming 'exhausted' and ineffective, like the T cells in older people. This is why we think it's important to vaccinate children," said Phan.<br /><br />The immune system has two modes. The innate immune system is the first line of defence, comprising physical barriers such as skin and mucosal surfaces that block viruses from entering.<br /><br />The innate immune system is also composed of cells that make chemicals to signal to other cells and ward off the viruses. The innate immune system does not distinguish between one type of virus or another.<br /><br />The second line of defence comprises B and T cells of the adaptive immune system. These cells have specific receptors that can recognise and distinguish different parts of a virus and generate a rapid response to neutralise or limit it.<br /><br />Infants start with an immune system blank slate, which has a much higher proportion of naive T cells, the researchers found. As they move through childhood into adulthood and become exposed to more viruses, the naive T cells are replaced by memory T cells that are locked in to making responses to viruses they have seen before, the study said.<br /><br />"Over time, as you get infections, your immune system becomes more 'educated', allowing you to make a faster immune response that's tightly matched to the viruses that have infected you before," said Philip Britton, Associate Professor and clinical lead in the study.<br /><br />"Children's immune systems move from relying mostly on the innate system to needing the adaptive system as a backup as they grow older and are unable to clear viruses as rapidly," said Britton.<br /><br />In this study, Phan, Britton and colleagues took a deep dive to investigate T cells and cellular immune responses of a small group of children and their household family contacts who had mild or no symptoms from coronavirus (SARS-CoV-2) infection, it said.<br /><br />The researchers sequenced white blood cell samples to analyse T cells in children and adults at the time of acute infection and one month later, the study said.<br /><br />Because they studied household family contacts who were infected, researchers could control for the impact of genetic or environmental influences on the immune response, the study said.<br /><br />The scientists found that children had many different naive T cells to fight SARS-CoV-2 and made poor memory T cell responses to the virus after they had recovered, whereas the adults had few naive T cells but made good memory T cell responses after recovery.<br /><br /><strong>SEE ALSO:<br /><a target="_blank" class="c-link c-message_attachment__title_link" href="https://www.businessinsider.in/budget/news/the-union-budget-is-round-the-corner-but-is-your-budget-sorted/articleshow/97370691.cms">The Union Budget is round the corner, but is your budget sorted?</a></strong><br /><strong><a target="_blank" class="c-link c-message_attachment__title_link" href="https://www.businessinsider.in/tech/news/google-makes-changes-to-android-and-google-play-services-in-india-after-cci-setback/articleshow/97373147.cms">Google makes changes to Android and Google Play services in India after CCI setback</a></strong><br />

Children's 'rushed' immune response makes them susceptible to Covid reinfection: Study

Sydney, <keyword id="6354645" type="ORGANIZATION" weightage="20" keywordseo="researchers">Researchers</keyword> have found new evidence about the <keyword id="1308746" type="PERSON" weightage="20" keywordseo="positive-role">positive role</keyword> of <keyword id="3124830" type="PERSON" weightage="20" keywordseo="androgens">androgens</keyword>, commonly thought of as male sex hormones but also found at lower levels in women, in breast cancer treatment.<br /><br />In normal breast development, <keyword id="10620878" type="UNKNOWN" weightage="20" keywordseo="estrogen-stimulates">estrogen stimulates</keyword> and androgen inhibits growth at puberty and throughout adult life. <br /><br />Abnormal estrogen activity is responsible for the majority of breast cancers, but the role of androgen activity in this disease has been controversial.<br /><br />The new research published in the journal <keyword id="298915" type="ORGANIZATION" weightage="20" keywordseo="Nature-Medicine">Nature Medicine</keyword> showed that androgens have potential for treatment of <keyword id="3157762" type="PERSON" weightage="20" keywordseo="estrogen-receptor-positive-breast-cancer">estrogen receptor positive breast cancer</keyword>.<br /><br />A cancer is called estrogen receptor positive if it has receptors for estrogen, according to Breastcancer.org.<br /><br />Using cell-line and patient-derived models, the global team, including researchers at the <keyword id="171120" type="COMPANY" weightage="20" keywordseo="University-of-Adelaide">University of Adelaide</keyword> and the Garvan Institute of Medical Research in Australia, demonstrated that androgen receptor activation by natural androgen or a new androgenic drug had potent anti-tumour activity in all estrogen receptor positive breast cancers, even those resistant to current standard-of-care treatments. <br /><br />In contrast, androgen receptor inhibitors had no effect.<br /><br />"This work has immediate implications for women with metastatic estrogen receptor positive breast cancer, including those resistant to current forms of endocrine therapy," said lead researcher Theresa Hickey, Associate Professor at the University of Adelaide.<br /><br />"We provide compelling new experimental evidence that androgen receptor stimulating drugs can be more effective than existing (e.g. Tamoxifen) or new (e.g. Palbociclib) standard-of-care treatments and, in the case of the latter, can be combined to enhance growth inhibition," said Wayne Tilley, Director of the Dame Roma Mitchell Cancer Research Laboratories, Adelaide Medical School, University of Adelaide.<br /><br />Androgens were historically used to treat breast cancer, but knowledge of hormone receptors in breast tissue was rudimentary at the time and the treatment's efficacy misunderstood.<br /><br />Androgen therapy was discontinued due to virilising side effects and the advent of anti-estrogenic endocrine therapies.<br /><br />While endocrine therapy is standard-of-care for estrogen receptor positive breast cancer, resistance to these drugs is the major cause of breast cancer mortality.<br /><br />"The new insights from this study should clarify the widespread confusion over the role of the androgen receptor in estrogen receptor driven breast cancer," said Elgene Lim, a breast oncologist and Head of the Connie Johnson Breast Cancer Research Lab at the Garvan Institute.<br /><br />"Given the efficacy of this treatment strategy at multiple stages of disease in our study, we hope to translate these findings into clinical trials as a new class of endocrine therapy for breast cancer."<br /><br /><br /><strong>SEE ALSO:<br /><a href="https://www.businessinsider.in/business/startups/news/zoom-dropbox-backer-salesforce-ventures-makes-its-first-investment-in-india-in-hr-tech-startup-darwinbox-which-claims-to-have-grown-by-200-during-lockdown/articleshow/80341562.cms">Zoom, Dropbox backer Salesforce Ventures makes its first investment in India in HR tech startup Darwinbox, which claims to have grown by 200% during lockdown</a><br /><a href="https://www.businessinsider.in/stock-market/news/home-first-finance-company-hffc-is-set-to-launch-its-1153-crore-ipo-on-january-21/articleshow/80341439.cms?upcache=2">Warburg Pincus-backed Home First Finance Company to launch ₹1,153 crore IPO on January 21</a><br /></strong><a href="https://www.businessinsider.in/international/news/top-ten-likely-global-risks-in-2021-according-to-the-world-economic-forum/slidelist/80346013.cms"><strong>From climate action failure to monopoly in the tech world — the world needs to wake up to these global risks in 2021, says the World Economic Forum</strong></a><br />

Male sex hormones could help in treating breast cancer, says new study

A new genetic mutation may be the cause of severe cases of <keyword id="22374" type="General" weightage="80" keywordseo="childhood" source="Orion">childhood</keyword> <keyword id="109031" type="General" weightage="100" keywordseo="glaucoma" source="Orion">glaucoma</keyword>, a debilitating condition that runs in families and can cause children to lose their vision by the age of three, according to a study.<br /><br />  The discovery was made by an international team of researchers led by Mass Eye and Ear, a division of Mass General Brigham, and Boston Children's Hospital and the findings were published in the Journal of Clinical Investigation.<br /><br /> Through advanced genome-sequencing technology, the researchers found a mutation in the thrombospondin-1 (THBS1) gene in three ethnically and geographically diverse families with childhood glaucoma histories. The researchers then confirmed their findings in a mouse model that possessed the genetic mutation and went on to develop symptoms of glaucoma driven by a previously unknown disease mechanism.<br /><br /> The new findings, could lead to improved screening for childhood glaucoma and earlier and more targeted treatments to prevent vision loss in children with the mutation, according to the study's authors.<br /><br /> "This is a very exciting finding for families affected by childhood glaucoma," said Janey L. Wiggs, MD, PhD, Associate Chief of Ophthalmology Clinical Research at Mass Eye and Ear and the Vice Chair for Ophthalmology Clinical Research and <keyword id="15693489" type="General" weightage="50" keywordseo="paul-austin-chandler" source="Orion">Paul Austin Chandler</keyword> Professor of Ophthalmology at <keyword id="20988" type="General" weightage="50" keywordseo="harvard-medical-school" source="Orion">Harvard Medical School</keyword>. "With this new knowledge, we can offer genetic testing to identify children in a family who may be at risk for the disease and start disease surveillance and conventional treatments earlier to preserve their vision. In the future, we would look to develop new therapies to target this genetic mutation."<br /><br /> Leading cause of childhood blindness<br /><br /> Childhood, or congenital, glaucoma is a rare but serious disease that presents in children as early as birth and as late as 3 years of age. Despite its rarity, childhood glaucoma is responsible for 5 percent of cases of child blindness worldwide.<br /><br /> Glaucoma causes irreversible damage to the eye's optic nerve, often due to buildup of pressure inside the eye (intraocular pressure, or IOP). In adults, this damage can occur over time without symptoms, which is why the disease is often referred to as a "sneak thief of sight."<br /><br /> Children and babies with childhood glaucoma, however, can be born with severe disease and vision loss or lose their vision later in childhood due to elevated IOP. This increase in pressure not only damages the optic nerve but can also affect other structures in a child's eye like the cornea. Children with childhood glaucoma typically require surgeries as early as the first three to six months of life, followed by several more operations throughout their childhood.<br /><br /> With childhood glaucoma, there is typically a strong hereditary component often with multiple members of a family affected by the condition. According to Dr. Wiggs, by better understanding the genes involved, genetic testing can give affected families peace of mind to learn whether their child might be at risk for developing the disease.<br /><br /> Uncovering the genetic underpinnings of disease<br /><br /> For decades, researchers have turned towards genetics to better understand the cause of glaucoma. When Dr. Wiggs first began this line of research 30 years ago, scientists were only able to identify regions of the genome affected in glaucoma. Thanks to advances in genomic technology, researchers gained the ability to review the complete genetic makeup of individuals with and without glaucoma to determine which specific genetic mutations play a role in the disease. Research led by Dr. Wiggs in 2021 used a dataset of more than 34,000 adults with glaucoma to identify 127 genes associated with the condition.<br /><br /> To better study the genetic mutations in childhood glaucoma, Dr. Wiggs and her Mass Eye and Ear team first looked at exome sequences from an American family of European-Caucasian descent who had been part of an earlier research project and found a striking and novel variant in thrombospondin-1, a well-known protein in the body involved in a number of important biological processes, such as the formation of new vessels (angiogenesis) and tissues. This mutated gene was not found in people without childhood glaucoma, nor in large population genetic databases. The amino acid altered by the mutation was evolutionarily conserved, indicating an important role in the protein function. This finding led Dr. Wiggs to connect with colleagues at Flinders University in Australia to see if they had any childhood glaucoma families with thrombospondin mutations. They surprisingly found two families with an alteration at the same amino acid: one of mixed European and Indian descent, and one Sudanese family originally from Africa.<br /><br /> "What was really striking about this finding is that these families all possessed this genetic variant, and it was not possible for them to be related because they were from such diverse backgrounds," said Dr. Wiggs. "That meant there was something really important about this mutation."<br /><br /> To further test this hypothesis, the researchers collaborated with Robert J. D'Amato, MD, PhD, the Judah Folkman Chair in Surgery in the Vascular Biology Program at Boston Children's Hospital, and a professor of Ophthalmology at Harvard Medical School. Dr. D'Amato's team developed a mouse model with the THBS1 mutation and found that the mouse also had features of glaucoma.<br /><br /> "Thrombospondin-1 is well known as a potent inhibitor of blood vessel growth, or angiogenesis," said Dr. D'Amato, who has studied angiogenesis for more than three decades. "I assumed at first that THBS1 mutations were disrupting blood vessel formation in the eye, but our animal models showed normal angiogenesis. We realized that there must be another mechanism."<br /><br /> Specifically, D'Amato's lab showed that the mutation caused abnormal thrombospondin proteins to accumulate in the intraocular drainage structures of the eye involved with regulating IOP, which in turn, led to a buildup of pressure that damaged the optic nerve and led to the loss of retinal ganglion cells, thereby causing vision loss.<br /><br /> This was the first time that researchers identified this kind of disease mechanism for causing childhood glaucoma.<br /><br /> "This work highlights the power of international collaborations," said study co-author Owen M. Siggs MD, DPhil, associate professor at Flinders University and the Garvan Institute of Medical Research in Australia. "There's such incredible genetic diversity across the globe, and comparing this information is becoming more and more critical for discoveries like this."<br /><br /> Personalizing care for families with future study<br /><br /> The new study has significant clinical implications, according to the researchers. While more work remains before comprehensive genetic testing can be offered, every gene that is found presents another opportunity to be able to identify causative mutations in these families through screening, according to the authors.<br /><br /> Therapeutically, knowledge of this gene mutation can lead to earlier treatments with conventional therapies. For example, if a baby is born with this mutation, their eye care specialist can better inform the parents of the risks and develop an appropriate disease-monitoring and treatment plan.<br /><br /> Identifying this new mechanism and gene at the root of childhood glaucoma could also lead to new therapies that would target the accumulation of abnormal proteins. The researchers also aim to determine if other THBS1 mutations are involved in adult-onset disease, like primary open-angle glaucoma, or milder forms of the disease if the mutation is not as pronounced.<br /><br /> The researchers will also continue to look for new genes associated with childhood glaucoma in the hopes of one day developing very comprehensive screening.<br /><br /> "Dr. Wiggs is an international expert in glaucoma genetics and has worked tirelessly to unravel the genetic contributions to these blinding diseases. These findings provide important insights into the causes of childhood glaucoma and offer the prospect of targeted therapy," said Joan W. Miller, MD, Chair of Ophthalmology at Mass Eye and Ear and <keyword id="576044" type="General" weightage="50" keywordseo="massachusetts-general-hospital" source="Orion">Massachusetts General Hospital</keyword>, Ophthalmologist-in-Chief at Brigham and Women's Hospital, and Chair of Ophthalmology and the David Glendenning Cogan Professor of Ophthalmology at Harvard Medical School. "The collaboration is a powerful demonstration of the strength of bedside-to-bench-to-bedside translational research, in uncovering disease pathogenesis and developing therapies for patients."<br /><br /><b>SEE ALSO:</b><br /><br /> <b><a href="https://www.businessinsider.in/science/health/news/postpartum-depression-in-mothers-can-have-serious-consequences-on-the-childs-health-and-development/articleshow/95946346.cms">Postpartum depression in mothers can have serious consequences on the child’s health and development</a></b><br /><br /> <b><a href="https://www.businessinsider.in/stock-market/markets/news/foreign-investors-upgrade-india-as-dedicated-allocation-in-investment-portfolios-say-equity-experts/articleshow/95974087.cms">Foreign investors upgrade India as dedicated allocation in investment portfolios, say equity experts</a></b><br />

Researchers reveal new genetic mutation cause of childhood glaucoma

<p dir="ltr"><div class="KonaFilter image-container display-table"><div><div class="image"><p class="source"><span>Paula Bronstein /Getty Images</span></p><p class="caption">Handicapped residents at the Ba Vi orphanage wander about the large campus posing for the camera. </p></div><p></p></div></div>During the Vietnam War, the U.S. military sprayed approximately 20 million gallons of herbicides across 5.5 million acres of Vietnamese jungle and countryside, an area roughly the size of New Jersey, according to The New York Times. U.S. soldiers sprayed these herbicides to flush out Vietcong soldiers, who used the foliage for cover.</p>
<p dir="ltr">The main herbicide, nicknamed Agent Orange, consisted of two herbicides, one of which had been tainted with a toxic strain of dioxin, according to The Times. Dioxins are a group of chemical compounds that have similar structures; the <span style="line-height: 1.5em;">World Health Organization has called these compounds </span><a href="http://www.who.int/mediacentre/factsheets/fs225/en/">"highly toxic</a><span style="line-height: 1.5em;">."</span><span style="line-height: 1.5em;"> The EPA characterizes dioxins as </span><a href="http://www.epa.gov/pbt/pubs/dioxins.htm">likely human carcinogens</a>, and it notes they've been linked to birth defects and a serious skin condition called <a href="http://en.wikipedia.org/wiki/Chloracne">chlorachne</a>.<span style="line-height: 1.5em;"><br /></span></p>
<p dir="ltr"><span style="font-size: 15px; line-height: 1.5em;">Nearly 40 years after the Vietnam War, a particularly harmful strain of dioxin still saturates Vietnamese lands, wildlife, and groundwater - ensuring Vietnamese villagers will feel its effects for generations more. The Vietnam Red Cross estimates that Agent Orange caused at <a href="http://www.redcross.int/EN/mag/magazine2004_3/22-23.html">least 150,000 birth defects</a> since the end of the Vietnam War.</span></p>
<p><span id="docs-internal-guid-03eafa16-8318-c9f9-0009-9664c0b7e68d"><a href="http://www.paulaphoto.com/#/agent-orange--vietnams-legacy/agentorangewebsite001">Getty photographer Paula Bronstein</a> traveled to Vietnam in 2011 to document the third generation of Vietnamese to suffer the effects of Agent Orange. The impoverished villagers continue to have health problems, and orphanages often care for children disabled by Agent Orange. </span></p>
<p><span style="line-height: 1.5em;">In recent years, the U.S. has </span><a href="http://www.nytimes.com/2012/08/10/world/asia/us-moves-to-address-agent-orange-contamination-in-vietnam.html?pagewanted=all&amp;_r=0">made efforts to clean up dioxin sites</a><span style="line-height: 1.5em;"> and </span><a href="http://www.gpo.gov/fdsys/pkg/CHRG-111hhrg57498/html/CHRG-111hhrg57498.htm">has provided $46 million in general aid for disabled Vietnamese</a><span style="line-height: 1.5em;">. Still, some lawmakers have argued the U.S. hasn't done enough to </span><a href="http://www.gpo.gov/fdsys/pkg/CHRG-111hhrg57498/html/CHRG-111hhrg57498.htm">accept culpability</a><span style="line-height: 1.5em;"> for the harmful effects of Agent Orange. </span></p>
<h3>Bronstein traveled to villages in the north of Vietnam near Cam L?, Ba Vì, and Da Nang. <div class="KonaFilter image-container display-table"><div><div class="image"><p class="source"><span>Google Maps/Screenshot</span></p></div><p></p></div></div>The U.S. sprayed Agent Orange mostly in the south but also spread the herbicide in many areas in the north. This is a U.S. Army map of spray missions conducted during the war. <div class="KonaFilter image-container display-table"><div><div class="image"><p class="source"><span>U.S. Department of the Army</span></p></div><p></p></div></div> </h3>
<h3>During the war, <a href="http://articles.chicagotribune.com/2009-12-08/health/chi-agent-orange3-dec08_1_defoliants-vietnam-war-agent-orange">the U.S. said Agent Orange was harmless</a>, according to the Chicago Tribune. While the U.S. now offers benefits to veterans who suffer certain Agent Orange-related illnesses, it <a href="http://www.aspeninstitute.org/policy-work/agent-orange/program-home/agent-orange-us-veterans">still refuses to acknowledge</a> Agent Orange caused<a href="http://www.aspeninstitute.org/policy-work/agent-orange/program-home/agent-orange-us-veterans"> health problems in Vietnam</a>, according to the Aspen Institute. The Vietnam Red Cross estimates Agent Orange affected as <a href="http://www.mcclatchydc.com/2013/07/22/197318/4-decades-after-war-ended-agent.html#.UhumOmTF2nQ">many as 3 million Vietnamese</a>.<div class="KonaFilter image-container display-table"><div><div class="image"><p class="source"><span>Paula Bronstein /Getty Images</span></p><p class="caption">Le Van Khanh,38 (left) stands next to his mother Nguyen Thi Huyen in Cam Lo, Vietnam. Le Van was born deaf, mentally handicapped with legs that are deformed, he is wheelchair bound most of the time and his elderly mother can't physically handle the responsibility of her handicapped son. Nguyen lost 2 children in addition as well and gets a small stipend from the government.</p></div><p></p></div></div>Children in areas where Agent Orange was used have been affected with hydrocephalus (brain swelling), cleft palates, mental disabilities, hernias, extra fingers and toes, spina bifida, and various genetic diseases. Still, it's tough to prove Agent Orange caused these problems <a href="http://ije.oxfordjournals.org/content/35/5/1220.full">due to some studies finding inconsistent results</a>, according to a 2006 study by researchers at the Garvan Institute of Medical Research.<div class="KonaFilter image-container display-table"><div><div class="image"><p class="source"><span>Paula Bronstein /Getty Images</span></p><p class="caption">Nguyen Xuan Minh, 4 years, lays in a crib at the Tu Du Hospital in Ho Chi Minh City, Vietnam. He has been deformed since birth from what may be the effects of the defoliant Agent Orange.</p></div><p></p></div></div>Dioxin exposure is linked to non-Hodgkin's lymphoma, soft-tissue sarcoma, type-2 diabetes, and several types of cancer, <a href="http://www.publichealth.va.gov/PUBLICHEALTH/exposures/agentorange/conditions/index.asp">according to the Department of Veterans Affairs.<div class="KonaFilter image-container display-table"><div><div class="image"><p class="source"><span>Paula Bronstein /Getty Images</span></p><p class="caption">Le Thi Mit feeds her son Nguyen Van Choui, 26, at their home in Cam Lo, Vietnam.</p></div><p></p></div></div>The 2006 Garvan study</a>, which conducted a review of 22 Agent Orange studies, concluded parental exposure to Agent Orange unequivocally increased the risk of birth defects.<div class="KonaFilter image-container display-table"><div><div class="image"><a href="http://www.publichealth.va.gov/PUBLICHEALTH/exposures/agentorange/conditions/index.asp"></a><p class="source"><span>Paula Bronstein /Getty Images</span></p><p class="caption">A mother parks her handicapped son who she claims is suffering from the effects of Agent Orange parks outside a shopping center begging for money.</p></div><p></p></div></div><a href="http://www.publichealth.va.gov/PUBLICHEALTH/exposures/agentorange/conditions/index.asp">In order to receive aid from the Vietnamese government,</a> affected Vietnamese must prove Agent Orange caused their ailments or birth defects, according to Bronstein. Since it's tough for poor villagers to pay for tests to provide this proof, she says they often don't get the aid to help them pay for their children's medical care.</h3>
<h3><div class="KonaFilter image-container display-table"><div><div class="image"><p class="source"><span>Paula Bronstein /Getty Images</span></p><p class="caption">Trong Thi Kiev, 17, rests in a hammock. She is blind and deaf suffering, with Spina Bifida. As a single mother, her mother has to balance caring for her severely handicapped daughter with working. She struggles everyday to make ends meet. Trong also lost her first child after 45 days due to severe birth defects from dioxin.</p></div><p></p></div></div>Since many Vietnamese can barely eek out a living as farmers, some leave their children at orphanages run by charities and aid organizations. <div class="KonaFilter image-container display-table"><div><div class="image"><p class="source"><span>Paula Bronstein /Getty Images</span></p><p class="caption">Handicapped orphans get fed by the medical staff at the Ba Vi orphanage.</p></div><p></p></div></div>The problem is so bad that many orphanages are overcrowded, with new children arriving every day. At 17, the disabled children move to an adult-care home. It's unlikely they will ever live independently.<div class="KonaFilter image-container display-table"><div><div class="image"><p class="source"><span>Paula Bronstein /Getty Images</span></p><p class="caption"> Handicapped orphans get bathed by the medical staff at the Ba Vi orphanage.</p></div><p></p></div></div>Those who don't give up their children must care for them through their adult years. It's a stressful proposition. Few completely understand why they have the issues that they do, says Bronstein. They only know it's the U.S. government's fault. <div class="KonaFilter image-container display-table"><div><div class="image"><p class="source"><span>Paula Bronstein /Getty Images</span></p><p class="caption">Le Thi Mit sits with her one of her two handicapped sons, Nguyen VanTrong, 22, at their home in Cam Lo, Vietnam. His handicap was caused due to the effects of the dioxin. They live a life without physical therapy or education.</p></div><p></p></div></div>Da Nang is one of the areas most affected by Agent Orange. The U.S. military used the airport there as a major military base and storage site for Agent Orange. In 2011, the U.S. began an operation to decontaminate the soil in dioxin "hot spots." Da Nang <a href="http://www.nytimes.com/2012/08/10/world/asia/us-moves-to-address-agent-orange-contamination-in-vietnam.html?pagewanted=all">was the first site of the operation</a>. <div class="KonaFilter image-container display-table"><div><div class="image"><p class="source"><span>Paula Bronstein /Getty Images</span></p><p class="caption"> Handicapped children play games at the Thanh Tam Special school in Da Nang. The brand new privately funded school is run by Catholic charities with help from various non-governmental organizations like Children of Vietnam.</p></div><p></p></div></div>The program, costing $43 million and to be completed in four years, will <a href="http://www.nytimes.com/2012/08/10/world/asia/us-moves-to-address-agent-orange-contamination-in-vietnam.html?pagewanted=all&amp;action=click&amp;module=Search&amp;region=searchResults&amp;mabReward=relbias%3As%2C[%22RI%3A1%22%2C%22RI%3A3%22]&amp;url=http%3A%2F%2Fquery.nytimes.com%2Fsearch%2Fsitesearch%2F%23%2Fagent%2Borange%2F">render the dioxins in the soil harmless</a>, according to The New York Times. It does nothing to help those already affected by Agent Orange.<div class="KonaFilter image-container display-table"><div><div class="image"><p class="source"><span>REUTERS/Kham </span></p><p class="caption">Soldiers detect Unexploded Ordnance (UXO) and defoliant Agent Orange during the launch of the "environmental remediation of dioxin contamination" project, in Vietnam's central Da Nang City in 2011. </p></div><p></p></div></div></h3>

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