The Imperfect Nutritionist – by Jennifer Medhurst
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The idea of the “imperfect nutritionist” is to note that we’re all different with slightly different needs and sometimes very different preferences (or circumstances!) and having a truly perfect diet is probably a fool’s errand. Should we just give up, then? Not at all:
What we can do, Medhust argues, is find what’s best for us, realistically.
It’s better to have an 80% perfect diet 80% of the time, than to have a totally perfect diet for four and a half meals before running out of steam (and ingredients).
As for the “seven principles” mentioned in the title… we’re not going to keep those a mystery; they are:
- Focusing on wholefood
- Being diverse
- Knowing your fats
- Including fermented, prebiotic and probiotic foods
- Reducing refined carbohydrates
- Being aware of liquids
- Eating mindfully
The first part of the book is a treatise on how to implement those principles in your diet generally; the second part of the book is a recipe collection—70 recipes, with “these ingredients will almost certainly be available at your local supermarket” as a baseline. No instances of “the secret to being a good chef is knowing how to source fresh ingredients; ask your local greengrocer where to find spring-harvested perambulatory truffle-cones” here!
Basically, it focusses on adding healthy foods per your personal preferences and circumstances, and building these up into a repertoire of meals that will keep you and your family happy and healthy.
Pick Up Your Copy Of The Imperfect Nutritionist From Amazon Today!
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Why Do We Have Pores, And Could We Not?
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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
❝Do we really need pores, and why are they bigger on the face?❞
Pores secrete sweat or sebum (there are different kinds of pores for each).
If we didn’t have sweat pores, we’d be unable to sweat, which superficially may seem like a bonus, but it’d make us prone to overheating (like dogs, pigs, and other mammals that cannot sweat).
If we didn’t have sebum pores (usually called hair follicles, which are supplied by a sebaceous gland), we’d be completely hairless, and also unable to supply our skin with natural oils that keep it healthy. So we’d have no hair and very unhappy skin.
Which is ironic, because to believe beauty magazines, we must at all costs minimize our pores (and indeed, interventions like botox* can kill them).
*Let’s give that its full name though:
Suffice it to say, we do not recommend getting injected with neurotoxins unless it is truly necessary to ward off a greater harm.
As for being bigger on the face, they need not be, but sebaceous glands are more active and numerous there, being most active and numerous in the face/forehead—which is why oily skin is more likely to appear there than other parts of the body.
If your facial sebaceous glands are too active for your liking…
…there are ways to reduce that, a simple and relatively gentle way (relative, for example, botox) is with retinoids, including retinols or retinoic acids. Here’s some of the science of that; the paper is about treating acne, but the mechanism of action is the same (down-regulating the sebaceous glands’ action):
The potential side-effects, however were noted as:
- Cheilitis
- Desquamation of the skin
- Pruritus
Which, in translation from sciencese, means:
- Chapped lips
- Flaky skin
- Itchiness
Which aren’t necessarily fun, which is why with retinoids are best taken in very small doses at first to see how your skin reacts.
Remember when we said what your skin would be like without pores? This is what would happen, only much worse.
Take care!
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Prolonged Grief: A New Mental Disorder?
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The issue is not whether certain mental conditions are real—they are. It is how we conceptualize them and what we think treating them requires.
The latest edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) features a new diagnosis: prolonged grief disorder—used for those who, a year after a loss, still remain incapacitated by it. This addition follows more than a decade of debate. Supporters argued that the addition enables clinicians to provide much-needed help to those afflicted by what one might simply consider a too much of grief, whereas opponents insisted that one mustn’t unduly pathologize grief and reject an increasingly medicalized approach to a condition that they considered part of a normal process of dealing with loss—a process which in some simply takes longer than in others.
By including a condition in a professional classification system, we collectively recognize it as real. Recognizing hitherto unnamed conditions can help remove certain kinds of disadvantages. Miranda Fricker emphasizes this in her discussion of what she dubs hermeneutic injustice: a specific sort of epistemic injustice that affects persons in their capacity as knowers1. Creating terms like ‘post-natal depression’ and ‘sexual harassment’, Fricker argues, filled lacunae in the collectively available hermeneutic resources that existed where names for distinctive kinds of social experience should have been. The absence of such resources, Fricker holds, put those who suffered from such experiences at an epistemic disadvantage: they lacked the words to talk about them, understand them, and articulate how they were wronged. Simultaneously, such absences prevented wrong-doers from properly understanding and facing the harm they were inflicting—e.g. those who would ridicule or scold mothers of newborns for not being happier or those who would either actively engage in sexual harassment or (knowingly or not) support the societal structures that helped make it seem as if it was something women just had to put up with.
For Fricker, the hermeneutical disadvantage faced by those who suffer from an as-of-yet ill-understood and largely undiagnosed medical condition is not an epistemic injustice. Those so disadvantaged are not excluded from full participation in hermeneutic practices, or at least not through mechanisms of social coercion that arise due to some structural identity prejudice. They are not, in other words, hermeneutically marginalized, which for Fricker, is an essential characteristic of epistemic injustice. Instead, their situation is simply one of “circumstantial epistemic bad luck”2. Still, Fricker, too, can agree that providing labels for ill-understood conditions is valuable. Naming a condition helps raise awareness of it, makes it discursively available and, thus, a possible object of knowledge and understanding. This, in turn, can enable those afflicted by it to understand their experience and give those who care about them another way of nudging them into seeking help.
Surely, if adding prolonged grief disorder to the DSM-5 were merely a matter of recognizing the condition and of facilitating assistance, nobody should have any qualms with it. However, the addition also turns intense grief into a mental disorder—something for whose treatment insurance companies can be billed. With this, significant forces of interest enter the scene. The DSM-5, recall, is mainly consulted by psychiatrists. In contrast to talk-therapists like psychotherapists or psychoanalysts, psychiatrists constitute a highly medicalized profession, in which symptoms—clustered together as syndromes or disorders—are frequently taken to require drugs to treat them. Adding prolonged grief disorder thus heralds the advent of research into various drug-based grief therapies. Ellen Barry of the New York Times confirms this: “naltrexone, a drug used to help treat addiction,” she reports, “is currently in clinical trials as a form of grief therapy”, and we are likely to see a “competition for approval of medicines by the Food and Drug Administration.”3
Adding diagnoses to the DSM-5 creates financial incentives for players in the pharmaceutical industry to develop drugs advertised as providing relief to those so diagnosed. Surely, for various conditions, providing drug-induced relief from severe symptoms is useful, even necessary to enable patients to return to normal levels of functioning. But while drugs may help suppress feelings associated with intense grief, they cannot remove the grief. If all mental illnesses were brain diseases, they might be removed by adhering to some drug regimen or other. Note, however, that ‘mental illness’ is a metaphor that carries the implicit suggestion that just like physical illnesses, mental afflictions, too, are curable by providing the right kind of physical treatment. Unsurprisingly, this metaphor is embraced by those who stand to massively benefit from what profits they may reap from selling a plethora of drugs to those diagnosed with any of what seems like an ever-increasing number of mental disorders. But metaphors have limits. Lou Marinoff, a proponent of philosophical counselling, puts the point aptly:
Those who are dysfunctional by reason of physical illness entirely beyond their control—such as manic-depressives—are helped by medication. For handling that kind of problem, make your first stop a psychiatrist’s office. But if your problem is about identity or values or ethics, your worst bet is to let someone reify a mental illness and write a prescription. There is no pill that will make you find yourself, achieve your goals, or do the right thing.
Much more could be said about the differences between psychotherapy, psychiatry, and the newcomer in the field: philosophical counselling. Interested readers may benefit from consulting Marinoff’s work. Written in a provocative, sometimes alarmist style, it is both entertaining and—if taken with a substantial grain of salt—frequently insightful. My own view is this: from Fricker’s work, we can extract reasons to side with the proponents of adding prolonged grief disorder to the DSM-5. Creating hermeneutic resources that allow us to help raise awareness, promote understanding, and facilitate assistance is commendable. If the addition achieves that, we should welcome it. And yet, one may indeed worry that practitioners are too eager to move from the recognition of a mental condition to the implementation of therapeutic interventions that are based on the assumption that such afflictions must be understood on the model of physical disease. The issue is not whether certain mental conditions are real—they are. It is how we conceptualize them and what we think treating them requires.
No doubt, grief manifests physically. It is, however, not primarily a physical condition—let alone a brain disease. Grief is a distinctive mental condition. Apart from bouts of sadness, its symptoms typically include the loss of orientation or a sense of meaning. To overcome grief, we must come to terms with who we are or can be without the loved one’s physical presence in our life. We may need to reinvent ourselves, figure out how to be better again and whence to derive a new purpose. What is at stake is our sense of identity, our self-worth, and, ultimately, our happiness. Thinking that such issues are best addressed by popping pills puts us on a dangerous path, leading perhaps towards the kind of dystopian society Aldous Huxley imagined in his 1932 novel Brave New World. It does little to help us understand, let alone address, the moral and broader philosophical issues that trouble the bereaved and that lie at the root not just of prolonged grief but, arguably, of many so-called mental illnesses.
Footnotes:
1 For this and the following, cf. Fricker 2007, chapter 7.
2 Fricker 2007: 152
3 Barry 2022
References:
Barry, E. (2022). “How Long Should It Take to Grieve? Psychiatry Has Come Up With an Answer.” The New York Times, 03/18/2022, URL = https://www.nytimes.com/2022/03/18/health/prolonged-grief-
disorder.html [last access: 04/05/2022])
Fricker, M. (2007). Epistemic Injustice. Power & the Ethics of knowing. Oxford/New York: Oxford University Press.
Huxley, A. (1932). Brave New World. New York: Harper Brothers.
Marinoff, L. (1999). Plato, not Prozac! New York: HarperCollins Publishers.Professor Raja Rosenhagen is currently serving as Assistant Professor of Philosophy, Head of Department, and Associate Dean of Academic Affairs at Ashoka University. He earned his PhD in Philosophy from the University of Pittsburgh and has a broad range of philosophical interests (see here). He wrote this article a) because he was invited to do so and b) because he is currently nurturing a growing interest in philosophical counselling.
This article is republished from OpenAxis under a Creative Commons license. Read the original article.
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Bell Pepper vs Sweetcorn – Which is Healthier?
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Our Verdict
When comparing bell pepper to sweetcorn, we picked the corn.
Why?
If you’re thinking “but wait, which color bell pepper, don’t they have different nutritional properties?” then firstly, well-remembered, and secondly, it doesn’t matter in this case. The main things that it affects are vitamins A and C and various polyphenols, and even the weakest bell pepper for them wins on both of those vitamins (while the strongest bell peppers for them still lose on vitamins in total) and even the strongest bell pepper for them loses on polyphenols, so the results go the same with any color.
In terms of macros, the corn has more carbs, protein, and fiber; however, both are low in glycemic index, so we’ll go with the “more food per food” option, the corn.
In the category of vitamins, even green bell peppers (the least well-endowed) have more of vitamins A, B6, C, E, and K, while sweetcorn has more of vitamins B1, B2, B3, B5, B9, and choline, compared to even yellow or red bell peppers (which are the best peppers for vitamins). So, a moderate win for the corn.
When it comes to minerals, bell peppers have more calcium and copper, while sweetcorn has more iron, magnesium, manganese, phosphorus, potassium, selenium, and zinc. An easy win for sweetcorn.
In short, enjoy both, but the corn is the overall winner today!
Want to learn more?
You might like to read:
- Brain Food? The Eyes Have It! ← green bell peppers are a good source of lutein, as is sweetcorn
- A Spectrum Of Specialties: Which Bell Peppers To Pick?
Take care!
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Five Supplements That Actually Work Vs Arthritis
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This is Dr. Diana Girnita, a double board-certified physician (internal medicine & rheumatology) who, in addition to her MD, also has a PhD in immunology—bearing in mind that rheumatoid arthritis is an autoimmune condition.
Her mission is to help people with any form of arthritis (rheumatoid or otherwise) and those with many non-arthritic autoimmune conditions (ranging from tendonitis to lupus) to live better.
Today, we’ll be looking at her recommendations of 5 supplements that actually help alleviate arthritis:
Collagen
Collagen famously supports skin, nails, bones, and joint cartilage; Dr. Girnita advises that it’s particularly beneficial for osteoarthritis.
Specifically, she recommends either collagen peptides or hydrolyzed collagen, as they are most absorbable. However, collagen can also be sourced from foods like bone broth, fish with skin and bones, and gelatin-based foods.
If you’re vegetarian/vegan, then it becomes important to simply consume the ingredients for collagen, because like most animals, we can synthesize it ourselves provided we get the necessary nutrients. For more on that, see:
We Are Such Stuff As Fish Are Made Of
Glucosamine & chondroitin
Technically two things, but almost always sold/taken together. Naturally found in joint cartilage, it can slow cartilage breakdown and reduce pain in osteoarthritis.
Studies show pain relief, especially in moderate-to-severe cases; best taken long-term. Additionally, it’s a better option than NSAIDs for patients with heart or gastrointestinal issues.
10almonds tip: something that’s tricker to find as a supplement than glucosamine and chondroitin, but you might want to check it out:
Cucumber Extract Beats Glucosamine & Chondroitin… At 1/135th Of The Dose?!
Omega-3 fatty acids
Dr. Girnita recommends this one because unlike the above recommendations that mainly help reduce/reverse the joint damage itself, omega-3 reduces inflammation, pain, and stiffness, and can decrease or eliminate the need for NSAIDs in rheumatoid arthritis and psoriatic arthritis.
She recommends 2-4g EPA/DHA daily; ideally taken with a meal for better absorption.
She also recommends to look for mercury-free options—algae-derived are usually better than fish-derived, but check for certification either way! See also:
What Omega-3 Fatty Acids Really Do For Us
Boswellia serrata (frankincense)
Popularly enjoyed as an incense but also available in supplement form, it contains boswellic acid, which reduces inflammation and cartilage damage.
Dr. Girnita recommends 100 mg daily, but advises that it may interact with some antidepressants, anti-anxiety medications, and NSAIDs—so speak with your pharmacist/doctor if unsure.
We also wrote about this one here:
Science-Based Alternative Pain Relief
Curcumin (turmeric)
Well-known for its potent anti-inflammatory properties, it’s comparable to NSAIDs in pain relief for most common forms of arthritis.
Dr. Girnita recommends 1–1.5g of curcumin daily, ideally combined with black pepper for better absorption:
Why Curcumin (Turmeric) Is Worth Its Weight In Gold
Lastly…
Dr. Girnita advises to not blindly trust supplements, but rather, to test them for 2–3 months while keeping a journal of your symptoms. If it improves things for you, keep it up, if not, discontinue. Humans can be complicated and not everything will work exactly the same way for everyone!
For more on dealing with chronic pain specifically, by the way, check out:
Managing Chronic Pain (Realistically!)
Take care!
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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.
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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Overcoming Gravity – by Steven Low
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The author, a professional gymnast and coach with a background in the sciences, knows his stuff here. This is what it says on the tin: it’s rigorously systematic. It’s also the most science-based calisthenics book this reviewer has read to date.
If you just wanted to know how to do some exercises, then this book would be very much overkill, but if you want to be able to go from no knowledge to expert knowledge, then the nearly 600 pages of this weighty tome will do that for you.
This is a textbook, it’s a “the bible of…” style book, it’s the one that if you’re serious, will engage you thoroughly and enable you to craft the calisthenics-forged body you want, head to toe.
As if it weren’t already overdelivering, it also has plenty of information on injury avoidance (or injury/condition management if you have some existing injury or chronic condition), and building routines in a dynamic fashion that avoids becoming a grind, because it’s going from strength to strength while cycling through different body parts.
Bottom line: if you’d like to get serious about calisthenics, then this is the book for you.
Click here to check out Overcoming Gravity, and do just that!
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