Kevin Tracey, a neurosurgeon based in New York, is a man haunted by personal events – a man with a mission. “My mother died from a brain tumor when I was five years old. It was very sudden and unexpected,” he says. “And I learned from that experience that the brain – nerves – are responsible for health.”
This background made him a neurosurgeon who thinks a lot about inflammation. He believes it was this perspective that enabled him to interpret the results of an accidental experiment in a new way.
In the late 1990s, Tracey was experimenting with a rat’s brain. “We’d injected an anti-inflammatory drug into the brain because we were studying the beneficial effect of blocking inflammation during a stroke,” he recalls. “We were surprised to find that when the drug was present in the brain, it also blocked inflammation in the spleen and in other organs in the rest of the body. Yet the amount of drug we’d injected was far too small to have got into the bloodstream and traveled to the rest of the body.”
After months puzzling over this, he finally hit upon the idea that the brain might be using the nervous system – specifically the vagus nerve – to tell the spleen to switch off inflammation everywhere.
It was an extraordinary idea – if Tracey was right, inflammation in body tissues was being directly regulated by the brain. Communication between the immune system’s specialist cells in our organs and bloodstream and the electrical connections of the nervous system had been considered impossible. Now Tracey was apparently discovering that the two systems were intricately linked.
The first critical test of this exciting hypothesis was to cut the vagus nerve. When Tracey and his team did, injecting the anti-inflammatory drug into the brain no longer had an effect on the rest of the body. The second test was to stimulate the nerve without any drug in the system. “Because the vagus nerve, like all nerves, communicates information through electrical signals, it meant that we should be able to replicate the experiment by putting a nerve stimulator on the vagus nerve in the brainstem to block inflammation in the spleen,” he explains. “That’s what we did and that was the breakthrough experiment.”
Let’s wallow in semen a little while longer, shall we? We have already seen that, even in humans, there is more to this substance than meets the eye. It contains proteins that, when mixed together, can forge a mating plug. It also contains sugars as sperm fuel, proteins that protect the sperm cells from the acidic vaginal environment, zinc that keeps the sperm’s DNA in good shape, and chemical compounds that prevent the sperm cells from becoming overenthusiastic prematurely.
But this list of ingredients is just the tip of the iceberg. Human ejaculates are home to hundreds of different proteins (which in certain women cause a kind of “sperm hay fever,” an allergic reaction to semen). And those are not trace amounts either; most of them occur in considerable concentrations, so they must be doing something important—we just don’t know what. Even in the ejaculate of the lowly banana fly Drosophila melanogaster, researchers have identified no fewer than 133 different kinds of proteins. One hundred and thirty-three! And this excludes the many proteins that are in the sperm cells themselves. These 133 are all produced by the banana fly version of the prostate, which releases them into the liquid portion of the semen.
For most of the common cancers, a major cause has been identified: smoking causes 90% of lung cancer worldwide, hepatitis viruses cause most liver cancer, H pylori bacteria causes stomach cancer, human papillomavirus causes almost all cases of cervical cancer, colon cancer is largely explained by physical activity, diet and family history.
But for breast cancer, there is no smoking gun. It is almost unique among the common cancers of the world in that there is not a known major cause; there is no consensus among experts that proof of a major cause has been identified.
Yet, breast cancer is the most common form of cancer in women worldwide. The risk is not equally distributed around the globe, though. Women in North America and Northern Europe have long had five times the risk of women in Africa and Asia, though recently risk has been increasing fast in Africa and Asia for unknown reasons.
Exposure to high levels of ionizing radiation is extremely bad for human health. Witness the effects of acute radiation sickness suffered by early scientists studying radioactive elements, or by survivors of atomic bomb blasts. Witness the complex procedures through which doctors must shield cancer patients from radiation therapy, and the long-term complications of adult survivors of cancer who were treated with earlier technology. In light of all this, it’s clear that high doses of ionizing radiation are dangerous.
But the science is less clear when it comes to low dose radiation (LDR). Medical science, the nuclear industry, and government regulatory agencies generally take a play-it-safe approach when considering LDR. In recent years, however, an increasing number of researchers (though still firmly in the minority) have questioned the assumption that all radiation is bad – and have begun studying whether low doses might in fact aid in genetic repair, prevent tissue damage, and other benefits.
One day in October 2010, at a school in the Gaibandha district of northwest Bangladesh, a pupil noticed that the label on a packet of crackers she was eating had darkened. Fearing the crackers were contaminated – “the devil’s deed”, as she put it – she almost immediately fell ill, complaining of heartburn, headache and severe abdominal pain.
The condition quickly spread among her fellow pupils, and later to other schools in the area. Yet toxicologists could trace no contaminant, and all those affected were quickly discharged from the hospital after doctors found no trace of illness. The following week, investigators diagnosed “mass sociogenic illness,” otherwise known as mass hysteria. The children, it seemed, had developed their symptoms simply because they had seen their classmates succumb.
Mass hysteria is thought to be an extreme example of a phenomenon that affects us all day-to-day: emotional contagion. Short of living in hermitic isolation, it is hard to escape it; we are vulnerable to the moods and behaviors of others to an extraordinary degree.
Emotional contagion caused the failure of successive banks at the start of the Great Depression in the 1930s, when investors suffered a collective loss of faith in the ability of these institutions to pay out. It is the force behind fuel crises, health scares and the spread of public grief (for example in Britain after the death of Princess Diana in August 1997). It is the reason why you are more likely to be obese if you have obese friends, and depressed if you are living with a depressed roommate.
But emotional contagion is not all bad – far from it. The mechanism behind it – our tendency to mimic each other’s expressions and behaviors – is crucial to social interaction. Without it, anything beyond superficial communication would be impossible.
Human genetic engineering is not new; it has been going on for a long, long time — naturally. Ancient viruses are really good at inserting themselves and modifying human gene code. Over millennia, constant infections would come to mean that 8 percent of the entire human genome is made up of inserted virus code. All this gene recoding of our bodies occurred under Darwin’s rules, natural selection and random mutation. But nonrandom, deliberate human genetic engineering is new, and it is a big deal.
As of 1990, increasingly genetically modified humans walk among us. More and more gene therapies carry new instructions into our bodies and place them in the right spots; in so doing, they modify our most fundamental selves, our core, heretofore slow-evolving DNA. We are still in the very early stages of effectively hijacking viruses for human-driven purposes; just a few years ago it took a long time to identify and isolate a single faulty gene and figure out what was wrong, never mind finding a way to replace it with a properly functioning alternative. Early gene therapy focused on obscure, deadly orphan diseases like ADA-SCID (the immune disease that “Bubble Boy” had), adrenoleukodystrophy (say that five times fast), Wiskott-Aldrich syndrome, various leukemias, and hemophilia.
In theory the technique is relatively simple: Take a neutered virus, one that is engineered to not harm you but that readily infects human cells to ferry in new DNA instructions, write a new set of genetic instructions into the virus, and let it loose to infect a patient’s cells. And ta‑da! You have a genetically modified human. (Think of this as deliberately sneezing on someone but instead of giving them a cold, you give them a benign infection that enters their body, recodes their cells, and fixes a faulty gene.)
You might have heard that men are wimps when it comes to pain. It can make for lighthearted argument, but in fact it’s not true. Women have a lower pain threshold. Take a man and a woman, put a piece of ice on the backs of their hands, and wait. The woman will almost certainly complain about the pain first.
Not all pain is equal, but women are definitely worse off. In some quite macabre experiments, researchers have shown that women are much more sensitive to electric shocks, muscle pain, hot and cold, and chemical pain, such as the discomfort of eating a vindaloo curry.
If this comes as a surprise to you, you’re not alone. According to surveys, two-thirds of women still think that men feel more pain than they do. (Men are far less convinced of that; only one third think they are worse off when it comes to pain.)
And this isn’t some half-witted attempt to make out that men are the stronger sex. It’s a serious call to the medical system to improve the way they treat women’s pain.
Last fall as the Ebola epidemic continued unabated, experts started discussing something that had never before been bandied about: the idea of Ebola becoming endemic in parts of West Africa. Endemic diseases, like malaria and Lassa fever in that region of Africa, are constant presences. Instead of surfacing periodically, as it always has before now, Ebola in an endemic form would persist in the human population, at low levels of transmission, indefinitely.
The debate was stoked by a paper written by the World Health Organization (WHO) Ebola Response Team and published in October in the New England Journal of Medicine. The sentence that grabbed the world’s attention was saved till near the very end: “For the medium term, at least, we must therefore face the possibility that EVD [Ebola virus] will become endemic among the human population of West Africa, a prospect that has never previously been contemplated.”
What would it mean exactly for Ebola to become endemic, and how would it change things?
This article was originally published on The Conversation.
Food labels seem to provide all the information a thoughtful consumer needs, so counting calories should be simple. But things get tricky because food labels tell only half the story.
A calorie is a measure of usable energy. Food labels say how many calories a food contains. But what they don’t say is that how many calories you actually get out of your food depends on how highly processed it is.
Food-processing includes cooking, blending and mashing, or using refined instead of unrefined flour. It can be done by the food industry before you buy, or in your home when you prepare a meal. Its effects can be big. If you eat your food raw, you will tend to lose weight. If you eat the same food cooked, you will tend to gain weight. Same calories, different outcome.
For our ancestors, it could have meant the difference between life and death. Hundreds of thousands of years ago, when early humans learned to cook they were able to access more energy in whatever they ate. The extra energy allowed them to develop big brains, have babies faster and travel more efficiently. Without cooking, we would not be human.
While developing drugs to cure Ebola is crucial to end the current epidemic, a vaccine that prevents the infection altogether is the end-game for viral outbreaks – a way to protect healthcare workers on the front lines and to prevent future outbreaks.
It typically takes 10 or 20 years to develop and test a vaccine and get it to market. But in Ebola’s case, this time frame has been compressed into a matter of months, bringing pharmaceutical companies, scientists and regulators into uncharted territory, striving for a vaccine to curb the still-escalating epidemic without compromising safety.
“Never before has there been a push to develop a vaccine for an emerging public health threat in this short a time frame,” said Dr. Mark Feinberg, vice president and chief public health and science officer of the drug company Merck’s vaccine division.
Dr. Ripley Ballou, head of Ebola vaccine research for GlaxoSmithKline, concurs. “I’ve been doing this kind of work for 30 years, and this is the first time I’ve encountered anything with the compressed timeline and sense of urgency,” he said.