Archive for the ‘Fitness’ Category
Then you’re in the same boat as many Americans. This article describes how some have been helped.
The common thought is yes, but there are counterarguments, as Zazie Todd points out in an article in Pacific Standard:
Did you over-indulge during Thanksgiving? Could a dog be the answer? A new meta-analysis by an international team investigates whether dog owners are more physically active than people without dogs.
Contrary to popular belief, not all pet dogs are walked. And it’s possible that dog owners spend time walking their pets at the expense of participating in sports or going to the gym. A 155-pound adult uses 493kcals playing soccer or using a rowing machine at a moderate pace, compared to 211 walking. So the question is whether, on average, people who own dogs get more physical activity than those who don’t.
This is of particular interest to public health specialists who want to know how to leverage your dog to make you more active. The scientists, writing in the Journal of Physical Activity and Health, explain that “considering the large proportion of dog owners, and that many dogs enjoy being walked, dog walking could provide a potentially viable strategy for increasing population levels of physical activity.”
The team, led by the University of Western Australia’sHayley Christian, analyzed 29 research studies conducted between 1990 and 2010, mainly in the United States and Australia. They looked at dog owners and non-dog owners of all ages, from children to seniors.
Their results showed that dog owners . . .
Blog readers have noted the interesting findings recently reported that the gut microbiota of lean and obese mice differ, and when the microbiota of one is transferred to the other, the body goes along, either the lean becoming fat or the fat lean, depending on the direction of the transfer.
I thought I would try that at home to see what happens. I clearly do not have the gut microbiota of a lean person—I am no longer obese, but I am overweight once more.
So how do I achieve a different population of gut microbes? Changing diet is one way, and The Wife and I have gradually dropped meat, fish, and fowl from our diet. Fish is not such a problem, I imagine—we bought wild-caught rather than farmed—but meat and fowl not only change the composition of the but contents, which would encourage some microbes and discourage others, but (worse) meat and fowl in the US contain antibiotics (in general, though if you look you can find antibiotic-free meat, if you trust producers—mostly, I don’t), but now I read that half of China’s antibiotics now go to livestock. Obviously, antibiotics in the food can completely disrupt the microbe population of the gut and send it in new, perhaps unhealthy, directions. [See this article for how antibiotics in meat affect the body.]
So step 1: change the microbe fodder, and that we’ve done by switching to a plant-based diet, along with some eggs and dairy (but not all that much). Step 2 will be to introduce new microbes: ingesting various probiotics.
In the past, I have favored probiotics from dairy sources: yogurt, kefir, aged cheese, and the like. So to introduce a new population, I am eating now lots of sauerkraut, kimchi, and other fermented foods. I figure a couple of servings of those a day will in time result in a different sort of gut microbe population than I have now.
Will is be a lean-inclined population? No idea. But I thought it would be interesting to play around with it and see what happens.
UPDATE: I just realized that this experiment occurred to me just a day or two after posting this. Hah. Free will, is it?
Two recent articles of interest, more or less on the same topic and finding: gut microbes affect weight.
First, in Science News, Meghan Rosen reports on some fat and skinny mice:
Skinniness could be contagious. Gut bacteria from thin people can invade the intestines of mice carrying microbes from obese people. And these invaders can keep mice from getting tubby, researchers report in the Sept. 6 Science.
“It’s very surprising,” says molecular microbiologist Andreas Schwiertz of the University of Giessen in Germany, who was not involved in the work. “It’s like a beneficial infection.”
But the benefits come with a catch. The invading microbes drop in and get to work only when mice eat healthy food. Even fat-blocking bacteria can’t fight a bad diet, suggests study leader Jeffrey Gordon, a microbiologist at Washington University in St. Louis.
In recent years, researchers have collected clues that suggest that gut microbes can tweak people’s metabolism. Fat and thin people have different microbes teeming in their intestines, for example. And normal-weight mice given microbes from obese mice pack on extra fat, says coauthor Vanessa Ridaura, also of Washington University.
These and other hints have led researchers to experiment with fecal transplants to flush out bad gut microbes and dump in good ones. The transplants can clear up diarrhea and may even help some obese people regain insulin sensitivity. But feces can house dangerous microbes as well as friendly ones.
“We want to make therapies that are more standardized — and more appealing,” says gastroenterologist Josbert Keller of the Haga Teaching Hospital in The Hague, Netherlands.
Scientists are trying to pinpoint helpful gut microbes and figure out how diet guides their role in metabolism. Gordon, Ridaura and colleagues transplanted fecal microbes from obese and lean human twins into mice lacking gut bacteria of their own. Within two weeks, mice that received bacteria from obese people started to put on fat. Mice given bacteria from lean people stayed slim.
Next, the researchers wondered if the microbes could travel between animals and stake out new territory. So the team housed together mice carrying microbes from lean people with mice carrying microbes from obese people. “We called it ‘The battle of the microbiota,’” Gordon says.
Microbes from lean people won: The organisms claimed space in the guts of mice carrying microbes from obese people. What’s more, the invaders kept their new hosts from putting on weight.
The findings sparked a question about humans. If microbes from thin people can jump between animals and prevent pudginess, Gordon asks, “Why isn’t there an epidemic of leanness? The answer is . . . “
Next is an intriguing finding that low levels of antibiotics used to fatten meat animals may be wreaking havoc with our gut microbes (that is, those who eat meat). Ari LeVaux reports at AlterNet:
For decades, livestock producers have used low doses of antibiotics to expedite animal growth. The practice, dubbed sub-therapeutic antibiotic therapy (STAT), lowers feed costs while increasing meat production, and nearly 80 percent of the antibiotics used in the United States are for this purpose.
Because STAT can encourage the growth of antibiotic-resistant “superbugs,” it’s banned in many countries, but remains common in the U.S., despite recent public pleas to stop it by two former FDA commissioners . Although STAT has been in use since the 1950s, how it works has long been a mystery. But evidence is mounting that it might be due to antibiotics killing microorganisms that populate animals’ guts.
If so, antibiotics could do the same thing to humans. In support of this idea, a paper published last month in Nature identifies a correlation between diversity of gut microflora and human obesity. A nine-year study, led by S. Dusko Ehrlich of France’s National Institute for Agricultural Research, compared microbiotas—the 100-trillion-member microbial ecosystems that populate the body—of slim and obese people. The team found obese people have lower microbial diversity in their bellies. This is consistent with earlier research in mice, as well as a paper published last year in Journal of Obesitythat found a strong correlation between young children’s exposure to antibiotics and later obesity.
Perhaps more significantly, the team behind the Naturestudy found a correlation between low microbial diversity and heart disease, diabetes and cancer, regardless of weight. “Even lean people who are poor in bacterial species have a higher risk of developing these pathologies,” Ehrlich told NPR. 
Our understanding of human microbiota is in its infancy, but the possible implications of such research are profound. Could our frequent use of antibiotics, both to treat human sickness and to encourage animal growth, be having unintended consequences on our health?
There are strict limits on the amount of antibiotic residues allowed in commercial meat, and according to the USDA’s Food Safety and Inspection Service, violations of these limits are extremely rare. But this could be interpreted in two ways: maybe there isn’t much antibiotic residue in meat, or maybe the legal thresholds are set too high.
Research published last year in the journal of the American Society for Microbiology found that legal amounts of antibiotic residues in cured meats can still be high enough  to kill bacteria sausage manufacturers intentionally apply to their products. Sausage is treated with lactic acid-producing microbes to make it more acidic, which kills dangerous microbes like salmonella and E. coli. The researchers found that while legal levels of antibiotic residues in meat don’t kill the pathogenic microbes, they can kill the acidifying microbes intended to keep the “bad” bugs at bay.
The growing recognition of the importance of gut flora has spawned a probiotics industry valued at $8.7 billion, according to Carl Zimmer at National Geographic’s Phenomena blog. Currently, the retail products of that industry are regulated as food and cosmetics, not as medicine.
Zimmer notes : “It’s possible that the bottle of probiotics you buy in the drug store really will help your digestion, or your immune system, or your bad breath. But it’s also possible that the bacteria you’re buying will get annihilated in the ruthless jungle that is your body. A lot of species you’ll find in probiotic products do not actually belong to the dominant groups of species in the human microbiome. Stop eating them, and they’ll disappear from your body.”
That said, the Nature study did identify eight species of bacteria generally missing from underpopulated guts, and there is talk of putting those in a probiotic. But until such a product is available, there are other promising approaches to managing your microflora.
Another article by Ehrlich’s team, in the same issue of Nature, reports putting overweight people on low-calorie diets quickly increased their gut diversity. Together, the two studies suggest eating less could help enrich your gut flora, which could help you stay lean, in turn reducing your risk of associated diseases.
Another option is to consume microbe-rich fermented foods. In a recent New York Times article about the human microbiota, Michael Pollan wrote that several researchers he’d spoken to had added fermented foods like yogurt, kimchi and sauerkraut to their diets, as well as having cut back on processed foods. “In general they seemed to place less faith in probiotics (which few of them used) than in prebiotics—foods likely to encourage the growth of ‘good bacteria’ already present,” Pollan wrote. 
South Korea, the land of kimchi, has one of the lowest obesity rates  in the developed world. It may be a leap to connect that with richer gut flora, but it’s not inconsistent with the recent Nature papers.
And finally, no discussion of microbiota enrichment would be complete without mention of . . .
UPDATE: Another article, this one in The Scientist.
Obesity turns out to be a more complex phenomenon than anticipated. Chris Palmer reports at The Scientist:
Individuals with fewer numbers of so-called “good” bacteria are more likely to be obese and develop obesity-related ailments such as type 2 diabetes, high cholesterol, and heart disease. That’s according to research conducted by the international MetaHIT consortium published Thursday (August 29) inNature.
The MetaHIT team analyzed the genomes of gut bacteria from 123 non-obese and 169 obese Danish individuals. The resulting quantitative metagenomic analysis revealed stark differences between people with high versus low bacterial diversity. Individuals with more diversity had an average of 580,000 different microbial genes, compared to just 380,000 among the nearly 25 percent of the cohort with reduced diversity. Obesity was more prevalent in the reduced diversity population, as was increased resistance to insulin and higher levels of inflammatory agents and white blood cells.
“We also see that if you belong to the group with less intestinal bacteria and have already developed obesity, you will also gain more weight over a number of years,” Oluf Pederson, a geneticist at the University of Copenhagen, said in a statement. “We don’t know what came first, the chicken or the egg, but one thing is certain: it is a vicious circle that poses a health threat.”
Just six bacterial species appeared to protect against obesity, providing researchers with potential therapeutic targets to fight excessive weight gain.
Wow. Found through this post at Kafeneio—click link for backstory and more information, and by all means watch the short video. Fascinating:
Double wow. Just watched this episode:
An interesting report in Science News by Cristy Gelling:
Repairing a faulty communication line between the gut and the brain can quell the urge to overeat, an experiment that cured chubby mice of their junk food addiction indicates. A similar strategy might be used to treat compulsive eating in people.
Some scientists have proposed that, in both mice and humans, overeating can resemble drug addiction; the more food a person consumes, the less responsive the brain becomes to the pleasure of eating. By restoring normal communication between the gut and brain, researchers were able to resensitize overfed rodents to the pleasures of both fatty and healthy foods.
“The therapeutic implications are huge,” says neuroscientist Paul Kenny of the Scripps Research Institute in Jupiter, Fla., who was not involved in the study.
In the brain, a chemical called dopamine surges in response to pleasurable experiences like eating, sex and taking drugs. But brain-scanning studies suggest that obese individuals have muted dopamine increases in response to food. These changes could lead overeaters to seek more and more food to satisfy their cravings, suggests study leader Ivan de Araujo of Yale University.
De Araujo and his colleagues looked for ways to restore the dopamine response of overfed mice by studying the signals sent by their guts. In previous work, the researchers found that mice get a dopamine rush when fat is introduced directly into the small intestine via catheters. This shows that the gut communicates with the brain’s reward center even when the mouse can’t taste food.
But de Araujo’s team reports in the Aug. 16 Science that mice fed a high-fat diet for 15 weeks don’t experience the normal dopamine surge after an infusion of gut calories. In fact, fat delivered directly to the gut caused dopamine levels in these mice to fall.
The team hypothesized that the disruption in dopamine levels involved a molecule called oleoylethanolamine, which is thought to suppress appetite. In normal mice, eating boosts levels of the molecule in the small intestine. That increase is thought to help animals stop feeding when they are full. But rodents eating a high-fat diet have abnormally low levels of oleoylethanolamine.
The researchers gave the overfed mice injections of oleoylethanolamine and found that . . .
The Scientist also has a note by Ruth Williams on this research:
A chronic high-fat diet is thought to desensitize the brain to the feeling of satisfaction that one normally gets from a meal, causing a person to overeat in order to achieve the same high again. New research published today (August 15) in Science, however, suggests that this desensitization actually begins in the gut itself, where production of a satiety factor, which normally tells the brain to stop eating, becomes dialed down by the repeated intake of high-fat food.
“It’s really fantastic work,” said Paul Kenny, a professor of molecular therapeutics at The Scripps Research Institute in Jupiter, Florida, who was not involved in the study. “It could be a so-called missing link between gut and brain signaling, which has been something of a mystery.”
While pork belly, ice cream, and other high-fat foods produce an endorphin response in the brain when they hit the taste buds, according to Kenny, the gut also sends signals directly to the brain to control our feeding behavior. Indeed, mice nourished via gastric feeding tubes, which bypass the mouth, exhibit a surge in dopamine—a neurotransmitter promoting reinforcement in the brain’s reward circuitry—similar to that experienced by those eating normally.
This dopamine surge occurs in response to . . .
Laudon Aron writes in the New Scientist, reprinted in Slate:
Americans die younger and experience more injury and illness than people in other rich nations, despite spending almost twice as much per person on health care. That was the startlingconclusion of a major report released earlier this year by the U.S. National Research Council and the Institute of Medicine.
It received widespread attention. The New York Times concluded: “It is now shockingly clear that poor health is a much broader and deeper problem than past studies have suggested.”
What it revealed was the extent of the United States’ large and growing “health disadvantage,” which shows up as higher rates of disease and injury from birth to age 75 for men and women, rich and poor, across all races and ethnicities. The comparison countries—Australia, Austria, Canada, Denmark, Finland, France, Germany, Italy, Japan, Norway, Portugal, Spain, Sweden, Switzerland, the Netherlands and the United Kingdom—generally do much better, although the United Kingdom isn’t far behind the United States.
The poorer outcomes in the United States are reflected in measures as varied as infant mortality, the rate of teen pregnancy, traffic fatalities, and heart disease. Even those with health insurance, high incomes, college educations, and healthy lifestyles appear to be sicker than their counterparts in other wealthy countries. The U.S. Council on Foreign Relations, a nonpartisan think tank, described the report as “a catalog of horrors.”
Findings that prompted this reaction include the fact that the rate of premature births in the United States is the highest among the comparison countries and more closely resembles those of sub-Saharan Africa. Premature birth is the most frequent cause of infant death in the United States, and the cost to the health care system is estimated to top $26 billion a year.
As distressing as all this is, much less attention has been given to the obvious question: Why is the United States so unwell? The answer, it turns out, is simple and yet deceptively complex: . . .
Just do 30 seconds of each, at an intensity that is uncomfortable. Explanation (and link to research) here.
Interesting that fat plays in some respects the role of an endocrine gland. Edyta Zielinska reports in The Scientist:
The small protein aP2, thought to only be involved in shuttling lipids throughout fat cells, is actually excreted outside the cell where it acts as a long range signaling molecule or hormone, controlling glucose levels, according to new research published this week (May 7) in Cell Metabolism. The findings suggest a new target for treating obesity-related diabetes.
“It was surprising to find that a critical hormone playing a pathological role in diabetes turned out to be the secreted form of aP2, which for decades has been considered a protein that resides inside the fat cells,” senior author Gökhan Hotamisligil from Harvard School of Public Health said in press release.
The protein aP2 occurs in the blood of obese individuals at much higher levels than in lean individuals, although it is also secreted by fat tissues during times of fasting. To test whether the protein controls glucose retention, the researchers first increased the levels of aP2 in normal mice and saw that the animals were less capable of controlling their glucose levels. When the team performed the reverse experiment, reducing aP2 in obese mice to the levels seen in lean mice using an antibody against the protein, glucose metabolism appeared more similar to that of lean mice.
The group hopes that the antibody could help treat diabetes and have licensed the technology to the biopharmaceutical company Union Chimique Belge in Belgium for development.
I’m very pleased and proud to report that The Youngest Grandson, now aged just over 10 months, very much likes sardines as finger food. Excellent choice: high in protein, calcium, and omega-3, plus very low on the food chain (so no accumulation of toxins—cf. tuna, swordfish, mackerel).
It will take a while, but I’m starting to feel desperate for exercise—that is the state I apparently must reach before doing any. A 45-minute walk on Thursday from here to Lover’s Point seemed good on Thursday. Friday I did a shorter walk—to my ISP to turn in my old modem and buy a new one. Today I set out for Lover’s Point again, but this time the walk took only about 35 minutes: I’ll have to walk a little farther to reach 45 minutes. But it’s a pleasant walk, along the rocky shore.
I have found that it’s surprisingly easy to postpone a walk from day to day, but today—after yesterday’s beautiful day—I was determined to start, so I walked from here to Lover’s Point in Pacific Grove, about a 45-minute round trip. Not bad, and walking along the shore is nice. But now to keep it up.