What happens to your body when you give up sugar?


The brain becomes tolerant to sugar – which means more is needed to attain the same ‘high’. In ways that nicotine and heroin hijack the brain’s reward pathway and make users dependent, increasing neuro-chemical and behavioural evidence suggests sugar is addictive in the same way

Sugar addiction is real

Anyone who knows me also knows that I have a huge sweet tooth. I always have. My friend and fellow graduate student Andrew is equally afflicted, and living in Hershey, Pennsylvania – the “Chocolate Capital of the World” – doesn’t help either of us. But Andrew is braver than I am. Last year, he gave up sweets for Lent.

“The first few days are a little rough,” Andrew told me. “It almost feels like you’re detoxing from drugs. I found myself eating a lot of carbs to compensate for the lack of sugar.”

There are four major components of addiction: bingeing, withdrawal, craving, and cross-sensitisation (the notion that one addictive substance predisposes someone to becoming addicted to another). All of these components have been observed in animal models of addiction – for sugar, as well as drugs of abuse.

A typical experiment goes like this: rats are deprived of food for 12 hours each day, then given 12 hours of access to a sugary solution and regular chow. After a month of following this daily pattern, rats display behaviours similar to those on drugs of abuse. They’ll binge on the sugar solution in a short period of time, much more than their regular food. They also show signs of anxiety and depression during the food deprivation period. Many sugar-treated rats who are later exposed to drugs, such as cocaine andopiates, demonstrate dependent behaviours towards the drugs compared to rats who did not consume sugar beforehand.

Like drugs, sugar spikes dopamine release in the nucleus accumbens. Over the long term, regular sugar consumption actually changes the gene expression and availability of dopamine receptors in both the midbrain and frontal cortex. Specifically, sugar increases the concentration of a type of excitatory receptor called D1, but decreases another receptor type called D2, which is inhibitory. Regular sugar consumption also inhibits the action of the dopamine transporter, a protein which pumps dopamine out of the synapse and back into the neuron after firing.

In short, this means that repeated access to sugar over time leads to prolonged dopamine signalling, greater excitation of the brain’s reward pathways and a need for even more sugar to activate all of the midbrain dopamine receptors like before. The brain becomes tolerant to sugar – and more is needed to attain the same “sugar high.”

Sugar withdrawal is also real

Although these studies were conducted in rodents, it’s not far-fetched to say that the same primitive processes are occurring in the human brain, too. “The cravings never stopped, [but that was] probably psychological,” Andrew told me. “But it got easier after the first week or so.”

In a 2002 study by Carlo Colantuoni and colleagues of Princeton University, rats who had undergone a typical sugar dependence protocol then underwent “sugar withdrawal.” This was facilitated by either food deprivation or treatment with naloxone, a drug used for treating opiate addiction which binds to receptors in the brain’s reward system. Both withdrawal methods led to physical problems, including teeth chattering, paw tremors, and head shaking. Naloxone treatment also appeared to make the rats more anxious, as they spent less time on an elevated apparatus that lacked walls on either side.

Similar withdrawal experiments by others also report behaviour similar to depression in tasks such as the forced swim test. Rats in sugar withdrawal are more likely to show passive behaviours (like floating) than active behaviours (like trying to escape) when placed in water, suggesting feelings of helplessness.

A new study published by Victor Mangabeira and colleagues in this month’s Physiology & Behavior reports that sugar withdrawal is also linked to impulsive behaviour. Initially, rats were trained to receive water by pushing a lever. After training, the animals returned to their home cages and had access to a sugar solution and water, or just water alone. After 30 days, when rats were again given the opportunity to press a lever for water, those who had become dependent on sugar pressed the lever significantly more times than control animals, suggesting impulsive behaviour.

These are extreme experiments, of course. We humans aren’t depriving ourselves of food for 12 hours and then allowing ourselves to binge on soda and doughnuts at the end of the day. But these rodent studies certainly give us insight into the neuro-chemical underpinnings of sugar dependence, withdrawal, and behaviour.

Through decades of diet programmes and best-selling books, we’ve toyed with the notion of “sugar addiction” for a long time. There are accounts of those in “sugar withdrawal” describing food cravings, which can trigger relapse and impulsive eating. There are also countless articles and books about the boundless energy and new-found happiness in those who have sworn off sugar for good. But despite the ubiquity of sugar in our diets, the notion of sugar addiction is still a rather taboo topic.

Are you still motivated to give up sugar? You might wonder how long it will take until you’re free of cravings and side-effects, but there’s no answer – everyone is different and no human studies have been done on this. But after 40 days, it’s clear that Andrew had overcome the worst, likely even reversing some of his altered dopamine signalling. “I remember eating my first sweet and thinking it was too sweet,” he said. “I had to rebuild my tolerance.”

And as regulars of a local bakery in Hershey – I can assure you, readers, that he has done just that.

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Scientists hope to attract millions to ‘DNA.LAND’


Study to collect data from customers of genetic-testing services.

Researchers hope to create a massive, crowdsourced DNA database for genetic studies.

Geneticists have launched a project to test whether they can study millions of genomes — without collecting a drop of blood or tube of spit themselves.

The project, DNA.LAND, aims to entice people who have already had their genomes analysed by consumer genetics companies to share that data, allowing DNA.LAND geneticists to study the information.

Although some consumer genetic-testing companies share data with researchers, they provide only aggregate information about their customers, not individual genomes. Because the data are not always accompanied by detailed information on patients’ health, they are of limited use for drawing links between genes and disease.

“Millions of people have access to their genomes, and many more millions will join them in the near future,” says computational geneticist Yaniv Erlich. He is launching DNA.LAND with fellow geneticist Joseph Pickrell at the New York Genome Center and Columbia University in New York. “Can you get to the point that instead of paying for each study from scratch, we can use the crowd to collect and repurpose this data?” Erlich asks.

Erlich will present the project on 10 October at the annual meeting of the American Society of Human Genetics (ASHG) in Baltimore, Maryland. This is not the first time that he has sought to engage the public to assemble data for large research studies. For instance, Erlich has previously combined data from genealogy websites into the world’s largest family tree, with information on 13 million people.

DNA.Land is an example of the ‘participatory turn’ in human subjects research, says Michelle Meyer, a bioethicist and legal scholar at the Icahn School of Medicine at Mount Sinai in New York.This is a smart research model, since it keeps sequencing and data-storage costs low and doesn’t run into the patchwork of federal and state laws governing genetic testing itself.

DNA donors

Erlich hopes to tap the genomes of up to three million customers of companies such as 23andMe, Ancestry.com and Family Tree DNA. The companies allow people to download a file containing the readout of their genetic results.

By combining these data with other information about the participants, such as that on their health, Erlich hopes to assemble a very large data set. A recent analysis, for instance, suggested that as many as 2 billion genomes could be sequenced by 2025. “The sky is the limit,” he says.

Erlich has studied the potential for unmasking the identities of anonymous donors of genetic data, and the study’s consent document warns participants that “we cannot guarantee that your identity and/or data will never become known, which could have significant implications in some scenarios. We estimate that the risk for such a confidentiality breach is low but not zero.” Erlich and Pickrell have adopted what they call a “skin in the game” philosophy by making their own genomes publicly available.

Meyer, who supports the project, says that it might require a more detailed consent briefing — for instance, by spelling out what risks there are if participants’ identities are revealed, or suggesting that participants might want to consult with their families before entering information about them. When DNA.LAND participants create an account, for instance, they are asked for the names and dates of birth of their parents.

“Usually, genomics studies suggest discussing your decision to participate with close family members,” Meyer says. “Here, genomic data is combined with parents’ names and dates of birth, both identifiers, so it was surprising that there was no mention of risks to family members.”

Erlich says that his team wanted to keep the consent form succinct, and that DNA.LAND provides more detailed information as participants progress to relevant parts of the study. He adds that the team is open to making revisions to its consent documents.

Crowdsourced science

DNA.LAND will not pay participants, but uses other means to entice people to share their data. It will provide shareable digital contribution badges to participants as they contribute more information, and promises to provide new findings about their genomes in return.

For instance, to stitch together a coherent data set from genomes that have been analysed by multiple companies and which each test for different genetic markers, DNA.LAND will use a method called imputation. This allows the project to infer the identities of gene variants that were not originally tested, filling in gaps on the basis of knowledge about specific markers that are often inherited together. Participants will be told about newly identified genetic variants uncovered by imputation. The researchers also have promised to tell participants if the work uncovers that they have relatives in the project database.

Statistical geneticist Gonçalo Abecasis at the University of Michigan, Ann Arbor, has enlisted 7,200 research participants in a separate genetics study called Genes for Good. He says that both his project and DNA.LAND are motivated by geneticists’ growing awareness that it will take very large data sets to understand how genes influence human health. That may require finding new ways to recruit research participants — such as the Facebook app created by Genes for Good.

Going viral

Meyer says that the ability to learn more about their own genomes and find new relatives could attract genetic genealogists to the DNA.LAND project. Such people are interested in using DNA to explore their family histories, and are often avid users of genetic-testing services. But attracting other groups of people might be more difficult, she says.

“I have no doubt that genomics nerds will flock to the site, but a lot of interesting research they might want to do will require large sample sizes, so they’ll need to go beyond the community of early adopters and academics who attend ASHG each year,” Meyer says.

Geneticist and entrepreneur David Mittelman, who is based in Houston, Texas, says that people can be convinced to share their data if it is easy and fun, and if they get something in return. He noted that DNA.LAND’s creators understand this — on 5 October, Erlich tweeted that he had used the project’s relative finder to discover that he and human geneticist Nathan Pearson of the New York Genome Center are on the order of third or fourth cousins, prompting a flurry of tweets.

“That kind of engagement and viral promotion is how gaming companies like Zynga spread their games through Facebook and the Internet,” Mittelman says. “That’s the recipe for success: standardize the tools, engage folks and give them a value-add, and if it’s easy to share, they will do it.”

Cultivating sunflowers can brighten your life and improve your health in surprising ways


Sunflowers, with their tall stalks and bright yellow flowers, are often associated with optimism and cheer. However, they do more than evoke positive feelings; they can improve health — your own as well that of the environment — in many ways.

health

For example, it’s no secret that consuming their seeds does wonders for health.

According to the World’s Healthiest Foods website, sunflower seeds “are an excellent source of vitamin E, the body’s primary fat-soluble antioxidant.” Vitamin E plays a role in maintaining healthy cells and keeping free radicals from destroying the body; as such, sunflower seeds are listed on the site as one of the top 100 healthiest foods.(1)

Furthermore, the site explains that the seeds are good sources of selenium and magnesium, which aids in cancer prevention, improved detoxification and nerve and blood vessel health. Lowered blood pressure, reduced stroke risk, fewer muscle cramps and migraine relief are just a few benefits gained by incorporating more sunflower seeds into the diet.(1)

To really ramp up these nutritional benefits, sprout the seeds, which creates microgreens. Doing so provides nearly 100 times the enzymes of full-grown greens, so in actuality, your body is able to more easily absorb its vitamins E and A, as well as omega-3 fatty acids, folate and iron.(2)

The good news doesn’t stop with the seeds. Did you know that there are health benefits beyond the seeds?

Medicinal properties of sunflowers

Have a high fever? Turn to sunflower leaves. When used as an infusion, it can help bring the fever down. It also plays a role in improving lung issues and offering relief from diarrhea.

If you’ve developed a wound or other similar skin injury, you’ll be amazed by the healing wonders of sunflower stems. According to the United States Department of Agriculture’s Natural Resources Conservation Service, Charles H. Lange, an anthropologist at the University of Texas, touted the healing nature of the stems, calling them a “reliable ‘home remedy'” in which the juice of freshly-cut sunflower stems can be “smeared liberally over the wounds” then bandaged. Lange noted that doing so led to a fast, infection-free recovery.(3)

Natural way to preserve wildlife and protect other crops

In addition to human health, planting sunflowers also attracts birds (ranging from black-capped chickadees to house finches and meadowlarks) and bees to help other crops grow and be pollinated.(2,3)

Furthermore, sunflower stalks are ideal for climbing plants like squash or green beans; consider using stalks instead of bothering with purchasing or making your own stakes. They’re sturdy enough to support climbing plants, plus the sheer size of sunflowers helps protect crops from intense sunlight, creating shade while also boosting humidity. In turn, gardens and crops flourish.

When the SHTF, sunflowers are ideal

Because sunflowers are great for health and the environment, they’re also viewed as a great way to prepare for SHTF scenarios. In fact, a 2,500 square foot lot can produce about 20 pounds of
non-hulled seeds. This amount even includes plenty of broken seeds left over that feed birds. In the the likely event that economic, societal and environmental collapse occurs and people are left scurrying for food and shelter, cultivating sunflowers is important to consider.(2)

What’s not to love about bright and cheery sunflowers? They’re great for health, possess a wide range of nutritional qualities, aid in wound healing and ensure that other crops and wildlife are protected.

Learn more: http://www.naturalnews.com/051476_sunflowers_gardening_medicinal_plants.html#ixzz3oEQlBWtr

Many doctors uninformed about strokes of unknown cause .


1008-News-Cryptogenic stroke_Blog

A new survey shows that up to half of doctors feel uninformed about how to diagnose and treat the nearly 200,000 patients who suffer strokes of unknown cause each year.

The survey, released Thursday by the American Heart Association/American Stroke Association, found that depending on their specialty, 18 percent to 49 percent of physicians are unsure about the best approaches to diagnose and treat cryptogenic stroke, a stroke for which the underlying cause is still unknown after extensive testing.

The survey polled 652 neurologists, cardiologists, hospitalists, primary care physicians and stroke coordinators.

In response, the AHA/ASA will convene the Cryptogenic Stroke Public Health Conference on Friday in Washington, D.C. Leading healthcare providers will discuss the new survey findings and possibilities for a coordinated, systematic approach to diagnose and manage patients with cryptogenic stroke.

Statistics show that cryptogenic stroke patients should be concerned: A prior stroke is the No. 1 risk factor for a second stroke, and a second stroke is 16 times more likely to be fatal.

“The ability to discern the causes of cryptogenic strokes has profound implications for preventing secondary strokes and improving patient outcomes,” said Mary Ann Bauman, M.D., chair of the ASA’s advisory committee. “With the Cryptogenic Stroke Public Health Conference, we are coming together as a healthcare community to increase our knowledge about cryptogenic stroke and improve treatment.”

Healthcare professionals recognize that among other causes, atrial fibrillation, an irregular heartbeat that may occur only intermittently and thus be difficult to detect, can be a cause of cryptogenic stroke. Yet physicians are not always sure how best to detect the condition, according to the survey.

Other possible causes of cryptogenic stroke include patent foramen ovale, a hole between the heart’s upper chambers, and various blood clotting disorders.

“This is important,” Bauman said, “because stroke is the fifth-leading cause of death in the U.S. and a leading cause of severe, long-term disability.”

Water may be found on other planet.


Ghosh, who leads ‘Science Operations Working Group, Mission Operations, NASA Mars Exploration Rover Mission’, said, “Our satellites have sent signals of (suggesting) availability of water at few other planets including Pluto, Saturn and Jupiter which enhances the chances of (finding)life in those places.”

However, mere presence of water doesn’t guarantee that there would be living organisms, he added.

An alumnus of IIT-Kharagpur, Ghosh was associated with Pathfinder mission in 1997 at the age of 27 and is now leading the project ‘Opportunity’ on tactical rover operations including rover driving and science experiments.

He interacted with journalists at Mumbai Press Club this evening.

“Presence of water on Mars is a huge relief for us,” he said, because it can cut down the logistical provisions that a Human mission to Mars in future may have to carry.

“NASA also aims to collect a few rocks from Mars around (year) 2030 and bring it to earth to have further analysis inour labs..at various universities,” he said.

NASA would send its next spacecraft to Mars, named InSight in 2016, and it will study the activities under the crust of the planet.

Another spacecraft would be sent in 2020, he said.

Teaching Your Brain to Ward Off Bad Habits.


What’s the Latest?

The Chicago Tribune currently features an article by Danielle Braffdetailing strategies for breaking annoying habits. Braff explains that to tackle a bad habit, one must understand the anatomy of a habit. She evokes Charles Duhigg, author of The Power of Habit, who offers a tripartite explanation. Every habit, says Duhigg, consists of a cue, a routine and a reward:

“The reward is how our brain learns how to latch on to the habit,” Duhigg said, explaining that the reward is always something positive. Your brain tries to turn a repeatable pattern into a habit as long as it has a reward attached. So if you have a cup of coffee with a cookie, then your brain will use the coffee as a cue for a cookie. If you do this often enough (every other day for three weeks, for example), your brain will turn it into a repeatable pattern, and that pattern will become a habit.

Habit

As you can probably surmise, the secret to kicking habits is to train the brain away from this routine.

What’s the Big Idea?

Braff offers a number of examples of ingrained, trained habits and the ways one can re-train the brain to avoid falling into the subconscious pursuits of unhealthy rewards. She acknowledges that some strategies require more effort than others — some even requiring broad lifestyle changes.

Braff’s article also features strategies for how to avoid falling into bad habits, the classic “cure by prevention” method. She quotes author Tara Gidus:

“I think a lot of it is planning, as in having healthier substitutions, but it also has to do with plain old willpower and self-talk.”

New blood test determines which patients are at risk of heart attack.


Two out of three patients could be going home a lot sooner.

The levels of a protein called troponin in your blood could tell doctors whether you’re at risk of a heart attack, thanks to a new high-sensitivity blood test developed by researchers in the UK.

This quick, convenient method of testing patients could rule out the diagnosis of a heart attack for two-thirds of people in hospital emergency departments, researchers say, drastically simplifying the costs and procedures of hospital admissions for acute chest pain.

“Until now there were no quick ways to rule out a heart attack within the emergency department,” said lead author Anoop Shah from the University of Edinburgh. “We have identified a cardiac troponin concentration (less than 5 nanograms per decilitre; <5 ng/L) below which patients are at very low risk of heart attack either during the admission or in the ensuing 30 days.”

In the UK, hospital visits for chest pain stand at around 1 million every year, with guidelines requiring extensive monitoring of any patients who might experience a heart attack. This can take place in long visits to the emergency department, or some patients may be admitted to hospital and receive a bed in a ward.

The majority of those patients, however, never actually end up having a heart attack. Now thanks to this blood test, which can detect far lower levels of troponin in the blood than previous, less-precise tests could register, these patients could be sent home straight away.

The researchers trialled the system on 6,000 patients in hospitals in Scotland and the US and identified that almost two-thirds of patients (61 percent) could have been eligible for a safe early discharge, having presented less than 5 ng/L of troponin in their blood results.

“These patients are therefore potentially suitable for immediate and safe discharge from the emergency department,” said Shah. “These findings could dramatically reduce unnecessary hospital admissions and provide substantial cost savings for healthcare providers.”

Those with a higher level of troponin above 5 ng/L won’t be so lucky, however. Not only would they have to stay in hospital for ongoing monitoring and tests, but research shows that they’re also three times more likely to have a heart attack than patients with lower troponin levels.

While the study is promising, other physicians are cautious of the risks that could come with instant discharges of potentially ill patients on the outcome of a singular blood test, arguing that further research is required before this process can be safely adopted.

“The ultimate validation for the safety and efficacy of discharging patients … will be the report of clinical outcomes after this threshold is implemented in routine clinical practice,” writes a team of physicians from emergency departments in Australia and New Zealand, in a commentary on the study.

“[W]hat further assessment, if any, is needed for those patients identified as low risk and suitable for early discharge? Trials are needed to assess the safety and effectiveness of clinical pathways that involve no further testing for such patients.”

Scientists build a digital piece of a rat’s brain .


Summary:
If you want to learn how something works, one strategy is to take it apart and put it back together again. For 10 years, a global initiative called the Blue Brain Project has been attempting to do this digitally with a section of juvenile rat brain. The project presents a first draft of this reconstruction, which contains over 31,000 neurons, 55 layers of cells, and 207 different neuron subtypes.

This is a photo of a virtual brain slice.

If you want to learn how something works, one strategy is to take it apart and put it back together again. For 10 years, a global initiative called the Blue Brain Project–hosted at the Ecole Polytechnique Federale de Lausanne (EPFL)–has been attempting to do this digitally with a section of juvenile rat brain. The project presents a first draft of this reconstruction, which contains over 31,000 neurons, 55 layers of cells, and 207 different neuron subtypes, on October 8 in Cell.

Heroic efforts are currently being made to define all the different types of neurons in the brain, to measure their electrical firing properties, and to map out the circuits that connect them to one another. These painstaking efforts are giving us a glimpse into the building blocks and logic of brain wiring. However, getting a full, high-resolution picture of all the features and activity of the neurons within a brain region and the circuit-level behaviors of these neurons is a major challenge.

Henry Markram and colleagues have taken an engineering approach to this question by digitally reconstructing a slice of the neocortex, an area of the brain that has benefitted from extensive characterization. Using this wealth of data, they built a virtual brain slice representing the different neuron types present in this region and the key features controlling their firing and, most notably, modeling their connectivity, including nearly 40 million synapses and 2,000 connections between each brain cell type.

“The reconstruction required an enormous number of experiments,” says Markram, of the EPFL. “It paves the way for predicting the location, numbers, and even the amount of ion currents flowing through all 40 million synapses.”

Once the reconstruction was complete, the investigators used powerful supercomputers to simulate the behavior of neurons under different conditions. Remarkably, the researchers found that, by slightly adjusting just one parameter, the level of calcium ions, they could produce broader patterns of circuit-level activity that could not be predicted based on features of the individual neurons. For instance, slow synchronous waves of neuronal activity, which have been observed in the brain during sleep, were triggered in their simulations, suggesting that neural circuits may be able to switch into different “states” that could underlie important behaviors.

“An analogy would be a computer processer that can reconfigure to focus on certain tasks,” Markram says. “The experiments suggest the existence of a spectrum of states, so this raises new types of questions, such as ‘what if you’re stuck in the wrong state?'” For instance, Markram suggests that the findings may open up new avenues for explaining how initiating the fight-or-flight response through the adrenocorticotropic hormone yields tunnel vision and aggression.

The Blue Brain Project researchers plan to continue exploring the state-dependent computational theory while improving the model they’ve built. All of the results to date are now freely available to the scientific community at https://bbp.epfl.ch/nmc-portal.

Ancient human genome from Africa sequenced for first time .


Researchers have mapped the first ancient African genome from a 4,500-year-old Ethiopian and found that a “mysterious” wave of migration back into Africa from Western Eurasia around 3,000 years ago was much larger and more widespread then previously thought.

 The genome was taken from the skull of a man buried face-down 4,500 years ago in a cave called Mota in the highlands of Ethiopia - a cave cool and dry enough to preserve his DNA for thousands of years. File photo for representation

The genome was taken from the skull of a man buried face-down 4,500 years ago in a cave called Mota in the highlands of Ethiopia – a cave cool and dry enough to preserve his DNA for thousands of years.

The ancient genome predates a mysterious migratory event which occurred roughly 3,000 years ago, known as the ‘Eurasian backflow’, when people from regions of Western Eurasia such as the Near East and Anatolia suddenly flooded back into the Horn of Africa.

The genome enabled researchers to run a millennia-spanning genetic comparison and determine that these Western Eurasians were closely related to the Early Neolithic farmers who had brought agriculture to Europe 4,000 years earlier.

By comparing the ancient genome to DNA from modern Africans, the team has been able to show that not only do East African populations today have as much as 25 per cent Eurasian ancestry from this event, but that African populations in all corners of the continent – from the far West to the South – have at least 5 per cent of their genome traceable to the Eurasian migration.

Researchers at the University of Cambridge describe the findings as evidence that the ‘backflow’ event was of far greater size and influence than previously thought.

The massive wave of migration was perhaps equivalent to over a quarter of the then population of the Horn of Africa, which hit the area and then dispersed genetically across the whole continent.

The cause of the West Eurasian migration back into Africa is currently a mystery, with no obvious climatic reasons.

The researchers said it’s clear that the Eurasian migrants were direct descendants of, or a very close population to, the Neolithic farmers that had brought agriculture from the Near East into West Eurasia around 7,000 years ago, and then migrated into the Horn of Africa some 4,000 years later.

The ancient Mota genome allows researchers to jump to before another major African migration: the Bantu expansion, when speakers of an early Bantu language flowed out of West Africa and into central and southern areas around 3,000 years ago.

Researchers said the Bantu expansion may well have helped carry the Eurasian genomes to the continent’s furthest corners.

The genome also helped researchers identify genetic adaptations for living at altitude, and a lack of genes for lactose tolerance – all genetic traits shared by the current populations of the Ethiopian highlands. The findings are published in the journal Science. – See more at: http://m.deccanherald.com/content/505456/ancient-human-genome-africa-sequenced.html/#sthash.3dlkPcq7.dpuf

AIDS pioneer finally brings AIDS vaccine to clinic .


Human trials of more than 100 different AIDS vaccines have taken place since researchers proved in 1984 that HIV caused the disease. Robert Gallo, whose U.S. National Cancer Institute laboratory published the four landmark papers in Science that convinced the world of the link between this recently discovered retrovirus and the growing epidemic, has closely monitored—and often sharply critiqued—the AIDS vaccine search since it began. But Gallo, who now runs the Institute of Human Virology (IHV) in Baltimore, Maryland, has always been a spectator—until today.

Gallo’s team has been developing a vaccine with an unusual method of protection for 15 years and is now launching the first clinical trial of it in collaboration with Profectus BioSciences, a biotech that spun off from IHV recently. Known as a phase I study, the trial expects to enroll 60 people and will simply assess safety and immune responses of the “full-length single chain” vaccine. “It’s a terrible name,” says Gallo, who is not one to mince words.

The vaccine contains a version of HIV’s surface protein, gp120, engineered so that it links to a few portions of a protein called the CD4 receptor. When HIV infects cells, gp120 first binds to the CD4 receptor on white blood cells and then “transitions” in such a way that hidden parts of the virus are exposed, allowing it to bind to a second receptor on the immune cells called CCR5. Once bound to both receptors, HIV can enter the white blood cell and establish an infection. The IHV vaccine aims to generate antibodies that bind to HIV’s gp120 when it’s in this transitional state, ultimately blocking attachment to CCR5, aborting the infection process. The development of the vaccine is being led by IHV’s George Lewis, whose team includes Antonio DeVico and Timothy Fouts.

Gallo, 78, says it has taken a long time to move this vaccine into the clinic because he and his group have done extensive testing in monkeys, faced the typical vaccine challenges of manufacturing a human-grade product, and have had to scramble for funding. “Was anything a lack of courage?” asks Gallo, who frequently asks and answers his own questions. “Sure. We wanted more and more answers before going into people.”

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