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Barista milk—who knew?

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Rohini Chaki writes in Gastro Obscura:

IF THE HEART ON YOUR cappuccino foam looks extra-twirly, you might consider inquiring whether your favorite caffeine purveyor is using the newest tool in the coffee kit: barista milk. Specifically formulated for coffee shops, barista milk’s higher protein content helps create a more stable foam for latte art, and its creamy richness boosts the flavor of the roasted bean. For a global dairy industry that has seen dropping demand for conventional, liquid milk, this is a promising development.

“I think the specialty coffee industry has really upped the ante with the beans and roasting, and so the milk had to follow,” says Joanna Heart, an owner and barista at The Palm Coffee Bar in Burbank, California. “You’re working with this beautiful bean, it’s fair trade, it’s organic, and you’re putting all this effort into it, and then you’re just dumping whatever milk in it? I think baristas began to realize that milk is also something to be researched and played with as an artist.”

Don’t expect to find this milk for use at home. For now, barista milk, which is priced between 30 to 60 percent higher than conventional dairy milk, is exclusively sold to culinary professionals.

“Barista milk is crucial because of the way it behaves in tandem with good, flavorsome coffee to create an overall balance in the drink,” says Joe Towers, who handles the marketing and public relations for Brades Farm, his family’s dairy in Lancaster, England.

Barista milk is rich in . . .

Continue reading.

Written by LeisureGuy

9 February 2019 at 12:32 pm

We’ve just had a lot of snow, so I’m using it as an excuse to have pork belly

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Really, a stupendous amount of snow, compared to what we got in Pacific Grove (none). But perhaps 10cm accumulated, and I have a leftover piece of pork belly I got from Farm & Field. They braise it (this time in “Saigon sauce”), so you just have to heat it up. I put it on a piece of parchment paper in my little carbon-steel skillet and leave it in a 300ºF for an hour or a little more (fairly big cuts, this time). I’ll add photo if I think of it.

Written by LeisureGuy

8 February 2019 at 4:27 pm

Posted in Food, Low carb, Recipes

A typical breakfast for me

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I use my 2-qt All Clad Stainless sauté pan because it has vertical sides (food doesn’t slide out) and a lid.

This morning I used 2 tsp duck fat since I had a tub on hand, but generally I use 2 tsp extra-virgin olive oil. Then I sauté:

1 bunch scallions, chopped (including leaves)
several stalks of asparagus, chopped
1 baby Shanghai bok choy, chopped
1 large jalapeño pepper, chopped
oyster mushrooms, caps and stems, chopped
skin from one large salmon fillet, cut to pieces with kitchen shears
10-12 San Marzano cherry tomatoes, sliced
salt, pepper, and a dash of Maggi

I sauté that covered, stirring occasionally with a wooden spatula, until the vegetables have cooked down a bit. While it cooks and between stirrings, I wipe off and put away the chopping board and rinse, dry, and put away the knife.

2 eggs, cracked on top of the veggies

I cover and let that steam for 2 minutes, then scoop contents into a large bowl and enjoy with a glass of iced tea that has the juice of 1 lemon or (this morning) 1 lime. I also drink:

1/4 cup pomegranate juice

I think that’s a pretty good breakfast, and you’ll note that it is low carb.

When I don’t have salmon skin, I’ll used some chicken breast or fillet of sole or chopped ham or the like.

 

Written by LeisureGuy

6 February 2019 at 8:50 am

Posted in Food, Low carb, Recipes

Tasty health: Salmon-Red Chard Stew

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As always, improvised. This time I used the 6-qt All Clad pot (wide diameter so good for sautéing). I had steamed green beans (first cut into 1″ lengths) and then refrigerated. I stopped steaming just before they were done, since I planned on cooking them in various dishes—like this one

2 tablespoons extra-virgin olive oil
2 bunches scallions, chopped—thick ones if possible (I wasn’t so lucky)
1 cup leafy celery, chopped—the leafy-ness was unexpected but welcome
1 large carrot, cut on diagonal, rotating carrot 90º after each cut
1 cup steamed green beans cut into 1″ lengths, not quite done
chopped stems from one bunch of red chard
1/2 cup pitted Kalamata olives, coarsely chopped
1 tablespoon dried marjoram
1 tablespoon herbes de Provence
big pinch of salt
1 tablespoon freshly ground black pepper

Sauté, stirring occasionally (I use a wooden spatula because it stirs better than a spoon) until the vegetables start to soften a bit (8-10 minutes, I’d guess).

Add:

I large zucchini, halved lengthways, cut into strips and then crossways into chunks—large enough to hold the texture when cooked

Continue sautéing for a bit longer (4-6 minutes), then add:

1 bunch red chard, chopped (stems chopped and sautéed with above)
dash Worcestershire sauce
juice of 1 lemon

Stir to mix, cover and cook for 8-10 minutes over medium heat. Then add:

1 large salmon fillet, skin removed and then cut into chunks
1/4 cup good sherry (cream sherry or Amontillado or the like)

Cover and simmer for another 8-10 minutes. Really yummy. 8 WW points for olive oil, probably 8 for Kalamata olives: 16 total, or 4 points a serving.

Written by LeisureGuy

5 February 2019 at 5:36 pm

Is Sugar Toxic?

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This article by Gary Taubes appeared in the NY Times on April 13, 2011—but it’s still of interest:

On May 26, 2009, Robert Lustig gave a lecture called “Sugar: The Bitter Truth,” which was posted on YouTube the following July. Since then, it has been viewed well over 800,000 times, gaining new viewers at a rate of about 50,000 per month, fairly remarkable numbers for a 90-minute discussion of the nuances of fructose biochemistry and human physiology.

Lustig is a specialist on pediatric hormone disorders and the leading expert in childhood obesity at the University of California, San Francisco, School of Medicine, which is one of the best medical schools in the country. He published his first paper on childhood obesity a dozen years ago, and he has been treating patients and doing research on the disorder ever since.

The viral success of his lecture, though, has little to do with Lustig’s impressive credentials and far more with the persuasive case he makes that sugar is a “toxin” or a “poison,” terms he uses together 13 times through the course of the lecture, in addition to the five references to sugar as merely “evil.” And by “sugar,” Lustig means not only the white granulated stuff that we put in coffee and sprinkle on cereal — technically known as sucrose — but also high-fructose corn syrup, which has already become without Lustig’s help what he calls “the most demonized additive known to man.”

It doesn’t hurt Lustig’s cause that he is a compelling public speaker. His critics argue that what makes him compelling is his practice of taking suggestive evidence and insisting that it’s incontrovertible. Lustig certainly doesn’t dabble in shades of gray. Sugar is not just an empty calorie, he says; its effect on us is much more insidious. “It’s not about the calories,” he says. “It has nothing to do with the calories. It’s a poison by itself.”

If Lustig is right, then our excessive consumption of sugar is the primary reason that the numbers of obese and diabetic Americans have skyrocketed in the past 30 years. But his argument implies more than that. If Lustig is right, it would mean that sugar is also the likely dietary cause of several other chronic ailments widely considered to be diseases of Western lifestyles — heart disease, hypertension and many common cancers among them.

The number of viewers Lustig has attracted suggests that people are paying attention to his argument. When I set out to interview public health authorities and researchers for this article, they would often initiate the interview with some variation of the comment “surely you’ve spoken to Robert Lustig,” not because Lustig has done any of the key research on sugar himself, which he hasn’t, but because he’s willing to insist publicly and unambiguously, when most researchers are not, that sugar is a toxic substance that people abuse. In Lustig’s view, sugar should be thought of, like cigarettes and alcohol, as something that’s killing us.

This brings us to the salient question: Can sugar possibly be as bad as Lustig says it is?

It’s one thing to suggest, as most nutritionists will, that a healthful diet includes more fruits and vegetables, and maybe less fat, red meat and salt, or less of everything. It’s entirely different to claim that one particularly cherished aspect of our diet might not just be an unhealthful indulgence but actually be toxic, that when you bake your children a birthday cake or give them lemonade on a hot summer day, you may be doing them more harm than good, despite all the love that goes with it. Suggesting that sugar might kill us is what zealots do. But Lustig, who has genuine expertise, has accumulated and synthesized a mass of evidence, which he finds compelling enough to convict sugar. His critics consider that evidence insufficient, but there’s no way to know who might be right, or what must be done to find out, without discussing it.

If I didn’t buy this argument myself, I wouldn’t be writing about it here. And I also have a disclaimer to acknowledge. I’ve spent much of the last decade doing journalistic research on diet and chronic disease — some of the more contrarian findings, on dietary fat, appeared in this magazine —– and I have come to conclusions similar to Lustig’s.

The history of the debate over the health effects of sugar has gone on far longer than you might imagine. It is littered with erroneous statements and conclusions because even the supposed authorities had no true understanding of what they were talking about. They didn’t know, quite literally, what they meant by the word “sugar” and therefore what the implications were.

So let’s start by clarifying a few issues, beginning with Lustig’s use of the word “sugar” to mean both sucrose — beet and cane sugar, whether white or brown — and high-fructose corn syrup. This is a critical point, particularly because high-fructose corn syrup has indeed become “the flashpoint for everybody’s distrust of processed foods,” says Marion Nestle, a New York University nutritionist and the author of “Food Politics.”

This development is recent and borders on humorous. In the early 1980s, high-fructose corn syrup replaced sugar in sodas and other products in part because refined sugar then had the reputation as a generally noxious nutrient. (“Villain in Disguise?” asked a headline in this paper in 1977, before answering in the affirmative.) High-fructose corn syrup was portrayed by the food industry as a healthful alternative, and that’s how the public perceived it. It was also cheaper than sugar, which didn’t hurt its commercial prospects. Now the tide is rolling the other way, and refined sugar is making a commercial comeback as the supposedly healthful alternative to this noxious corn-syrup stuff. “Industry after industry is replacing their product with sucrose and advertising it as such — ‘No High-Fructose Corn Syrup,’ ” Nestle notes.

But marketing aside, the two sweeteners are effectively identical in their biological effects. “High-fructose corn syrup, sugar — no difference,” is how Lustig put it in a lecture that I attended in San Francisco last December. “The point is they’re each bad — equally bad, equally poisonous.”

Refined sugar (that is, sucrose) is made up of a molecule of the carbohydrate glucose, bonded to a molecule of the carbohydrate fructose — a 50-50 mixture of the two. The fructose, which is almost twice as sweet as glucose, is what distinguishes sugar from other carbohydrate-rich foods like bread or potatoes that break down upon digestion to glucose alone. The more fructose in a substance, the sweeter it will be. High-fructose corn syrup, as it is most commonly consumed, is 55 percent fructose, and the remaining 45 percent is nearly all glucose. It was first marketed in the late 1970s and was created to be indistinguishable from refined sugar when used in soft drinks. Because each of these sugars ends up as glucose and fructose in our guts, our bodies react the same way to both, and the physiological effects are identical. In a 2010 review of the relevant science, Luc Tappy, a researcher at the University of Lausanne in Switzerland who is considered by biochemists who study fructose to be the world’s foremost authority on the subject, said there was “not the single hint” that H.F.C.S. was more deleterious than other sources of sugar.

The question, then, isn’t whether high-fructose corn syrup is worse than sugar; it’s what do they do to us, and how do they do it? The conventional wisdom has long been that the worst that can be said about sugars of any kind is that they cause tooth decay and represent “empty calories” that we eat in excess because they taste so good.

By this logic, sugar-sweetened beverages (or H.F.C.S.-sweetened beverages, as the Sugar Association prefers they are called) are bad for us not because there’s anything particularly toxic about the sugar they contain but just because people consume too many of them.

Those organizations that now advise us to cut down on our sugar consumption — the Department of Agriculture, for instance, in its recent Dietary Guidelines for Americans, or the American Heart Association in guidelines released in September 2009 (of which Lustig was a co-author) — do so for this reason. Refined sugar and H.F.C.S. don’t come with any protein, vitamins, minerals, antioxidants or fiber, and so they either displace other more nutritious elements of our diet or are eaten over and above what we need to sustain our weight, and this is why we get fatter.

Whether the empty-calories argument is true, it’s certainly convenient. It allows everyone to assign blame for obesity and, by extension, diabetes — two conditions so intimately linked that some authorities have taken to calling them “diabesity” — to overeating of all foods, or underexercising, because a calorie is a calorie. “This isn’t about demonizing any industry,” as Michelle Obama said about her Let’s Move program to combat the epidemic of childhood obesity. Instead it’s about getting us — or our children — to move more and eat less, reduce our portion sizes, cut back on snacks.

Lustig’s argument, however, is not about the consumption of empty calories — and biochemists have made the same case previously, though not so publicly. It is that sugar has unique characteristics, specifically in the way the human body metabolizes the fructose in it, that may make it singularly harmful, at least if consumed in sufficient quantities.

The phrase Lustig uses when he describes this concept is “isocaloric but not isometabolic.” This means we can eat 100 calories of glucose (from a potato or bread or other starch) or 100 calories of sugar (half glucose and half fructose), and they will be metabolized differently and have a different effect on the body. The calories are the same, but the metabolic consequences are quite different.

The fructose component of sugar and H.F.C.S. is metabolized primarily by the liver, while the glucose from sugar and starches is metabolized by every cell in the body. Consuming sugar (fructose and glucose) means more work for the liver than if you consumed the same number of calories of starch (glucose). And if you take that sugar in liquid form — soda or fruit juices — the fructose and glucose will hit the liver more quickly than if you consume them, say, in an apple (or several apples, to get what researchers would call the equivalent dose of sugar). The speed with which the liver has to do its work will also affect how it metabolizes the fructose and glucose.

In animals, or at least in laboratory rats and mice, it’s clear that if the fructose hits the liver in sufficient quantity and with sufficient speed, the liver will convert much of it to fat. This apparently induces a condition known as insulin resistance, which is now considered the fundamental problem in obesity, and the underlying defect in heart disease and in the type of diabetes, type 2, that is common to obese and overweight individuals. It might also be the underlying defect in many cancers.

If what happens in laboratory rodents also happens in humans, and if we are eating enough sugar to make it happen, then we are in trouble.

The last time an agency of the federal government looked into the question of sugar and health in any detail was in 2005, in a report by the Institute of Medicine, a branch of the National Academies. The authors of the report acknowledged that plenty of evidence suggested that sugar could increase the risk of heart disease and diabetes — even raising LDL cholesterol, known as the “bad cholesterol”—– but did not consider the research to be definitive. There was enough ambiguity, they concluded, that they couldn’t even set an upper limit on how much sugar constitutes too much. Referring back to the 2005 report, an Institute of Medicine report released last fall reiterated, “There is a lack of scientific agreement about the amount of sugars that can be consumed in a healthy diet.” This was the same conclusion that the Food and Drug Administration came to when it last assessed the sugar question, back in 1986. The F.D.A. report was perceived as an exoneration of sugar, and that perception influenced the treatment of sugar in the landmark reports on diet and health that came after.

The Sugar Association and the Corn Refiners Association have also portrayed the 1986 F.D.A. report as clearing sugar of nutritional crimes, but what it concluded was actually something else entirely. To be precise, the F.D.A. reviewers said that other than its contribution to calories, “no conclusive evidence on sugars demonstrates a hazard to the general public when sugars are consumed at the levels that are now current.” This is another way of saying that the evidence by no means refuted the kinds of claims that Lustig is making now and other researchers were making then, just that it wasn’t definitive or unambiguous.

What we have to keep in mind, says Walter Glinsmann, the F.D.A. administrator who was the primary author on the 1986 report and who now is an adviser to the Corn Refiners Association, is that sugar and high-fructose corn syrup might be toxic, as Lustig argues, but so might any substance if it’s consumed in ways or in quantities that are unnatural for humans. The question is always at what dose does a substance go from being harmless to harmful? How much do we have to consume before this happens?

When Glinsmann and his F.D.A. co-authors decided no conclusive evidence demonstrated harm at the levels of sugar then being consumed, they estimated those levels at 40 pounds per person per year beyond what we might get naturally in fruits and vegetables — 40 pounds per person per year of “added sugars” as nutritionists now call them. This is 200 calories per day of sugar, which is less than the amount in a can and a half of Coca-Cola or two cups of apple juice. If that’s indeed all we consume, most nutritionists today would be delighted, including Lustig.

But 40 pounds per year happened to be 35 pounds less than what Department of Agriculture analysts said we were consuming at the time — 75 pounds per person per year — and the U.S.D.A. estimates are typically considered to be the most reliable. By the early 2000s, according to the U.S.D.A., we had increased our consumption to more than 90 pounds per person per year.

That this increase happened to coincide with the current epidemics of obesity and diabetes is one reason that it’s tempting to blame sugars — sucrose and high-fructose corn syrup — for the problem. In 1980, roughly one in seven Americans was obese, and almost six million were diabetic, and the obesity rates, at least, hadn’t changed significantly in the 20 years previously. By the early 2000s, when sugar consumption peaked, one in every three Americans was obese, and 14 million were diabetic.

This correlation between sugar consumption and diabetes is what defense attorneys call circumstantial evidence. It’s more compelling than it otherwise might be, though, because the last time sugar consumption jumped markedly in this country, it was also associated with a diabetes epidemic.

In the early 20th century, many of the leading authorities on diabetes in North America and Europe (including Frederick Banting, who shared the 1923 Nobel Prize for the discovery of insulin) suspected that sugar causes diabetes based on the observation that the disease was rare in populations that didn’t consume refined sugar and widespread in those that did. In 1924, Haven Emerson, director of the institute of public health at Columbia University, reported that diabetes deaths in New York City had increased as much as 15-fold since the Civil War years, and that deaths increased as much as fourfold in some U.S. cities between 1900 and 1920 alone. This coincided, he noted, with an equally significant increase in sugar consumption — almost doubling from 1890 to the early 1920s — with the birth and subsequent growth of the candy and soft-drink industries.

Emerson’s argument was countered by Elliott Joslin, a leading authority on diabetes, and Joslin won out. But his argument was fundamentally flawed. Simply put, it went like this: The Japanese eat lots of rice, and Japanese diabetics are few and far between; rice is mostly carbohydrate, which suggests that sugar, also a carbohydrate, does not cause diabetes. But sugar and rice are not identical merely because they’re both carbohydrates. Joslin could not know at the time that the fructose content of sugar affects how we metabolize it.

Joslin was also unaware that the Japanese ate little sugar.  . .

Continue reading. There’s much more.

Later in the article:

. . . Until Lustig came along, the last time an academic forcefully put forward the sugar-as-toxin thesis was in the 1970s, when John Yudkin, a leading authority on nutrition in the United Kingdom, published a polemic on sugar called “Sweet and Dangerous.” Through the 1960s Yudkin did a series of experiments feeding sugar and starch to rodents, chickens, rabbits, pigs and college students. He found that the sugar invariably raised blood levels of triglycerides (a technical term for fat), which was then, as now, considered a risk factor for heart disease. Sugar also raised insulin levels in Yudkin’s experiments, which linked sugar directly to type 2 diabetes. Few in the medical community took Yudkin’s ideas seriously, largely because he was also arguing that dietary fat and saturated fat were harmless. This set Yudkin’s sugar hypothesis directly against the growing acceptance of the idea, prominent to this day, that dietary fat was the cause of heart disease, a notion championed by the University of Minnesota nutritionist Ancel Keys.

A common assumption at the time was that if one hypothesis was right, then the other was most likely wrong. Either fat caused heart disease by raising cholesterol, or sugar did by raising triglycerides. “The theory that diets high in sugar are an important cause of atherosclerosis and heart disease does not have wide support among experts in the field, who say that fats and cholesterol are the more likely culprits,” as Jane E. Brody wrote in The Times in 1977.

At the time, many of the key observations cited to argue that dietary fat caused heart disease actually support the sugar theory as well. During the Korean War, pathologists doing autopsies on American soldiers killed in battle noticed that many had significant plaques in their arteries, even those who were still teenagers, while the Koreans killed in battle did not. The atherosclerotic plaques in the Americans were attributed to the fact that they ate high-fat diets and the Koreans ate low-fat. But the Americans were also eating high-sugar diets, while the Koreans, like the Japanese, were not. . .

Written by LeisureGuy

31 January 2019 at 4:07 pm

Germs in Your Gut Are Talking to Your Brain. Scientists Want to Know What They’re Saying.

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Carl Zimmer reports in the NY Times:

In 2014 John Cryan, a professor at University College Cork in Ireland, attended a meeting in California about Alzheimer’s disease. He wasn’t an expert on dementia. Instead, he studied the microbiome, the trillions of microbes inside the healthy human body.

Dr. Cryan and other scientists were beginning to find hints that these microbes could influence the brain and behavior. Perhaps, he told the scientific gathering, the microbiome has a role in the development of Alzheimer’s disease.

The idea was not well received. “I’ve never given a talk to so many people who didn’t believe what I was saying,” Dr. Cryan recalled.

A lot has changed since then: Research continues to turn up remarkable links between the microbiome and the brain. Scientists are finding evidence that microbiome may play a role not just in Alzheimer’s disease, but Parkinson’s disease, depression, schizophrenia, autism and other conditions.

For some neuroscientists, new studies have changed the way they think about the brain.

One of the skeptics at that Alzheimer’s meeting was Sangram Sisodia, a neurobiologist at the University of Chicago. He wasn’t swayed by Dr. Cryan’s talk, but later he decided to put the idea to a simple test.

“It was just on a lark,” said Dr. Sisodia. “We had no idea how it would turn out.”

He and his colleagues gave antibiotics to mice prone to develop a version of Alzheimer’s disease, in order to kill off much of the gut bacteria in the mice. Later, when the scientists inspected the animals’ brains, they found far fewer of the protein clumps linked to dementia.

Just a little disruption of the microbiome was enough to produce this effect. Young mice given antibiotics for a week had fewer clumps in their brains when they grew old, too.

“I never imagined it would be such a striking result,” Dr. Sisodia said. “For someone with a background in molecular biology and neuroscience, this is like going into outer space.”

Following a string of similar experiments, he now suspects that just a few species in the gut — perhaps even one — influence the course of Alzheimer’s disease, perhaps by releasing chemical that alters how immune cells work in the brain.

He hasn’t found those microbes, let alone that chemical. But “there’s something’s in there,” he said. “And we have to figure out what it is.”

Scientists have long known that microbes live inside us. In 1683, the Dutch scientist Antonie van Leeuwenhoek put plaque from his teeth under a microscope and discovered tiny creatures swimming about.

But the microbiome has stubbornly resisted scientific discovery. For generations, microbiologists only studied the species that they could grow in the lab. Most of our interior occupants can’t survive in petri dishes.

In the early 2000s, however, the science of the microbiome took a sudden leap forward when researchers figured out how to sequence DNA from these microbes. Researchers initially used this new technology to examine how the microbiome influences parts of our bodies rife with bacteria, such as the gut and the skin.

Few of them gave much thought to the brain — there didn’t seem to be much point. The brain is shielded from microbial invasion by the so-called blood-brain barrier. Normally, only small molecules pass through.

“As recently as 2011, it was considered crazy to look for associations between the microbiome and behavior,” said Rob Knight, a microbiologist at the University of California, San Diego.

He and his colleagues discovered some of the earliest hints of these links. Investigators took stool from mice with a genetic mutation that caused them to eat a lot and put on weight. They transferred the stool to mice that had been raised germ-free — that is, entirely without gut microbiomes — since birth.

After receiving this so-called fecal transplant, the germ-free mice got hungry, too, and put on weight.

Altering appetite isn’t the only thing that the microbiome can do to the brain, it turns out. Dr. Cryan and his colleagues, for example, have found that mice without microbiomes become loners, preferring to stay away from fellow rodents.

The scientists eventually discovered changes in the brains of these antisocial mice. One region, called the amygdala, is important for processing social emotions. In germ-free mice, the neurons in the amygdala make unusual sets of proteins, changing the connections they make with other cells.

Studies of humans revealed some surprising patterns, too. Children with autism have unusual patterns of microbial species in their stool. Differences in the gut bacteria of people with a host of other brain-based conditions also have been reported.

But none of these associations proves cause and effect. Finding an unusual microbiome in people with Alzheimer’s doesn’t mean that the bacteria drive the disease. It could be the reverse: People with Alzheimer’s disease often change their eating habits, for example, and that switch might favor different species of gut microbes.

Fecal transplants can help pin down these links. In his research on Alzheimer’s, Dr. Sisodia and his colleagues transferred stool from ordinary mice into the mice they had treated with antibiotics. Once their microbiomes were restored, the antibiotic-treated mice started developing protein clumps again.

“We’re extremely confident that it’s the bacteria that’s driving this,” he said. Other researchers have taken these experiments a step further by using human fecal transplants.

If you hold a mouse by its tail, it normally wriggles in an effort to escape. If you give it a fecal transplant from humans with major depression, you get a completely different result: The mice give up sooner, simply hanging motionless.

As intriguing as this sort of research can be, it has a major limitation. Because researchers are transferring hundreds of bacterial species at once, the experiments can’t reveal which in particular are responsible for changing the brain.

Now researchers are pinpointing individual strains that seem to have an effect.

To study autism, Dr. Mauro Costa-Mattioli and his colleagues at the Baylor College of Medicine in Houston investigated different kinds of mice, each of which display some symptoms of autism. A mutation in a gene called SHANK3 can cause mice to groom themselves repetitively and avoid contact with other mice, for example.

In another mouse strain, Dr. Costa-Mattioli found that feeding mothers a high-fat diet makes it more likely their pups will behave this way.

When the researchers investigated the microbiomes of these mice, they found the animals lacked a common species called Lactobacillus reuteri. When they added a strain of that bacteria to the diet, the animals became social again.

Dr. Costa-Mattioli found evidence that L. reuteri releases compounds that send a signal to nerve endings in the intestines. The vagus nerve sends these signals from the gut to the brain, where they alter production of a hormone called oxytocin that promotes social bonds.

Other microbial species also send signals along the vagus nerve, it turns out. Still others communicate with the brain via the bloodstream.

It’s likely that this influence begins before birth, as a pregnant mother’s microbiome releases molecules that make their way into the fetal brain.

Mothers seed their babies with microbes during childbirth and breast feeding. During the first few years of life, both the brain and the microbiome rapidly mature.

To understand the microbiome’s influence on the developing brain, Rebecca Knickmeyer, a neuroscientist at Michigan State University, is studying fMRI scans of infants.

In her first study, published in January, she focused on the amygdala, the emotion-processing region of the brain that Dr. Cryan and others have found to be altered in germ-free mice.

Dr. Knickmeyer and her colleagues measured the strength of the connections between the amygdala and other regions of the brain. Babies with a lower diversity of species in their guts have stronger connections, the researchers found.

Does that mean a low-diversity microbiome makes babies more fearful of others? It’s not possible to say yet — but Dr. Knickmeyer hopes to find out by running more studies on babies.

As researchers better understand how the microbiome influences the brain, they hope doctors will be able to use it to treat psychiatric and neurological conditions.

It’s possible they’ve been doing it for a long time — without knowing.

In the early 1900s, neurologists found that putting people with epilepsy on a diet low in carbohydrates and high in protein and fat sometimes reduced their seizures.

Epileptic mice experience the same protection from a so-called ketogenic diet. But no one could say why. Elaine Hsiao, a microbiologist at the University of California, Los Angeles, suspected that the microbiome was the reason.

To test the microbiome’s importance, Dr. Hsiao and her colleagues raised mice free of microbes. When they put the germ-free epileptic mice on a ketogenic diet, they found that the animals got no protection from seizures.

But if they gave the germ-free animals stool from mice on a ketogenic diet, seizures were reduced.

Dr. Hsiao found that two types of gut bacteria in particular thrive in mice on a ketogenic diet. They may provide their hosts with building blocks for neurotransmitters that put a brake on electrical activity in the brain.

It’s conceivable that people with epilepsy wouldn’t need to go on a ketogenic diet to get its benefits — one day, they may just take a pill containing the bacteria that do well on the diet.

Sarkis Mazmanian, a microbiologist at Caltech, and his colleagues have identified a single strain of bacteria that triggers symptoms of Parkinson’s disease in mice. He has started a company that is testing a compound that may block signals that the microbe sends to the vagus nerve.  . .

Continue reading.

Written by LeisureGuy

29 January 2019 at 1:19 pm

Intermittent fasting: Surprising update from Harvard Medical School

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I have never tried intermittent fasting (IF) and have never been interested in it. But after reading this report from Harvard Medical School, I’m going to give it a try:

There’s a ton of incredibly promising intermittent fasting (IF) research done on fat rats. They lose weight, their blood pressure, cholesterol, and blood sugars improve… but they’re rats. Studies in humans, almost across the board, have shown that IF is safe and incredibly effective, but really no more effective than any other diet. In addition, many people find it difficult to fast.

But a growing body of research suggests that the timing of the fast is key, and can make IF a more realistic, sustainable, and effective approach for weight loss, as well as for diabetes prevention.

The backstory on intermittent fasting

IF as a weight loss approach has been around in various forms for ages, but was highly popularized in 2012 by BBC broadcast journalist Dr. Michael Mosley’s TV documentary Eat Fast, Live Longer and book The Fast Diet, followed by journalist Kate Harrison’s book The 5:2 Diet based on her own experience, and subsequently by Dr. Jason Fung’s 2016 bestseller The Obesity Code. IF generated a steady positive buzz as anecdotes of its effectiveness proliferated.

As a lifestyle-leaning research doctor, I needed to understand the science. The Obesity Codeseemed the most evidence-based summary resource, and I loved it. Fung successfully combines plenty of research, his clinical experience, and sensible nutrition advice, and also addresses the socioeconomic forces conspiring to make us fat. He is very clear that we should eat more fruits and veggies, fiber, healthy protein, and fats, and avoid sugar, refined grains, processed foods, and for God’s sake, stop snacking. Check, check, check, I agree. The only part that was still questionable in my mind was the intermittent fasting part.

Intermittent fasting can help weight loss

IF makes intuitive sense. The food we eat is broken down by enzymes in our gut and eventually ends up as molecules in our bloodstream. Carbohydrates, particularly sugars and refined grains (think white flours and rice), are quickly broken down into sugar, which our cells use for energy. If our cells don’t use it all, we store it in our fat cells as, well, fat. But sugar can only enter our cells with insulin, a hormone made in the pancreas. Insulin brings sugar into the fat cells and keeps it there.

Between meals, as long as we don’t snack, our insulin levels will go down and our fat cells can then release their stored sugar, to be used as energy. We lose weight if we let our insulin levels go down. The entire idea of IF is to allow the insulin levels to go down far enough and for long enough that we burn off our fat.

Intermittent fasting can be hard… but maybe it doesn’t have to be

Initial human studies that compared fasting every other day to eating less every day showed that both worked about equally for weight loss, though people struggled with the fasting days. So I had written off IF as no better or worse than simply eating less, only far more uncomfortable. My advice was to just stick with the sensible, plant-based, Mediterranean-style diet.

New research is suggesting that not all IF approaches are the same, and some are actually very reasonable, effective, and sustainable, especially when combined with a nutritious plant-based diet. So I’m prepared to take my lumps on this one (and even revise my prior post).

We have evolved to be in sync with the day/night cycle, i.e., a circadian rhythm. Our metabolism has adapted to daytime food, nighttime sleep. Nighttime eating is well associated with a higher risk of obesity, as well as diabetes.

Based on this, researchers from the University of Alabama conducted a study with a small group of obese men with prediabetes. They compared a form of intermittent fasting called “early time-restricted feeding,” where all meals were fit into an early eight-hour period of the day (7 am to 3 pm), or spread out over 12 hours (between 7 am and 7 pm). Both groups maintained their weight (did not gain or lose) but after five weeks, the eight-hours group had dramatically lower insulin levels and significantly improved insulin sensitivity, as well as significantly lower blood pressure. The best part? The eight-hours group also had significantly decreased appetite. They weren’t starving.

Just changing the timing of meals, by eating earlier in the day and extending the overnight fast, significantly benefited metabolism even in people who didn’t lose a single pound.

So is this as good as it sounds?

I was very curious about this, so I asked the opinion of metabolic expert Dr. Deborah Wexler, Director of the Massachusetts General Hospital Diabetes Center and associate professor at Harvard Medical School. Here is what she told me. “There is evidence to suggest that the circadian rhythm fasting approach, where meals are restricted to an eight to 10-hour period of the daytime, is effective,” she confirmed, though generally she recommends that people “use an eating approach that works for them and is sustainable to them.”

So here’s the deal. There is some good scientific evidence suggesting that circadian rhythm fasting, when combined with a healthy diet and lifestyle, can be a particularly effective approach to weight loss, especially for people at risk for diabetes. (However, people with advanced diabetes or who are on medications for diabetes, people with a history of eating disorders like anorexia and bulimia, and pregnant or breastfeeding women should not attempt intermittent fasting unless under the close supervision of a physician who can monitor them.)

4 ways to use this information for better health

  1. Avoid sugars and refined grains. Instead, eat fruits, vegetables, beans, lentils, whole grains, lean proteins, and healthy fats (a sensible, plant-based, Mediterranean-style diet).
  2. Let your body burn fat between meals. Don’t snack. Be active throughout your day. Build muscle tone.
  3. Consider a simple form of intermittent fasting. Limit the hours of the day when you eat, and for best effect, make it earlier in the day (between 7 am to 3 pm, or even 10 am to 6 pm, but definitely not in the evening before bed).
  4. Avoid snacking or eating at nighttime, all the time.

Sources . . .

Continue reading.

Written by LeisureGuy

28 January 2019 at 11:31 am

Posted in Food, Health, Medical, Science

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