William Howard Taft (1857-1930), Weight Conscious President
William Howard Taft, the United States’ heaviest president, used a weight-loss program that researchers have found to be startlingly contemporary.
William Howard Taft (September 15, 1857 – March 8, 1930) was the 27th President of the United States (1909-1913) and later the tenth Chief Justice of the United States (1921-1930). He is the only person to have served in both of these offices.
Before becoming President, Taft, a Republican, was appointed to serve on the Superior Court of Cincinnati in 1887. In 1890, Taft was appointed Solicitor General of the United States and in 1891 a judge on the United States Court of Appeals for the Sixth Circuit. In 1900, President William McKinley appointed Taft Governor-General of the Philippines. In 1904, President Theodore Roosevelt appointed Taft Secretary of War in an effort to groom Taft, then his close political ally, into his handpicked presidential successor. Taft assumed a prominent role in problem solving, assuming on some occasions the role of acting Secretary of State, while declining repeated offers from Roosevelt to serve on the Supreme Court.
Riding a wave of popular support for fellow Republican Roosevelt, Taft won an easy victory in his 1908 bid for the presidency. In his only term, Taft’s domestic agenda emphasized trust-busting, civil service reform, strengthening the Interstate Commerce Commission, improving the performance of the postal service, and passage of the Sixteenth Amendment. Abroad, Taft sought to further the economic development of nations in Latin America and Asia through “Dollar Diplomacy”, and showed decisiveness and restraint in response to revolution in Mexico. The task-oriented Taft was oblivious to the political ramifications of his decisions, often alienated his own key constituencies, and was overwhelmingly defeated in his bid for a second term in the presidential election of 1912. In surveys of presidential scholars, Taft is usually ranked near the middle of lists of all American Presidents.
After leaving office, Taft spent his time in academia, arbitration, and the pursuit of world peace through his self-founded League to Enforce Peace. In 1921, after the First World War, President Warren G. Harding appointed Taft Chief Justice of the United States. He served in this capacity until shortly before his death in 1930.
Taft is often remembered as being the most obese president. He was 6 feet 2 inches tall; his weight peaked at 335–340 pounds toward the end of his Presidency. He was definitely a weight conscious person who tried hard to win the battle of the bulge. Evidence from eyewitnesses, and from Taft himself, strongly suggests that during his presidency he had severe obstructive sleep apnea. His chief symptom was somnolence. While President, he fell asleep during conversations, and at the dinner table, and even while standing. He was also strikingly hypertensive, with a systolic blood pressure over 200.
Within a year of leaving the presidency, Taft lost approximately 80 pounds (36 kg). His somnolence problem resolved and, less obviously, his systolic blood pressure dropped 40–50 mmHg (from 210 mmHg). Undoubtedly, this weight loss extended his life. Soon after his weight loss, he had a revival of interest in the outdoors; this led him to explore Alaska. Beginning in 1920, Taft used a cane; this was a gift from Professor of Geology W. S. Foster, and was made of 250,000-year-old petrified wood.
Taft’s 1909 Inauguration
Taft retired as Chief Justice on February 3, 1930, because of ill health. Charles Evans Hughes, whom he had appointed as an Associate Justice while President, succeeded him as Chief Justice. Five weeks following his retirement, Taft died on March 8, 1930, the same date as Associate Justice Edward Terry Sanford’s unexpected death. As it was customary for members of the court to attend the funeral of deceased members, this posed a “logistical nightmare”, necessitating cross-country travel. The house at which Taft died is now the diplomatic mission of the Syrian Arab Republic to the United States. Three days following his death, on March 11, he became the first president to be buried at Arlington National Cemetery. James Earle Fraser sculpted his grave marker out of Stony Creek granite. Taft is one of two presidents buried at Arlington National Cemetery, and is one of four Chief Justices buried there. Taft was the only Chief Justice to have had a state funeral.
1921: Supreme Court Chief Justice, William Howard Taft
William Howard Taft, the only massively obese man ever to be president of the United States, struggled mightily to control his weight a century ago, worrying about his health and image, and endured humiliation from cartoonists who delighted in his corpulent figure. But new research has found that his weight-loss program was startlingly contemporary, and his difficulties keeping the pounds off would be familiar to many Americans today.
On the advice of his doctor, a famed weight-loss guru and author of popular diet books, he went on a low-fat, low-calorie diet. He avoided snacks. He kept a careful diary of what he ate and weighed himself daily. He hired a personal trainer and rode a horse for exercise. And he wrote his doctor, Nathaniel E. Yorke-Davies, with updates on his progress, often twice a week.
In a way, he was ahead of his time. Obesity became a medical issue by the middle of the 20th century, around the time the term “obesity” rather than “corpulence” came into vogue, said Abigail C. Saguy, a sociologist at the University of California, Los Angeles, who specializes in the study of obesity. Taft’s story shows that “at least in some cases, corpulence was already treated as a medical problem early in the century,” she added.
Like many dieters today, Taft, 6 feet 2 inches tall, lost weight and regained it, fluctuating from more than 350 to 255 pounds. He was 48 when he first contacted Dr. Yorke-Davies, and spent the remaining 25 years of his life corresponding with the doctor and consulting other physicians in a quest to control his weight. Taft’s struggles are also recounted by Deborah Levine, a medical historian at Providence College in Rhode Island. She discovered the extensive correspondence between Taft and the diet doctor, including Taft’s diet program, his food diary, and a log of his weight. Her findings were published Monday in The Annals of Internal Medicine.
Obesity – often said to be a product of our sedentary lifestyle and fast foods – has been a concern for over a century. Obesity experts said Taft’s experience highlights how very difficult it is for many fat people to lose substantial amounts of weight and keep it off, and how little progress has been made in finding a combination of foods that lead to permanent weight loss.
“Maybe we are looking for something that doesn’t exist,” said David B. Allison, the director of the Nutrition Obesity Research Center at the University of Alabama at Birmingham. Doctors today would most likely offer Taft weight-loss surgery – which could have a big effect on weight – or drugs, which have a small effect at best. But the diet he was advised to follow would be largely unchanged, Dr. Allison said.
Dr. Levine became interested in Taft’s story when she read old newspaper articles that mentioned he was working with Dr. Yorke-Davies to lose weight. She found their letters in the Library of Congress. Dr. Yorke-Davies was known for creating strict personal diet plans for his patients. In a relationship sustained entirely by mail, he advised Taft to lose at least 60 to 80 pounds. Meals were to be eaten at certain times and meats were to be weighed. Taft was to eat a small portion of lean meat or fish at every meal, cooked vegetables at lunch and dinner (no butter), a plain salad, and stewed or baked fruit (unsweetened). He got a single glass of “unsweetened” wine at lunch. The doctor also allowed his own diet product, gluten biscuits, that were produced to his specifications in London. Taft bought them and had them shipped to the United States.
Taft tried to adhere to the program and also employed a personal trainer, known at the time as “a physical culture man.” By April 1905, six months after he first wrote to the doctor, Taft had lost 60 pounds. But even though people told him he looked good, he was “continuously hungry,” he wrote the doctor. Taft began to gain back the weight and stopped writing to the doctor, who asked Taft’s friends and family what was going on. After learning Taft had regained 19 pounds, he told Taft he needed to return to his diet program or “in another three or four years you will be almost back to your original weight.” By the time Taft was inaugurated as president in 1909, he had indeed regained all he had lost, and more, weighing 354 pounds. He became the butt of jokes, with many relishing a story that he had gotten stuck in a White House bathtub. But Taft never gave up. When he died in 1930, he weighed 280 pounds.
The tale is strikingly modern, obesity experts said. The self-monitoring – weighing himself daily, keeping a food diary – are “the fundamental tenets of changing behavior,” said Dr. Kimberly Gudzune, an obesity researcher at Johns Hopkins. “Keep yourself accountable.” In some ways Taft got the sort of medical care doctors today wish they could provide. He was in constant touch with his doctor over a period of many years. “That is really a model we try to strive for today,” Dr. Gudzune said. She sees her patients once a month, a frequency that, for most primary care doctors, “is almost unheard-of.” She and others were also struck by Taft’s persistent hunger pangs.
Dr. Jules Hirsch, an obesity researcher at Rockefeller University, said losing a substantial amount of weight and keeping it off amounts to telling the body it is starving. He saw this in his own pioneering studies decades ago. Fat people agreed to live in a hospital ward while they dieted to a normal weight. But they were ravenous and almost every one of them eventually succumbed to intense hunger and regained the weight that was so painfully lost. “One of the most important drives we have is to prevent starvation,” Dr. Hirsch said.
Sources: The New York Times, Wikipedia
Brain May Flush Out Toxins During Sleep
According to a recent study published online in Science (18 October 2013), a good night’s rest may literally clear the mind. Using mice, the study showed for the first time that the space between brain cells may increase during sleep, allowing the brain to flush out toxins that build up during waking hours. These results suggest a new role for sleep in health and disease.
For centuries, scientists and philosophers have wondered why people sleep and how it affects the brain. Only recently have scientists shown that sleep is important for storing memories. In the present study, it was serendipitously found that sleep may be also be the period when the brain cleanses itself of toxic molecules. During sleep, a plumbing system called the glymphatic system may open, letting fluid flow rapidly through the brain. The glymphatic system also helps control the flow of cerebrospinal fluid (CSF), a clear liquid surrounding the brain and spinal cord.
Initially the authors studied the system by injecting dye into the CSF of mice and watching it flow through their brains while simultaneously monitoring electrical brain activity. The dye flowed rapidly when the mice were unconscious, either asleep or anesthetized. In contrast, the dye barely flowed when the same mice were awake. According to the authors, they were surprised by how little flow there was into the brain when the mice were awake, and it suggested that the space between brain cells changed greatly between conscious and unconscious states.”
To test this hypothesis, the authors inserted electrodes into the brain to directly measure the space between brain cells. They found that the space inside the brains increased by 60% when the mice were asleep or anesthetized.
Certain brain cells, called glia, control flow through the glymphatic system by shrinking or swelling. Noradrenaline is an arousing hormone that is also known to control cell volume. Similar to using anesthesia, treating awake mice with drugs that block noradrenaline induced unconsciousness and increased brain fluid flow and the space between cells, further supporting the link between the glymphatic system and consciousness.
Previous studies suggest that toxic molecules involved in neurodegenerative disorders accumulate in the space between brain cells. In this study, the researchers tested whether the glymphatic system controls this by injecting mice with labeled beta-amyloid, a protein associated with Alzheimer’s disease, and measuring how long it lasted in their brains when they were asleep or awake. Beta-amyloid disappeared faster in mice brains when the mice were asleep, suggesting sleep normally clears toxic molecules from the brain.
NINDS is the nation’s leading funder of research on the brain and nervous system and its mission is to reduce the burden of neurological disease – a burden borne by every age group, by every segment of society, by people all over the world.
Tanning Gene Linked to Increased Risk of Testicular Cancer
The p53 stimulates skin tanning when ultraviolet light activates it in the skin. It then must bind a specific sequence of DNA located in a gene called the KIT ligand oncogene (KITLG), which stimulates melanocyte production, causing the skin to tan.
According to an article published online in the journal Cell (10 October 2013), the p53 gene has been linked to higher risk for testicular cancer in white men. Nearly 80% of white men carry a variant form of this gene, which increased risk of testicular cancer up to threefold in the study.
To conduct the analysis, a data mining expedition was performed to sieve through many different data sets. The team selected possible leads from the intersection of more than 20,000 p53 binding sites in the human genome, 10 million inherited genetic variations genotyped in the 1000 Genomes Project, and 62,000 genetic variations associated with human cancers identified in genome-wide association studies (GWAS). These data sets were gathered through joint efforts of thousands of researchers from around the world.
According to the authors, in the end, one variant in the p53 pathway was strongly associated with testicular cancer, but also, surprisingly, displayed a positive benefit that is probably related to tanning that has occurred as humans evolved.
White males with a single nucleotide variation in KITLG, called the G allele, have the highest odds of having testicular cancer. In fact, the twofold to threefold increased risk is one of the highest and most significant among all cancer GWAS conducted within the past few years. The high frequency of this allele in light skin individuals may explain why testicular cancer is so much more frequent in people of European descent than those of African descent.”
According to the authors, although the G allele increases testicular cancer risk, it may explain why testicular tumors are often easily cured with chemotherapy. The reason is that most other tumors have a mutant p53, but in these testicular cell tumors, the p53 is functioning properly, and the drugs used for testicular cancer appear to work in concert with p53’s tumor suppression function to kill the cancer cells.
TARGET HEALTH excels in Regulatory Affairs. Each week we highlight new information in this challenging area
FDA Approves Opsumit to Treat Pulmonary Arterial Hypertension
Pulmonary arterial hypertension (PAH) is a chronic, progressive and debilitating disease that can lead to death or the need for lung transplantation. In PAH, high blood pressure that occurs in the arteries that connect the heart to the lungs which causes the right side of the heart to work harder than normal. Sequelae of PAH include limitations on exercise ability and shortness of breath.
The FDA has approved Opsumit (macitentan), a new drug to treat adults with PAH. Opsumit belongs to a class of drugs called endothelin receptor blockers, which act to relax the pulmonary arteries, decreasing blood pressure in the lungs.
Opsumit’s safety and effectiveness were established in a long-term clinical trial where 742 participants were randomly assigned to take Opsumit or placebo. The average treatment duration was about two years. In the study, Opsumit was effective in delaying disease progression, a finding that included a decline in exercise ability, worsening symptoms of PAH or need for additional PAH medication.
Similar to other members of its drug class, Opsumit carries a Boxed Warning alerting patients and health care professionals that the drug should not be used in pregnant women because it can harm the developing fetus. Female patients can receive the drug only through the Opsumit Risk Evaluation and Mitigation Strategy (REMS) Program. This restricted-distribution program requires prescribers to be certified by enrolling in the program; all female patients to be enrolled in the program and comply with applicable pregnancy testing and contraception requirements before initiating treatment; and pharmacies to be certified and to dispense Opsumit only to patients who are authorized to receive it.
Common side effects observed in those treated with Opsumit include low red blood cell count (anemia), common cold-like symptoms (nasopharyngitis), sore throat, bronchitis, headache, flu and urinary tract infection.
Opsumit is marketed by San Francisco-based Actelion Pharmaceuticals US, Inc.
Easy Shrimp Salad, Appetizer, Dip or Spread
Shrimp pureed as a dip, as filling, or wonderful spread on toast or crackers
One 8-ounce container tofutti (soybean cream cheese)
Pinch black pepper, (grind to your taste)
Pinch salt (optional)
2 garlic cloves, juiced
1 teaspoon lemon zest
1 Tablespoon sherry (optional)
1/2 cup extra virgin olive oil (best olive oil)
1 teaspoon agar
2 Tablespoons chopped onion
1.5 to 2 lbs. shrimp, shelled, deveined, and cooked
Parsley, chopped for garnish only
Add all ingredients except shrimp to a large food processor. Process until well mixed. Drop in shrimp and process until either pureed or chopped to desired consistency. This recipe can be pureed to the consistency of butter or left with chunky pieces of shrimp. Garnish with a few little flakes of chopped parsley. Serve on crackers as an appetizer or on baguettes or on circles of cucumber, or fill pieces of celery (from celery hearts) with the shrimp butter. You could also make pumpernickel circles with a cookie cutter, and top with this dip.
Or consider filling tomatoes with the shrimp salad. This past Tuesday we had the dip, with small quarter pieces of toast, as an appetizer. Delicious!
As the photo below shows, this past Wednesday, I bought 2 large ugli tomatoes (or 2 large beefsteak tomatoes). Wash the tomatoes well, and then scoop out the insides of the tomatoes and fill them with the shrimp mixture (save the tomato for marinara sauce or soup). Make a salad plate for each shrimp/tomato and serve them on one lettuce leaf (romaine lettuce), along with quartered Italian bread, which I toasted, (in oven) with one quick swipe of a pastry brush dipped in our best extra virgin oil. Chop fresh parsley for garnish. We each had one tomato filled, as a beginning salad course.
Today, Friday, I bought these 4 peppers, just because I loved the colors, and thought they might make another nice salad presentation for tonight. Below, are these same peppers, filled with the shrimp salad, for another salad course. I simply washed them well, sliced the tops off, scooped out the insides, and stuck them in a preheated 400 degree oven, for about 5 to 10 minutes, just to get the skins a little softer. Keep your eye on the oven and check the peppers after 5 minutes to be sure they don’t burn. And, btw, even if they did burn a little, this might be just fine. Some people like peppers well done.
I removed the peppers from the oven, let them cool for 30+ minutes, then stuffed them with the shrimp salad. If you wanted smaller servings, do the following: just before putting in oven, cut each pepper in half. Roast for 30+ minutes, remove, cool and fill each pepper section with the shrimp salad. Arrange each section on a plate with a lettuce leaf and crackers. Garnish with chopped parsley.
We will probably share one pepper, because I also made a chicken-with-grapes-and- cashews dish. We’ll have a chilled New York State (North Fork) sauvignon blanc, that we discovered last night (Thursday) at “Rouge Tomate” 10 East 60th Street, last night with our friend and colleague, from Europe.
Have a wonderful weekend and until the next ON TARGET newsletter. Hope you enjoy doing this quick and easy shrimp recipe.
A bottle of sparkling Prosecco, to have as an aperitivo.
Researchers have developed a new kind of genetic engineering that may be safer, with the power to make never-before-seen types of protein.
On a genetic level, all of life on Earth speaks the same language. We’ve all got DNA and/or its close cousin, RNA. All of our genetic material is composed of the same batch of basic nucleotides, which are often called by the first letters of their full names—A, C, G and T for DNA; A, C, G and U for RNA. All cells on Earth even read those letters in much the same way, so cells from different species are often able to read each other’s DNA. That’s how pharmaceutical companies are able to put the human gene for insulin into bacteria and yeast to produce insulin medicine for diabetics. Want see a gross example? Early in the history of genetics, some biologists put the human gene for eyes onto a fruit fly’s leg… and the fruit fly’s cells made a fruit fly eye.
Now, however, a team of scientists from several U.S. universities has found a way to make small, but fundamental changes within that cellular language. It’s an entirely different kind of genetic engineering than scientists have ever done before.
“For the first time, we’ve created an organism with new or alternate code,” Farren Isaacs, a Yale University biologist and one of the lead scientists in the research, tells Popular Science.
“It’s like writing a new operating system,” says Danielle Tullman-Ercek, a bioengineer at the University of California, Berkeley, who was not involved in the research. In contrast, she compared previous genetic engineering to “adding a new piece of software.”
In traditional genetic engineering, scientists put entire genes — coherent strands of hundreds of nucleotides — into cells. Often they don’t mess with the cell’s own original genes at all. In contrast, Isaacs and his team made small, specific changes in E. coli‘s own native DNA.
This new kind of genetic engineering could help solve two major problems in the field. It could make bacteria more resilient against infections, which is great for companies churning out vats of engineered bacteria. That includes companies that try to grow bacteria engineered to make biofuels, or to gobble up pollution. (Yes, bacteria get infections, too!)
It could also make engineered stretches of DNA impossible for other cells to read, mitigating worries that engineered genes could escape into the environment and into wild organisms. This is no small concern: Just this August, a team of biologists showed genetically modified rice is able to transfer its modified genes to nearby weeds.
A new kind of GMO: the GRO
Isaacs and his team have coined a new term for their genetic code rewriting. They call it “recoding” and its results “genetically recoded organisms,” or GROs, which Isaacs says is a subset of genetically modified organisms, or GMOs.
The changes Isaacs and his colleagues made don’t seem like much, if you count them up. The scientists changed 321 individual nucleotides in the E. coli genome, which has about 4.5 million nucleotides. They also removed the cell’s ability to make one particular protein.
Nevertheless, in a series of experiments, Isaacs’ team showed these small changes allow the E. coli to do two major new things.
In one experiment, the team gave their GRO E. coli two types of viruses. Viruses normally hijack a cell’s machinery to reproduce themselves. However, the GRO E. coli‘s machinery was so different, one of the viruses had trouble infecting the bacteria. The other virus infected the E. colinormally. Further re-coding to the E. coli genome should make the bacteria more unreadable—and therefore more resistant—to more types of viruses, says Julius Lucks, a Cornell University bioengineer who was not part of Isaacs’ team.
In another experiment, Isaacs and his colleagues added machinery to the E. coli to get it to make proteins with components that don’t exist in nature. Normally, proteins in living things are composed of different combinations of the 20 natural amino acids. Scientists have worked for years to create unnatural amino acids, or NSAAs (non-standard amino acids). They’ve gotten cells to make proteins with artificial amino acids, but it’s an inefficient process. Isaacs and his colleagues got their E. coli to churn out a 21st amino acid efficiently and effectively. The changes they made to the E. coli‘s DNA happened to remove one of the natural processes that previously interfered with the production of unnatural amino acids.
Unnatural amino acids are useful because they allow scientists to create proteins with entirely new functions. The proteins can then go into medicines or industrial chemical reactions. Isaacs gave an example of one company, Ambrx, that makes medicines with artificial amino acids.
In addition, because the coding for the 21st amino acid is in this altered genetic language, other cells shouldn’t be able to read it. That reduces the possibility that wild bacteria or plants could pick up the gene for the 21st amino acid and start producing it on their own. “You can imagine that that’s effectively a safe GMO,” Isaacs says. Isaacs and his team did not test this aspect of their GRO, but other bioengineers Popular Science talked with say it would be nearly impossible for a non-GRO to exchange genes with a GRO.
Although numerically, the changes in GROs are few, Lucks calls GROs “a huge breakthrough conceptually.” “It really opens the door for the complete rethinking of the genetic code,” he says.
Isaacs and his colleagues published their work today in the journal Science.
A new study argues that climate oscillations in East Africa resulted in human migration and adaptation.
Rift Valley, Ethiopia
Millions of years ago, slow changes in the Earth’s orbit changed the climate in East Africa dramatically. Every 20,000 years ago, the region vacillated between very dry and very wet periods. These extreme changes may have played a vital role in driving human evolution, according to what’s called the pulsed climate variability hypothesis.
A new paper from the researcher who first introduced the idea in 2009, University College London geography professor Mark Maslin, links periods of change in the East African Rift Valley—namely the increase in freshwater lakes—with evidence of human evolution. “It seems modern humans were born from climate change,” Maslin explained in a press statement, “as they had to deal with rapid switching from famine to feast—and back again.” This, he says, was what drove the evolution of new species with bigger brains, and later forced them to migrate out of East Africa, moving down toward South Africa and north to Europe and Asia.
Along with University of Manchester research fellow Susanne Shultz, Maslin compared all lakes known to have existed in the East Africa Rift System over the last 5 million years with climate records and records of human evolution. Major events in human history, including when humans first started to migrate out of East Africa, happened during wetter periods. Around 1.9 million years ago, for example, when a number of deep freshwater lakes appeared, early Homo erectus arrived on the scene, at the same time as quite a few new species. The researchers believe the new species developed as a direct result of the changing ecology in the region.
Maslin says “the climate of East Africa seems to go through extreme oscillations from having huge deep freshwater lakes surrounded by rich lush vegetation to extremely arid conditions—like today—with sand dunes in the floor of the Rift Valley.” More water would have forced early humans to migrate by increasing the availability of food and water (and tributaries to follow as they travelled) while decreasing the amount of space in the valley they could inhabit.
Lake Tanganyika From Space, 1985
“The occurrence of deep freshwater lakes would have forced expanding hominin populations both northwards and southwards,” the researchers write, generating “a pumping effect pushing them out of East Africa.” In other periods, the lakes would dry up, forcing them to adapt to survive, which may have helped them evolve to be more flexible. This could be linked to other changes in hominin populations, such as bigger brains, increased use of throwing projectiles, and changes in social behavior:
The link between bigger brains and the changing environment is a little more tenuous. Homo erectus represented an 80 percent increase in brain size over previous species, at the same time that there was the greatest amount of water covering the region—potentially one huge lake covering something near 1,000 miles of territory. But other periods of brain expansion occurred during very dry periods, suggesting that brain size increases were driven by aridity.
However, the researchers allow that their hypothesis may not capture the whole of human evolution:
The study appears today in PLOS ONE.
An anti-dopamine drug could block the addictive rush associated with THC.
Researchers from the National Institute on Drug Abuse and the University of Massachusetts Medical School have found a way to block the dopamine rush associated with THC, the main psychoactive chemical in marijuana, in order to reduce pot use among people with a psychological dependence on the drug. Though the risk of dependence is relatively low compared to other drugs, for those people who do seek help for an out-of-control pot habit, there’s no current medical cure available.
THC is one of the ingredients that makes marijuana fun for the brain. According to some modelsof how cannabis works in the brain—though other studies have disputed this—THC stimulates the dopamine neurons in the brain’s ventral segmental area (VTA), which then increases the amount of dopamine released in the shell of the nucleus accumbens, a region of the brain associated with reward. So if you alter that process so the dopamine rush doesn’t arrive, pot isn’t so fun anymore, these researchers hypothesized.
Giving rats and squirrel monkeys a drug called Ro 61-8048, which increases the levels of kynurenic acid (KYNA) in the brain and in turn reduces dopamine levels, seems to have reduced the rewarding aspect of both THC and a synthetic variant of the cannabinoid. The rats stopped pushing their levers to self-administer the synthetic cannabinoid. In monkeys trained to self-administer food and cocaine as well as THC, the drug kept them from pushing the THC lever. It also reduced THC-seeking behavior when abstinent, formerly-dependent rats and monkeys were re-introduced to the drug. The researchers hypothesize that this is because the increase in KYNA blocked THC-induced dopamine elevation in the shell of the nucleus accumbens. The brain may not have been getting the same reward, so the animals stopped wanting THC.
The Substance Abuse and Mental Health Services Administration reports that more than a million people seek treatment for their marijuana habit every year in the U.S., more than the number of people that seek treatment for any other drug except alcohol. Pro-marijuana policy groups point out that many people opt to seek treatment as a condition of their arrest for marijuana use, which doesn’t necessarily mean they were addicted, just that they didn’t want to go to jail, so the number of people who actually suffer from marijuana dependence may be a bit lower.
Whether or not Ro 61-8048 would be a safe drug to give to humans, in any case, remains questionable. As the paper points out, high levels of KYNA have been associated with cognitive deficits in some studies. So much more research will be necessary.
The study appears in Nature Neuroscience.
Happy Colobus Day, an infinitely superior replacement for Columbus Day!
The colobi are a group of Old World monkeys (meaning, from Africa or Asia) that are widespread throughout Africa. They are better than Christopher Columbus for the following reasons.
1. Amazing Jumpers
The various species of colobus monkey–there are about five distinct species, some with subspecies–are probably the most arboreal of all African monkeys. They live in rainforests and cloud forests, and can leap absurdly long distances. It’s not uncommon to see colobus monkeys leaping 20 feet from tree to tree. These aren’t big monkeys; that’s the equivalent of a weak bad-jumping human leaping about 50 feet from a standstill. I could not find any documentation of Christopher Columbus’s jumping ability, which indicates to me that he was not as good a jumper as a colobus monkey.
2. Great Tails
Colobus monkeys have very long tails with delightful poofs at the end of them. The best-known colobus monkey, the mantled guereza (also called the Abyssinian black-and-white colobus), has an enormous poof, sometimes taking up most of the length of the tail, like a big white bottlebrush. The mantled guereza uses the tail, we think, for balance as it jumps back and forth amongst the trees.
Christopher Columbus was tailless, like the rest of his species.
3. Super Stylish
Colobus monkeys have cool beards; the mantled guereza has a dignified and well-trimmed white beard that contrasts beautifully with its black undercoat, bright white tail, and long white western-inspired fringes. The western red colobus has great bushy mutton-chops and a calico-patterned coat of bright rust, white, and black. Christopher Columbus, on the other hand, wears unflatteringly baggy pilgrim-nun clothes and has no beard.
4. Sustainable Diets
Colobus monkeys are almost exclusively leaf-eaters, filling an important niche in the tops of the African forest. Most dense forests have lots of leaves and fruits that are poisonous or indigestible to most animals; think of the eucalyptus of Australia or the bamboo forests of China. The colobus monkeys eat this abundant food, and are able to digest it thanks to gut bacteria that ferments and breaks down the plant product. This is unusual for a primate; gut bacteria of this sort is more often associated with ruminants like cows. But there are no cows in the upper rainforest! And colobi are important seed dispersal vectors in their habitat.
Christopher Columbus mostly ate pickled and preserved meat and fish and bread products. His voyage also included livestock, beginning a legacy that would lead to the extermination of many native animals in the New World through predation or overcompetition for resources.
5. Overcoming Adversity
Colobus monkeys have very small stumps instead of thumbs, unique among primates. The name comes from the Greek word kolobós, meaning, variously, “mangled” or “docked” and referring to the lack of thumb. The evolutionary theory is that the thumb was irrelevant to the semi-brachiation mode of transport (swinging through trees) that the colobus uses; if you look at the king of brachiation, the gibbon, you can see that its thumb is very far from its fingers and its mostly irrelevant for moving around. The colobus uses its fingers like a hook to grab onto and swing from branches.
Nobody seems to have liked Columbus very much. I guess he “overcame adversity” by getting a day named after him despite a dubious humanitarian record. Not good enough, Chris. You have been bested by a monkey.