Tuna vs Catfish – Which is Healthier?

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Our Verdict

When comparing tuna to catfish, we picked the tuna.

Why?

Today in “that which is more expensive and/or harder to get is not necessarily healthier”…

Looking at their macros, tuna has more protein and less fat (and overall, less saturated fat, and also less cholesterol).

In the category of vitamins, both are good but tuna distinguishes itself: tuna has more of vitamins A, B1, B2, B3, B6, and D, while catfish has more of vitamins B5, B9, B12, E, and K. They are both approximately equal in choline, and as an extra note in tuna’s favor (already winning 6:5), tuna is a very good source of vitamin D, while catfish barely contains any. All in all: a moderate, but convincing, win for tuna.

When it comes to minerals, things are clearer still: tuna has more copper, iron, magnesium, phosphorus, potassium, and selenium, while catfish has more calcium, manganese, and zinc. Oh, and catfish is also higher in one other mineral: sodium, which most people in industrialized countries need less of, on average. So, a 6:3 win for tuna, before we even take into account the sodium content (which makes the win for tuna even stronger).

In short: tuna wins the day in every category!

Want to learn more?

You might like to read:

Farmed Fish vs Wild Caught (It Makes Quite A Difference)

Take care!

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  • Could not getting enough sleep increase your risk of type 2 diabetes?

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    Not getting enough sleep is a common affliction in the modern age. If you don’t always get as many hours of shut-eye as you’d like, perhaps you were concerned by news of a recent study that found people who sleep less than six hours a night are at higher risk of type 2 diabetes.

    So what can we make of these findings? It turns out the relationship between sleep and diabetes is complex.

    The study

    Researchers analysed data from the UK Biobank, a large biomedical database which serves as a global resource for health and medical research. They looked at information from 247,867 adults, following their health outcomes for more than a decade.

    The researchers wanted to understand the associations between sleep duration and type 2 diabetes, and whether a healthy diet reduced the effects of short sleep on diabetes risk.

    As part of their involvement in the UK Biobank, participants had been asked roughly how much sleep they get in 24 hours. Seven to eight hours was the average and considered normal sleep. Short sleep duration was broken up into three categories: mild (six hours), moderate (five hours) and extreme (three to four hours). The researchers analysed sleep data alongside information about people’s diets.

    Some 3.2% of participants were diagnosed with type 2 diabetes during the follow-up period. Although healthy eating habits were associated with a lower overall risk of diabetes, when people ate healthily but slept less than six hours a day, their risk of type 2 diabetes increased compared to people in the normal sleep category.

    The researchers found sleep duration of five hours was linked with a 16% higher risk of developing type 2 diabetes, while the risk for people who slept three to four hours was 41% higher, compared to people who slept seven to eight hours.

    One limitation is the study defined a healthy diet based on the number of servings of fruit, vegetables, red meat and fish a person consumed over a day or a week. In doing so, it didn’t consider how dietary patterns such as time-restricted eating or the Mediterranean diet may modify the risk of diabetes among those who slept less.

    Also, information on participants’ sleep quantity and diet was only captured at recruitment and may have changed over the course of the study. The authors acknowledge these limitations.

    Why might short sleep increase diabetes risk?

    In people with type 2 diabetes, the body becomes resistant to the effects of a hormone called insulin, and slowly loses the capacity to produce enough of it in the pancreas. Insulin is important because it regulates glucose (sugar) in our blood that comes from the food we eat by helping move it to cells throughout the body.

    We don’t know the precise reasons why people who sleep less may be at higher risk of type 2 diabetes. But previous research has shown sleep-deprived people often have increased inflammatory markers and free fatty acids in their blood, which impair insulin sensitivity, leading to insulin resistance. This means the body struggles to use insulin properly to regulate blood glucose levels, and therefore increases the risk of type 2 diabetes.

    Further, people who don’t sleep enough, as well as people who sleep in irregular patterns (such as shift workers), experience disruptions to their body’s natural rhythm, known as the circadian rhythm.

    This can interfere with the release of hormones like cortisol, glucagon and growth hormones. These hormones are released through the day to meet the body’s changing energy needs, and normally keep blood glucose levels nicely balanced. If they’re compromised, this may reduce the body’s ability to handle glucose as the day progresses.

    These factors, and others, may contribute to the increased risk of type 2 diabetes seen among people sleeping less than six hours.

    A man checking the glucose monitor on his arm.
    Millions of people around the world have diabetes. WESTOCK PRODUCTIONS/Shutterstock

    While this study primarily focused on people who sleep eight hours or less, it’s possible longer sleepers may also face an increased risk of type 2 diabetes.

    Research has previously shown a U-shaped correlation between sleep duration and type 2 diabetes risk. A review of multiple studies found getting between seven to eight hours of sleep daily was associated with the lowest risk. When people got less than seven hours sleep, or more than eight hours, the risk began to increase.

    The reason sleeping longer is associated with increased risk of type 2 diabetes may be linked to weight gain, which is also correlated with longer sleep. Likewise, people who don’t sleep enough are more likely to be overweight or obese.

    Good sleep, healthy diet

    Getting enough sleep is an important part of a healthy lifestyle and may reduce the risk of type 2 diabetes.

    Based on this study and other evidence, it seems that when it comes to diabetes risk, seven to eight hours of sleep may be the sweet spot. However, other factors could influence the relationship between sleep duration and diabetes risk, such as individual differences in sleep quality and lifestyle.

    While this study’s findings question whether a healthy diet can mitigate the effects of a lack of sleep on diabetes risk, a wide range of evidence points to the benefits of healthy eating for overall health.

    The authors of the study acknowledge it’s not always possible to get enough sleep, and suggest doing high-intensity interval exercise during the day may offset some of the potential effects of short sleep on diabetes risk.

    In fact, exercise at any intensity can improve blood glucose levels.

    Giuliana Murfet, Casual Academic, Faculty of Health, University of Technology Sydney and ShanShan Lin, Senior Lecturer, School of Public Health, University of Technology Sydney

    This article is republished from The Conversation under a Creative Commons license. Read the original article.

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  • Gluten: What’s The Truth?

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    Gluten: What’s The Truth?

    We asked you for your health-related view of gluten, and got the above spread of results. To put it simply:

    Around 60% of voters voted for “Gluten is bad if you have an allergy/sensitivity; otherwise fine

    The rest of the votes were split fairly evenly between the other three options:

    • Gluten is bad for everyone and we should avoid it
    • Gluten is bad if (and only if) you have Celiac disease
    • Gluten is fine for all, and going gluten-free is a modern fad

    First, let’s define some terms so that we’re all on the same page:

    What is gluten?

    Gluten is a category of protein found in wheat, barley, rye, and triticale. As such, it’s not one single compound, but a little umbrella of similar compounds. However, for the sake of not making this article many times longer, we’re going to refer to “gluten” without further specification.

    What is Celiac disease?

    Celiac disease is an autoimmune disease. Like many autoimmune diseases, we don’t know for sure how/why it occurs, but a combination of genetic and environmental factors have been strongly implicated, with the latter putatively including overexposure to gluten.

    It affects about 1% of the world’s population, and people with Celiac disease will tend to respond adversely to gluten, notably by inflammation of the small intestine and destruction of enterocytes (the cells that line the wall of the small intestine). This in turn causes all sorts of other problems, beyond the scope of today’s main feature, but suffice it to say, it’s not pleasant.

    What is an allergy/intolerance/sensitivity?

    This may seem basic, but a lot of people conflate allergy/intolerance/sensitivity, so:

    • An allergy is when the body mistakes a harmless substance for something harmful, and responds inappropriately. This can be mild (e.g. allergic rhinitis, hayfever) or severe (e.g. peanut allergy), and as such, responses can vary from “sniffly nose” to “anaphylactic shock and death”.
      • In the case of a wheat allergy (for example), this is usually somewhere between the two, and can for example cause breathing problems after ingesting wheat or inhaling wheat flour.
    • An intolerance is when the body fails to correctly process something it should be able to process, and just ejects it half-processed instead.
      • A common and easily demonstrable example is lactose intolerance. There isn’t a well-defined analog for gluten, but gluten intolerance is nonetheless a well-reported thing.
    • A sensitivity is when none of the above apply, but the body nevertheless experiences unpleasant symptoms after exposure to a substance that should normally be safe.
      • In the case of gluten, this is referred to as non-Celiac gluten sensitivity

    A word on scientific objectivity: at 10almonds we try to report science as objectively as possible. Sometimes people have strong feelings on a topic, especially if it is polarizing.

    Sometimes people with a certain condition feel constantly disbelieved and mocked; sometimes people without a certain condition think others are imagining problems for themselves where there are none.

    We can’t diagnose anyone or validate either side of that, but what we can do is report the facts as objectively as science can lay them out.

    Gluten is fine for all, and going gluten-free is a modern fad: True or False?

    Definitely False, Celiac disease is a real autoimmune disease that cannot be faked, and allergies are also a real thing that people can have, and again can be validated in studies. Even intolerances have scientifically measurable symptoms and can be tested against nocebo.

    See for example:

    However! It may not be a modern fad, so much as a modern genuine increase in incidence.

    Widespread varieties of wheat today contain a lot more gluten than wheat of ages past, and many other molecular changes mean there are other compounds in modern grains that never even existed before.

    However, the health-related impact of these (novel proteins and carbohydrates) is currently still speculative, and we are not in the business of speculating, so we’ll leave that as a “this hasn’t been studied enough to comment yet but we recognize it could potentially be a thing” factor.

    Gluten is bad if (and only if) you have Celiac disease: True or False?

    Definitely False; allergies for example are well-evidenced as real; same facts as we discussed/linked just above.

    Gluten is bad for everyone and we should avoid it: True or False?

    False, tentatively and contingently.

    First, as established, there are people with clinically-evidenced Celiac disease, wheat allergy, or similar. Obviously, they should avoid triggering those diseases.

    What about the rest of us, and what about those who have non-Celiac gluten sensitivity?

    Clinical testing has found that of those reporting non-Celiac gluten sensitivity, nocebo-controlled studies validate that diagnosis in only a minority of cases.

    In the following study, for example, only 16% of those reporting symptoms showed them in the trials, and 40% of those also showed a nocebo response (i.e., like placebo, but a bad rather than good effect):

    Suspected Nonceliac Gluten Sensitivity Confirmed in Few Patients After Gluten Challenge in Double-Blind, Placebo-Controlled Trials

    This one, on the other hand, found that positive validations of diagnoses were found to be between 7% and 77%, depending on the trial, with an average of 30%:

    Re-challenge Studies in Non-celiac Gluten Sensitivity: A Systematic Review and Meta-Analysis

    In other words: non-Celiac gluten sensitivity is a thing, and/but may be over-reported, and/but may be in some part exacerbated by psychosomatic effect.

    Note: psychosomatic effect does not mean “imagining it” or “all in your head”. Indeed, the “soma” part of the word “psychosomatic” has to do with its measurable effect on the rest of the body.

    For example, while pain can’t be easily objectively measured, other things, like inflammation, definitely can.

    As for everyone else? If you’re enjoying your wheat (or similar) products, it’s well-established that they should be wholegrain for the best health impact (fiber, a positive for your health, rather than white flour’s super-fast metabolites padding the liver and causing metabolic problems).

    Wheat itself may have other problems, for example FODMAPs, amylase trypsin inhibitors, and wheat germ agglutinins, but that’s “a wheat thing” rather than “a gluten thing”.

    That’s beyond the scope of today’s main feature, but you might want to check out today’s featured book!

    For a final scientific opinion on this last one, though, here’s what a respected academic journal of gastroenterology has to say:

    From coeliac disease to noncoeliac gluten sensitivity; should everyone be gluten-free?

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  • Make Overnight Oats Shorter Or Longer For Different Benefits!

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    It’s Q&A Day at 10almonds!

    Have a question or a request? We love to hear from you!

    In cases where we’ve already covered something, we might link to what we wrote before, but will always be happy to revisit any of our topics again in the future too—there’s always more to say!

    As ever: if the question/request can be answered briefly, we’ll do it here in our Q&A Thursday edition. If not, we’ll make a main feature of it shortly afterwards!

    So, no question/request too big or small

    ❝How long do I have to soak oats for to get the benefits of “overnight oats”?❞

    The primary benefit of overnight oats (over cooked oats) is that they are soft enough to eat without having been cooked (as cooking increases their glycemic index).

    So, if it’s soft, it’s good to eat. A few hours should be sufficient.

    Bonus information

    If, by the way, you happen to leave oats and milk (be it animal or plant milk) sealed in a jar at room temperature for a 2–3 days (less if your “room temperature” is warmer than average), it will start to ferment.

    • Good news: fermentation can bring extra health benefits!
    • Bad news: you’re on your own if something pathogenic is present

    For more on this, you might like to read:

    Fermenting Everything: How to Make Your Own Cultured Butter, Fermented Fish, Perfect Kimchi, and Beyond

    Enjoy!

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  • Insights into Osteoporosis

    10almonds is reader-supported. We may, at no cost to you, receive a portion of sales if you purchase a product through a link in this article.

    It’s Q&A Day at 10almonds!

    Have a question or a request? You can always hit “reply” to any of our emails, or use the feedback widget at the bottom!

    In cases where we’ve already covered something, we might link to what we wrote before, but will always be happy to revisit any of our topics again in the future too—there’s always more to say!

    As ever: if the question/request can be answered briefly, we’ll do it here in our Q&A Thursday edition. If not, we’ll make a main feature of it shortly afterwards!

    So, no question/request too big or small

    ❝I would like to see some articles on osteoporosis❞

    You might enjoy this mythbusting main feature we did a few weeks ago!

    The Bare-Bones Truth About Osteoporosis

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  • How to Eat to Change How You Drink – by Dr. Brooke Scheller

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    Whether you want to stop drinking or just cut down, this book can help. But what makes it different from the other reduce/stop drinking books we’ve reviewed?

    Mostly, it’s about nutrition. This book focuses on the way that alcohol changes our relationship to food, our gut, our blood sugars, and more. The author also explains how reducing/stopping drinking, without bearing these things in mind, can be unnecessarily extra hard.

    The remedy? To bear them in mind, of course, but that requires knowing them. So what she does is explain the physiology of what’s going on in terms of each of the above things (and more), and how to adjust your diet to make up for what alcohol has been doing to you, so that you can reduce/quit without feeling constantly terrible.

    The style is very pop-science, light in tone, readable. She makes reference to a lot of hard science, but doesn’t discuss it in more depth than is necessary to convey the useful information. So, this is a practical book, aimed at all people who want to reduce/quit drinking.

    Bottom line: if you feel like it’s hard to drink less because it feels like something is missing, it’s probably because indeed something is missing, and this book can help you bridge that gap!

    Click here to check out How To Eat To Change How You Drink, and do just that!

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  • Can a drug like Ozempic help treat addictions to alcohol, opioids or other substances?

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    Semaglutide (sold as Ozempic, Wegovy and Rybelsus) was initially developed to treat diabetes. It works by stimulating the production of insulin to keep blood sugar levels in check.

    This type of drug is increasingly being prescribed for weight loss, despite the fact it was initially approved for another purpose. Recently, there has been growing interest in another possible use: to treat addiction.

    Anecdotal reports from patients taking semaglutide for weight loss suggest it reduces their appetite and craving for food, but surprisingly, it also may reduce their desire to drink alcohol, smoke cigarettes or take other drugs.

    But does the research evidence back this up?

    Animal studies show positive results

    Semaglutide works on glucagon-like peptide-1 receptors and is known as a “GLP-1 agonist”.

    Animal studies in rodents and monkeys have been overwhelmingly positive. Studies suggest GLP-1 agonists can reduce drug consumption and the rewarding value of drugs, including alcohol, nicotine, cocaine and opioids.

    Out team has reviewed the evidence and found more than 30 different pre-clinical studies have been conducted. The majority show positive results in reducing drug and alcohol consumption or cravings. More than half of these studies focus specifically on alcohol use.

    However, translating research evidence from animal models to people living with addiction is challenging. Although these results are promising, it’s still too early to tell if it will be safe and effective in humans with alcohol use disorder, nicotine addiction or another drug dependence.

    What about research in humans?

    Research findings are mixed in human studies.

    Only one large randomised controlled trial has been conducted so far on alcohol. This study of 127 people found no difference between exenatide (a GLP-1 agonist) and placebo (a sham treatment) in reducing alcohol use or heavy drinking over 26 weeks.

    In fact, everyone in the study reduced their drinking, both people on active medication and in the placebo group.

    However, the authors conducted further analyses to examine changes in drinking in relation to weight. They found there was a reduction in drinking for people who had both alcohol use problems and obesity.

    For people who started at a normal weight (BMI less than 30), despite initial reductions in drinking, they observed a rebound increase in levels of heavy drinking after four weeks of medication, with an overall increase in heavy drinking days relative to those who took the placebo.

    There were no differences between groups for other measures of drinking, such as cravings.

    Man shops for alcohol

    Some studies show a rebound increase in levels of heavy drinking. Deman/Shutterstock

    In another 12-week trial, researchers found the GLP-1 agonist dulaglutide did not help to reduce smoking.

    However, people receiving GLP-1 agonist dulaglutide drank 29% less alcohol than those on the placebo. Over 90% of people in this study also had obesity.

    Smaller studies have looked at GLP-1 agonists short-term for cocaine and opioids, with mixed results.

    There are currently many other clinical studies of GLP-1 agonists and alcohol and other addictive disorders underway.

    While we await findings from bigger studies, it’s difficult to interpret the conflicting results. These differences in treatment response may come from individual differences that affect addiction, including physical and mental health problems.

    Larger studies in broader populations of people will tell us more about whether GLP-1 agonists will work for addiction, and if so, for whom.

    How might these drugs work for addiction?

    The exact way GLP-1 agonists act are not yet well understood, however in addition to reducing consumption (of food or drugs), they also may reduce cravings.

    Animal studies show GLP-1 agonists reduce craving for cocaine and opioids.

    This may involve a key are of the brain reward circuit, the ventral striatum, with experimenters showing if they directly administer GLP-1 agonists into this region, rats show reduced “craving” for oxycodone or cocaine, possibly through reducing drug-induced dopamine release.

    Using human brain imaging, experimenters can elicit craving by showing images (cues) associated with alcohol. The GLP-1 agonist exenatide reduced brain activity in response to an alcohol cue. Researchers saw reduced brain activity in the ventral striatum and septal areas of the brain, which connect to regions that regulate emotion, like the amygdala.

    In studies in humans, it remains unclear whether GLP-1 agonists act directly to reduce cravings for alcohol or other drugs. This needs to be directly assessed in future research, alongside any reductions in use.

    Are these drugs safe to use for addiction?

    Overall, GLP-1 agonists have been shown to be relatively safe in healthy adults, and in people with diabetes or obesity. However side effects do include nausea, digestive troubles and headaches.

    And while some people are OK with losing weight as a side effect, others aren’t. If someone is already underweight, for example, this drug might not be suitable for them.

    In addition, very few studies have been conducted in people with addictive disorders. Yet some side effects may be more of an issue in people with addiction. Recent research, for instance, points to a rare risk of pancreatitis associated with GLP-1 agonists, and people with alcohol use problems already have a higher risk of this disorder.

    Other drugs treatments are currently available

    Although emerging research on GLP-1 agonists for addiction is an exciting development, much more research needs to be done to know the risks and benefits of these GLP-1 agonists for people living with addiction.

    In the meantime, existing effective medications for addiction remain under-prescribed. Only about 3% of Australians with alcohol dependence, for example, are prescribed medication treatments such as like naltrexone, acamprosate or disulfiram. We need to ensure current medication treatments are accessible and health providers know how to prescribe them.

    Continued innovation in addiction treatment is also essential. Our team is leading research towards other individualised and effective medications for alcohol dependence, while others are investigating treatments for nicotine addiction and other drug dependence.

    Read the other articles in The Conversation’s Ozempic series here.

    Shalini Arunogiri, Addiction Psychiatrist, Associate Professor, Monash University; Leigh Walker, , Florey Institute of Neuroscience and Mental Health, and Roberta Anversa, , The University of Melbourne

    This article is republished from The Conversation under a Creative Commons license. Read the original article.

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