Later On

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Archive for August 24th, 2021

Feeding mice high-fructose corn syrup increases gut surface area, leading to weight gain

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Fructose, the variant of sugar commonly found in fruit (thus the name), is a healthy sugar when consumed in the whole food that carries it (see video). But if you refine it and mainline it, as it were, by consuming the refined sugar, then it’s definitely unhealthy (as are other refined sugars). 

I’m a type 2 diabetic and I currently eat 3 pieces of fruit for breakfast and also a bowl of mixed berries (bought frozen and then thawed) every afternoon. Despite the relatively high sugar content — fructose, in fact — my HbA1c most recently was 5.2% and my fasting blood glucose the last three mornings was 5.7 mmol/L, 5.8, and 5.9. (The US uses mg/dL, and the corresponding figures are 103.6, 104.5, and 106.3.) From time to time I get a reading of 5.4 (97.3) or 5.5 (99.1). (I get lower readings if I am walking regularly.)

So fructose is not the problem; refined fructose is. And high-fructose corn syrup is a refined form of fructose commonly used in highly processed foods (manufactured from refined ingredients using industrial process — not the kind of “processing” you do at home, which generally consists of rinse, chop, and cook. 

Patrícia M. Nunes and Dimitrios Anastasiou write in Nature (emphasis added):

The incidence of obesity has been steadily increasing, tripling globally between 1975 and 2016, at a high cost to public health1. Obesity predisposes individuals to various diseases, including cancer, and the number of obesity-associated deaths globally each year1 (estimated at 2.8 million) is similar in scale to the reported COVID-19-associated deaths in the ongoing pandemic. Although fat-rich diets have taken much of the blame for the rise in obesity, excess consumption of processed sugars, and high-fructose corn syrup (HFCS) in particular, is strongly implicated in diet-induced obesity. Whether and how fructose causes obesity in humans remains a hotly debated question2,3. In a report in Nature that should make one think twice before gulping down sugar-sweetened drinks with fatty snacks, Taylor et al.4 propose that HFCS promotes obesity by boosting the ability of the intestine to absorb nutrients.

Evidence has emerged58 that the small intestine acts as the gatekeeper for the mammalian body against the harmful effects of fructose, the main one being the aberrant accumulation of fat (termed steatosis) in the liver. Moderate amounts of fructose — for example, those ingested when consuming fruits — are taken up and broken down by intestinal cells. Excess amounts, such as those that might be ingested after drinking a sugary beverage, overwhelm the intestine’s absorptive capacity and the fructose either ‘leaks’ into the bloodstream to reach the liver intact, or it spills over from the small intestine and reaches the colon5.

The breakdown of fructose in cells starts with its conversion to fructose 1-phosphate (F1-P). This modification involves the transfer of a phosphate group to fructose from the energy-providing molecule ATP, through the action of the enzyme ketohexokinase (KHK). Excess fructose in the liver fuels high KHK activity, which is thought to stimulate the expression of lipid-synthesis genes by diverse mechanisms9. The depletion of KHK in the liver of mice is enough to prevent fructose-induced liver steatosis6.

Fructose that ends up in the colon is broken down by resident bacteria to produce molecules that can then fuel lipid synthesis in the liver7. Furthermore, fructose increases intestinal ‘leakiness’, a condition in which loose connections between gut cells enable ingested nutrients, and toxins from bacteria in the colon, to escape to the liver, where they activate inflammatory signals from immune cells that boost steatosis8. Therefore, excess fructose harms the liver both directly and indirectly through changes in the intestine.

Taylor and colleagues’ study reveals that fructose has a previously unknown effect on the structure of the intestine (Fig. 1). Previous work10 had shown that HFCS promotes metabolic pathways that support the formation of colon tumours, so the authors wondered what consequences a HFCS-rich diet might have for non-cancerous intestinal cells. Taylor et al. found that HFCS-fed mice had longer intestinal protrusions — structures known as villi — and absorbed more dietary nutrients compared with mice that did not receive HFCS in their diet. Furthermore, fatty diets caused an even greater weight gain in mice if such diets also contained fructose than if they did not.

As a villus elongates when new cells are formed, the older intestinal cells move to the tip of the villus, away from blood vessels, and experience a gradually increasing limitation in oxygen availability (entering a state called hypoxia). The authors report evidence that at the tip of the villus, where hypoxia was extreme, cells were dying. Taylor and colleagues also found that new cells in the growing villi of HFCS-fed mice formed at similar rates to those of mice without HFCS in their diet. Together these observations suggest that hypoxia-induced cell death restricts villus length, and that the villi of HFCS-fed mice were longer because their cells were less likely to die compared with hypoxic cells in the villi of mice that were not fed HFCS.

Taylor et al. investigated how fructose might promote the survival of hypoxic cells. The authors’ analysis of cells grown in vitro revealed that . . .

Continue reading. There’s more. And note that food manufacturers have become aware of the unhealthy effects of HFCS and of consumer concerns about those, and they have responded — but their response has been to change the name in the hopes of fooling the consumer, a clear example of how corporations are concerned about their profits, not about their customers’ health (cf. cigarette companies).

Figure 1 | Fructose-mediated gut changes. Nutrients in the gut enter the bloodstream after passing through cells in an intestinal protrusion called a villus. Cells at the tip of a villus have limited access to oxygen (a state called hypoxia), and they die for reasons such as energy depletion and oxidative stress. Taylor et al.4 report that, if mice received high-fructose corn syrup (HFCS) in their diet, they had longer villi and higher levels of lipids in their blood compared with animals that did not receive HFCS. The authors suggest that villus lengthening arises due to increased survival of hypoxic cells through changes triggered by the presence of fructose. Glucose from HFCS is metabolized, gaining two phosphate groups (red circles) to generate the molecule fructose 1,6-bisphosphate (F1,6-BP), which favours the formation of the high-activity, tetrameric version of the enzyme PKM2. This enzyme functions in a metabolic pathway called glycolysis. When the fructose from HFCS enters cells through the GLUT5 transporter, the enzyme ketohexokinase (KHK) converts it to fructose 1-phosphate (F1-P), which is structurally similar to F1,6-BP. In contrast to F1,6-BP, F1-P causes the dissociation of PKM2 subunits and shifts the balance from active PKM2 tetramers to low-activity PKM2 monomers. PKM2 monomers boost the survival of villus cells in hypoxia by suppressing oxidative stress and by inducing the expression of genes that help to sustain energy levels.

Written by Leisureguy

24 August 2021 at 3:39 pm

Genetic patterns offer clues to evolution of homosexuality

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Conservatives — particularly, I believe, evangelicals — think that being homosexual is a choice rather than a genetically-determined preference (thus “pray the gay away,” as though the object of prayer can change his/her decision (with, of course, the help of God Almighty, who works night and day to obey all those prayers). See, for example, But I’m a Cheerleader on Amazon Prime Video. Deciding not to be homosexual is akin to deciding not to have, say, brown eye: it’s not something a person decides.

Sara Reardon in Nature discusses the genetic differences among homosexuals, those who are promiscuous, and the monogamously inclined:

To evolutionary biologists, the genetics of homosexuality seems like a paradox. In theory, humans and other animals who are exclusively attracted to others of the same sex should be unlikely to produce many biological children, so any genes that predispose people to homosexuality would rarely be passed on to future generations. Yet same-sex attraction is widespread in humans, and research suggests that it is partly genetic.

In a study of data from hundreds of thousands of people, researchers have now identified genetic patterns that could be associated with homosexual behaviour, and showed how these might also help people to find different-sex mates, and reproduce. The authors say their findings, published on 23 August in Nature Human Behaviour1could help to explain why genes that predispose people to homosexuality continue to be passed down. But other scientists question whether these data can provide definitive conclusions.

Evolutionary geneticist Brendan Zietsch at the University of Queensland in Brisbane, Australia, and his colleagues used data from the UK Biobank, the US National Longitudinal Study of Adolescent to Adult Health and the company 23andMe, based in Sunnyvale, California, which sequence genomes and use questionnaires to collect information from their participants. The team analysed the genomes of 477,522 people who said they had had sex at least once with someone of the same sex, then compared these genomes with those of 358,426 people who said they’d only had heterosexual sex. The study looked only at biological sex, not gender, and excluded participants whose gender and sex did not match.

In earlier research, the researchers had found that people who’d had at least one same-sex partner tended to share patterns of small genetic differences scattered throughout the genome2. None of these variations seemed to greatly affect sexual behaviour on its own, backing up previous research that has found no sign of a ‘gay gene’. But the collection of variants seemed to have a small effect overall, explaining between 8% and 25% of heritability.

Next, the researchers used a computer algorithm to simulate human evolution over 60 generations. They found that the array of genetic variations associated with same-sex behaviour would have eventually disappeared, unless it somehow helped people to survive or reproduce.

Overlapping genes

Zietsch and his team decided to test whether these genetic patterns might provide an evolutionary edge by increasing a person’s number of sexual partners. They sorted the participants who had only had heterosexual sex by the number of partners they said they had had, and found that those with numerous partners tended to share some of the markers that the team had found in people who had had a same-sex partner.

The researchers also found that people who’d had same-sex encounters shared genetic markers with people who described themselves as risk-taking and open to new experiences. And there was a small overlap between heterosexual people who had genes linked to same-sex behaviour and those whom interviewers rated as physically attractive. Zietsch suggests that traits such as charisma and sex drive could also share genes that overlap with same-sex behaviour, but he says that those traits were not included in the data, so “we’re just guessing”.

The authors acknowledge . . .

Continue reading.

Written by Leisureguy

24 August 2021 at 2:59 pm

The Brain Doesn’t Think the Way You Think It Does

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Jordana Cepelewicz writes in Quanta:

Neuroscientists are the cartographers of the brain’s diverse domains and territories — the features and activities that define them, the roads and highways that connect them, and the boundaries that delineate them. Toward the front of the brain, just behind the forehead, is the prefrontal cortex, celebrated as the seat of judgment. Behind it lies the motor cortex, responsible for planning and coordinating movement. To the sides: the temporal lobes, crucial for memory and the processing of emotion. Above them, the somatosensory cortex; behind them, the visual cortex.

Not only do researchers often depict the brain and its functions much as mapmakers might draw nations on continents, but they do so “the way old-fashioned mapmakers” did, according to Lisa Feldman Barrett, a psychologist at Northeastern University. “They parse the brain in terms of what they’re interested in psychologically or mentally or behaviorally,” and then they assign the functions to different networks of neurons “as if they’re Lego blocks, as if there are firm boundaries there.”

But a brain map with neat borders is not just oversimplified — it’s misleading. “Scientists for over 100 years have searched fruitlessly for brain boundaries between thinking, feeling, deciding, remembering, moving and other everyday experiences,” Barrett said. A host of recent neurological studies further confirm that these mental categories “are poor guides for understanding how brains are structured or how they work.”

Neuroscientists generally agree about how the physical tissue of the brain is organized: into particular regions, networks, cell types. But when it comes to relating those to the task the brain might be performing — perception, memory, attention, emotion or action — “things get a lot more dodgy,” said David Poeppel, a neuroscientist at New York University.

No one disputes that the visual cortex enables sight, that the auditory cortex enables hearing, or that the hippocampus is essential for memory. Damage to those regions impairs those abilities, and researchers have identified mechanisms underlying them in those areas. But memory, for example, also requires brain networks other than the hippocampus, and the hippocampus is turning out to be key to a growing number of cognitive processes other than memory. Sometimes the degree of overlap is so great that the labels start to lose their meaning.

“The idea that there’s some kind of strong parallelism between mental categories that neuroscientists use to try and understand the brain and the neural implementation of mental events is just wrong,” Barrett said.

And while the current framework has led to important insights, “it’s gotten us stuck in certain traps that are really stifling research,” said Paul Cisek, a neuroscientist at the University of Montreal — an outcome that has also directly hobbled the development of treatments for neurological and psychological conditions.

That is why Barrett, Cisek and other scientists argue that for us to truly understand how the brain works, concepts at the field’s core may need to be revised, perhaps radically. As they grapple with that challenge, they are uncovering new ways to frame their questions about the brain, and new answers: This month alone, one such approach revealed an unexpected link between memory formation and metabolic regulation. But even if a new framework succeeds in explaining the brain’s operation, some researchers wonder whether the price of that success will be a loss of connection to our human experience.

‘More Aliases Than Sherlock Holmes’

When functional magnetic resonance imaging (fMRI) and other powerful technologies made it possible to examine living brains in increasingly sophisticated ways, neuroscientists enthusiastically started searching for the physical basis of our mental faculties. They made great strides in understanding the neural foundations of perception, attention, learning, memory, decision-making, motor control and other classic categories of mental activity.

But they also found unsettling evidence that those categories and the neural networks that support them don’t work as expected. It’s not just that the architecture of the brain disrespects the boundaries between the established mental categories. It’s that there’s so much overlap that a single brain network “has more aliases than Sherlock Holmes,” Barrett said.

Recent work has found, for instance, that two-thirds of the brain is involved in simple eye movements; meanwhile, half of the brain gets activated during respiration. In 2019, several teams of scientists found that most of the neural activity in “perception” areas such as the visual cortex was encoding information about the animals’ movements rather than sensory inputs.

This identity crisis isn’t limited to neural centers of perception or other cognitive functions. The cerebellum, a structure in the brains of all vertebrates, was thought to be dedicated almost exclusively to motor control, but scientists have found that it’s also instrumental in attention processes, the regulation of emotions, language processing and decision-making. The basal ganglia, another ancient part of the brain usually associated with motor control, has been similarly implicated in several high-level cognitive processes.

Some of these confusing results may come from methodological problems. To find where the human brain performs different functions, for instance, neuroscientists typically correlate cognitive processes with patterns of brain activity measured by fMRI. But studies suggest that researchers need to be more alert to irrelevant muscle twitches and fidgets that may contaminate the readings.

“You think that your results are telling you something about high-level cognition,” said György Buzsáki, a neuroscientist at the NYU School of Medicine, “when in fact, it may reflect nothing else except that, because of the task, [the subject’s] eyes are moving differently.”

But he and other scientists believe the recent findings also highlight a deeper conceptual problem in neuroscience. “We divide the real estate of the brain according to our preconceived ideas, assuming — wrongly, as far as I’m concerned — that those preconceived ideas have boundaries, and the same boundaries exist in brain function,” Buzsáki said.

In 2019, Russell Poldrack, a neuroscientist at Stanford University, and his colleagues set out to test how appropriate the recognized categories for mental function are. They gathered a massive amount of behavioral data — obtained from experiments designed to test different aspects of cognitive control, including working memory, response inhibition and learning — and ran it through a machine learning classifier. The resulting classifications defied expectations, mixing up  . . .

Continue reading. There’s more.

Written by Leisureguy

24 August 2021 at 2:26 pm

Posted in Daily life, Science

Eating a Hot Dog Shortens Your Life by 36 Minutes

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Note how efficient is the hot dog, how much leverage it brings: it shortens your life by an order of magnitude more than the time it takes to consume it, assuming you eat the hot dog in 3 minutes 36 seconds.

Nicolaus Li reports in Hypebeast:

According to a new study by University of Michigan researchers, eating a hot dog shortens your life by 36 minutes while a peanut butter and jelly sandwich adds 33 minutes to your life.

A nutritional index published by the School of Public Health, Department of Environmental Health Sciences in the Nature Food journal ranked 5,800 foods in the United States based on minutes gained or lost of “healthy” life per serving. With “healthy life gains” explained as an increase in “good-quality and disease-free life expectancy.” The Health Nutritional Index reveals that beef, processed meat, pork, lamb, cheese and sugar-based drinks cause the most healthy minutes lost, while nuts, fruits, vegetables and whole grains provide the most healthy minutes gained.

The Health Nutritional Index is based on harmful health effects tracked by a 2016 Global Burden of Disease study, along with information regarding the nutritional and environmental impact of foods. Aside from pushing for more conscious diets, the University of Michigan researchers behind the index note that the argument for plant-based versus animal-based foods cannot be generalized.

Head over to  . . .

Continue reading.

Written by Leisureguy

24 August 2021 at 2:14 pm

The Art of the Focus Pull

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Written by Leisureguy

24 August 2021 at 1:34 pm

Downsides of having wealth

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Carolyn Gregoire has an interesting article in Greater Good Magazine. It begins:

The term “affluenza”—a portmanteau of affluence and influenza, defined as a “painful, contagious, socially transmitted condition of overload, debt, anxiety, and waste, resulting from the dogged pursuit of more”—is often dismissed as a silly buzzword created to express our cultural disdain for consumerism. Though often used in jest, the term may contain more truth than many of us would like to think.

Whether affluenza is real or imagined, money really does change everything, as the song goes—and those of high social class do tend to see themselves much differently than others. Wealth (and the pursuit of it) has been linked with immoral behavior—and not just in movies like The Wolf of Wall Street.

sychologists who study the impact of wealth and inequality on human behavior have found that money can powerfully influence our thoughts and actions in ways that we’re often not aware of, no matter our economic circumstances. Although wealth is certainly subjective, most of the current research measures wealth on scales of income, job status, or socioeconomic circumstances, like educational attainment and intergenerational wealth.

Here are seven things you should know about the psychology of money and wealth.

More money, less empathy?

Several studies have shown that wealth may be at odds with empathy and compassion. Research published in the journal Psychological Science found that people of lower economic status were better at reading others’ facial expressions—an important marker of empathy—than wealthier people.

“A lot of what we see is a baseline orientation for the lower class to be more empathetic and the upper class to be less [so],” study co-author Michael Kraus told Time. “Lower-class environments are much different from upper-class environments. Lower-class individuals have to respond chronically to a number of vulnerabilities and social threats. You really need to depend on others so they will tell you if a social threat or opportunity is coming, and that makes you more perceptive of emotions.”

While a lack of resources fosters greater emotional intelligence, having more resources can cause bad behavior in its own right [cf. the Sackler family, owners of Purdue Pharmacy, who gained great wealth by actively promoting use of the opioids they made and sold — and who are determined to hang on to that money. – LG]. UC Berkeley research found that even fake money could make people behave with less regard for others. Researchers observed that when two students played Monopoly, one having been given a great deal more Monopoly money than the other, the wealthier player expressed initial discomfort, but then went on to act aggressively, taking up more space and moving his pieces more loudly, and even taunting the player with less money.

Wealth can cloud moral judgment.

It is no surprise in this post-2008 world to learn that wealth may cause a sense of moral entitlement. A UC Berkeley study found that in San Francisco—where the law requires that cars stop at crosswalks for pedestrians to pass—drivers of luxury cars were four times less likely than those in less expensive vehicles to stop and allow pedestrians the right of way. They were also more likely to cut off other drivers.

Another study suggested that merely thinking about money could lead to unethical behavior. Researchers from Harvard and the University of Utah found that study participants were more likely to lie or behave immorally after being exposed to money-related words.

“Even if we are well-intentioned, even if we think we know right from wrong, there may be factors influencing our decisions and behaviors that we’re not aware of,” University of Utah associate management professor Kristin Smith-Crowe, one of the study’s co-authors, told MarketWatch.

Wealth has been linked with addiction

While money itself doesn’t cause addiction or substance abuse, wealth has been linked with a higher susceptibility to addiction problems. A number of . . .

Continue reading. There’s much more.

People believe they possess wealth, but it’s more as though wealth possesses them. They must care for their wealth, protect it, and in general act as its servants, doing its bidding.

Written by Leisureguy

24 August 2021 at 12:54 pm

First Night on Planet Earth and Rockwell’s Model T2

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Exceptionally good shave today, I must say. First Night on Planet Earth (FNOPE) is a big “yes” for me: it’s a CK-6 soap (though also available at a lower cost in the Kokum Butter formulation, which is also excellent). I love the lather from CK-6 soaps — the consistency and glide and the way they nourish my skin — and FNOPE’s fragrance is extremely nice:

Top Notes: Raspberry, Pine Resin, Lavender, Basil, Bergamot, and Sicilian Cedrat
Middle Notes: Carnation, Leather, Sandalwood, Patchouli, and Geranium
Base Notes: Leather, Tonka Bean, Amber, Benzoin, Oakmoss, and Bourbon Vanilla Bean

The Edwin Jagger synthetic is a lot like the Mühle synthetics, and quite unlike the usual Plissoft/angelhair knots: coarser and more akin to the badger knots they aim to emulate. The lather was easily aroused — it’s a CK-6 soap — and lathering provided pleasure.

My T2 had quite a bit of blade feel on “3,” but withal it was quite comfortable — and by that, I never felt at risk from a nick, and also the razor is agile and easy to handle. Three passes easily spread smoothness over my face, and a splash of FNOPE aftershave — augmented with a squirt of Grooming Dept Hydrating Gel — finished the job.

My face feels extremely good right now — the skin not only smooth but softened and supple (because of, I imagine, the combined effects of Grooming Dept Moisturizing Pre-Shave, the ingredients in the CK-6 formula, the fine job the T2 did, and the aftershave-plus-hydrating-gel combo. 

What a fine way to start the day!

Written by Leisureguy

24 August 2021 at 8:31 am

Posted in Shaving

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