What’s the difference between physical and chemical sunscreens? And which one should you choose?
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Sun exposure can accelerate ageing, cause skin burns, erythema (a skin reaction), skin cancer, melasmas (or sun spots) and other forms of hyperpigmentation – all triggered by solar ultraviolet radiation.
Approximately 80% of skin cancer cases in people engaged in outdoor activities are preventable by decreasing sun exposure. This can be done in lots of ways including wearing protective clothing or sunscreens.
But not all sunscreens work in the same way. You might have heard of “physical” and “chemical” sunscreens. What’s the difference and which one is right for you?
How sunscreens are classified
Sunscreens are grouped by their use of active inorganic and organic ultraviolet (UV) filters. Chemical sunscreens use organic filters such as cinnamates (chemically related to cinnamon oil) and benzophenones. Physical sunscreens (sometimes called mineral sunscreens) use inorganic filters such as titanium and zinc oxide.
These filters prevent the effects of UV radiation on the skin.
Organic UV filters are known as chemical filters because the molecules in them change to stop UV radiation reaching the skin. Inorganic UV filters are known as physical filters, because they work through physical means, such as blocking, scattering and reflection of UV radiation to prevent skin damage.
Nano versus micro
The effectiveness of the filters in physical sunscreen depends on factors including the size of the particle, how it’s mixed into the cream or lotion, the amount used and the refraction index (the speed light travels through a substance) of each filter.
When the particle size in physical sunscreens is large, it causes the light to be scattered and reflected more. That means physical sunscreens can be more obvious on the skin, which can reduce their cosmetic appeal.
Nanoparticulate forms of physical sunscreens (with tiny particles smaller than 100 nanometers) can improve the cosmetic appearance of creams on the skin and UV protection, because the particles in this size range absorb more radiation than they reflect. These are sometimes labelled as “invisible” zinc or mineral formulations and are considered safe.
So how do chemical sunscreens work?
Chemical UV filters work by absorbing high-energy UV rays. This leads to the filter molecules interacting with sunlight and changing chemically.
When molecules return to their ground (or lower energy) state, they release energy as heat, distributed all over the skin. This may lead to uncomfortable reactions for people with skin sensitivity.
Generally, UV filters are meant to stay on the epidermis (the first skin layer) surface to protect it from UV radiation. When they enter into the dermis (the connective tissue layer) and bloodstream, this can lead to skin sensitivity and increase the risk of toxicity. The safety profile of chemical UV filters may depend on whether their small molecular size allows them to penetrate the skin.
Chemical sunscreens, compared to physical ones, cause more adverse reactions in the skin because of chemical changes in their molecules. In addition, some chemical filters, such as dibenzoylmethane tend to break down after UV exposure. These degraded products can no longer protect the skin against UV and, if they penetrate the skin, can cause cell damage.
Due to their stability – that is, how well they retain product integrity and effectiveness when exposed to sunlight – physical sunscreens may be more suitable for children and people with skin allergies.
Although sunscreen filter ingredients can rarely cause true allergic dermatitis, patients with photodermatoses (where the skin reacts to light) and eczema have higher risk and should take care and seek advice.
What to look for
The best way to check if you’ll have a reaction to a physical or chemical sunscreen is to patch test it on a small area of skin.
And the best sunscreen to choose is one that provides broad-spectrum protection, is water and sweat-resistant, has a high sun protection factor (SPF), is easy to apply and has a low allergy risk.
Health authorities recommend sunscreen to prevent sun damage and cancer. Chemical sunscreens have the potential to penetrate the skin and may cause irritation for some people. Physical sunscreens are considered safe and effective and nanoparticulate formulations can increase their appeal and ease of use.
Yousuf Mohammed, Dermatology researcher, The University of Queensland and Khanh Phan, Postdoctoral research associate, Frazer Institute, The University of Queensland
This article is republished from The Conversation under a Creative Commons license. Read the original article.
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Reasons to Stay Alive – by Matt Haig
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We’ve previously reviewed Matt Haig’s (excellent) The Comfort Book, and now it’s time for his more famous book: Reasons To Stay Alive. So, what’s this one, beyond the obvious?
It narrates the experience of anxiety, depression, and suicidality, and discovering how to find beauty and joy in the world despite it all. It’s not that the author found a magical cure—he still experiences depression and anxiety (cannot speak for suicidality) but he knows now how to manage it, and live his life.
You may be wondering: is this book instructional; is it reproducible, or is it just an autobiography? It’s centered around his own experience and learnings, but it gives a huge sense of not feeling alone, of having hope, and it gives a template for making sense of one’s own experience, even if every person will of course have some points of differences, the commonalities are nonetheless of immense value.
The writing style is similar to The Comfort Book; it’s lots of small chapters, and all very easy-reading. Well, the subject matter is sometimes rather heavy, but the language is easy-reading! In other words, just the thing for when one is feeling easily overwhelmed, or not feeling up to reading a lot.
Bottom line: whether or not you suffer with anxiety and/or depression, whether or not you sometimes feel suicidal, the contents of this book are important, valuable insights for everyone.
Click here to check out Reasons To Stay Alive, and see through the highs and lows of life.
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Is alcohol good or bad for you? Yes.
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This article originally appeared in Harvard Public Health magazine.
It’s hard to escape the message these days that every sip of wine, every swig of beer is bad for your health. The truth, however, is far more nuanced.
We have been researching the health effects of alcohol for a combined 60 years. Our work, and that of others, has shown that even modest alcohol consumption likely raises the risk for certain diseases, such as breast and esophageal cancer. And heavy drinking is unequivocally harmful to health. But after countless studies, the data do not justify sweeping statements about the effects of moderate alcohol consumption on human health.
Yet we continue to see reductive narratives, in the media and even in science journals, that alcohol in any amount is dangerous. Earlier this month, for instance, the media reported on a new study that found even small amounts of alcohol might be harmful. But the stories failed to give enough context or probe deeply enough to understand the study’s limitations—including that it cherry-picked subgroups of a larger study previously used by researchers, including one of us, who concluded that limited drinking in a recommended pattern correlated with lower mortality risk.
“We need more high-quality evidence to assess the health impacts of moderate alcohol consumption. And we need the media to treat the subject with the nuance it requires. Newer studies are not necessarily better than older research.”
Those who try to correct this simplistic view are disparaged as pawns of the industry, even when no financial conflicts of interest exist. Meanwhile, some authors of studies suggesting alcohol is unhealthy have received money from anti-alcohol organizations.
We believe it’s worth trying, again, to set the record straight. We need more high-quality evidence to assess the health impacts of moderate alcohol consumption. And we need the media to treat the subject with the nuance it requires. Newer studies are not necessarily better than older research.
It’s important to keep in mind that alcohol affects many body systems—not just the liver and the brain, as many people imagine. That means how alcohol affects health is not a single question but the sum of many individual questions: How does it affect the heart? The immune system? The gut? The bones?
As an example, a highly cited study of one million women in the United Kingdom found that moderate alcohol consumption—calculated as no more than one drink a day for a woman—increased overall cancer rates. That was an important finding. But the increase was driven nearly entirely by breast cancer. The same study showed that greater alcohol consumption was associated with lower rates of thyroid cancer, non-Hodgkin lymphoma, and renal cell carcinoma. That doesn’t mean drinking a lot of alcohol is good for you—but it does suggest that the science around alcohol and health is complex.
One major challenge in this field is the lack of large, long-term, high-quality studies. Moderate alcohol consumption has been studied in dozens of randomized controlled trials, but those trials have never tracked more than about 200 people for more than two years. Longer and larger experimental trials have been used to test full diets, like the Mediterranean diet, and are routinely conducted to test new pharmaceuticals (or new uses for existing medications), but they’ve never been done to analyze alcohol consumption.
Instead, much alcohol research is observational, meaning it follows large groups of drinkers and abstainers over time. But observational studies cannot prove cause-and-effect because moderate drinkers differ in many ways from non-drinkers and heavy drinkers—in diet, exercise, and smoking habits, for instance. Observational studies can still yield useful information, but they also require researchers to gather data about when and how the alcohol is consumed, since alcohol’s effect on health depends heavily on drinking patterns.
For example, in an analysis of over 300,000 drinkers in the U.K., one of us found that the same total amount of alcohol appeared to increase the chances of dying prematurely if consumed on fewer occasions during the week and outside of meals, but to decrease mortality if spaced out across the week and consumed with meals. Such nuance is rarely captured in broader conversations about alcohol research—or even in observational studies, as researchers don’t always ask about drinking patterns, focusing instead on total consumption. To get a clearer picture of the health effects of alcohol, researchers and journalists must be far more attuned to the nuances of this highly complex issue.
One way to improve our collective understanding of the issue is to look at both observational and experimental data together whenever possible. When the data from both types of studies point in the same direction, we can have more confidence in the conclusion. For example, randomized controlled trials show that alcohol consumption raises levels of sex steroid hormones in the blood. Observational trials suggest that alcohol consumption also raises the risk of specific subtypes of breast cancer that respond to these hormones. Together, that evidence is highly persuasive that alcohol increases the chances of breast cancer.
Similarly, in randomized trials, alcohol consumption lowers average blood sugar levels. In observational trials, it also appears to lower the risk of diabetes. Again, that evidence is persuasive in combination.
As these examples illustrate, drinking alcohol may raise the risk of some conditions but not others. What does that mean for individuals? Patients should work with their clinicians to understand their personal risks and make informed decisions about drinking.
Medicine and public health would benefit greatly if better data were available to offer more conclusive guidance about alcohol. But that would require a major investment. Large, long-term, gold-standard studies are expensive. To date, federal agencies like the National Institutes of Health have shown no interest in exclusively funding these studies on alcohol.
Alcohol manufacturers have previously expressed some willingness to finance the studies—similar to the way pharmaceutical companies finance most drug testing—but that has often led to criticism. This happened to us, even though external experts found our proposal scientifically sound. In 2018, the National Institutes of Health ended our trial to study the health effects of alcohol. The NIH found that officials at one of its institutes had solicited funding from alcohol manufacturers, violating federal policy.
It’s tempting to assume that because heavy alcohol consumption is very bad, lesser amounts must be at least a little bad. But the science isn’t there, in part because critics of the alcohol industry have deliberately engineered a state of ignorance. They have preemptively discredited any research, even indirectly, by the alcohol industry—even though medicine relies on industry financing to support the large, gold-standard studies that provide conclusive data about drugs and devices that hundreds of millions of Americans take or use daily.
Scientific evidence about drinking alcohol goes back nearly 100 years—and includes plenty of variability in alcohol’s health effects. In the 1980s and 1990s, for instance, alcohol in moderation, and especially red wine, was touted as healthful. Now the pendulum has swung so far in the opposite direction that contemporary narratives suggest every ounce of alcohol is dangerous. Until gold-standard experiments are performed, we won’t truly know. In the meantime, we must acknowledge the complexity of existing evidence—and take care not to reduce it to a single, misleading conclusion.
This article first appeared on The Journalist’s Resource and is republished here under a Creative Commons license.
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What is childhood dementia? And how could new research help?
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“Childhood” and “dementia” are two words we wish we didn’t have to use together. But sadly, around 1,400 Australian children and young people live with currently untreatable childhood dementia.
Broadly speaking, childhood dementia is caused by any one of more than 100 rare genetic disorders. Although the causes differ from dementia acquired later in life, the progressive nature of the illness is the same.
Half of infants and children diagnosed with childhood dementia will not reach their tenth birthday, and most will die before turning 18.
Yet this devastating condition has lacked awareness, and importantly, the research attention needed to work towards treatments and a cure.
More about the causes
Most types of childhood dementia are caused by mutations (or mistakes) in our DNA. These mistakes lead to a range of rare genetic disorders, which in turn cause childhood dementia.
Two-thirds of childhood dementia disorders are caused by “inborn errors of metabolism”. This means the metabolic pathways involved in the breakdown of carbohydrates, lipids, fatty acids and proteins in the body fail.
As a result, nerve pathways fail to function, neurons (nerve cells that send messages around the body) die, and progressive cognitive decline occurs.
Childhood dementia is linked to rare genetic disorders. maxim ibragimov/Shutterstock What happens to children with childhood dementia?
Most children initially appear unaffected. But after a period of apparently normal development, children with childhood dementia progressively lose all previously acquired skills and abilities, such as talking, walking, learning, remembering and reasoning.
Childhood dementia also leads to significant changes in behaviour, such as aggression and hyperactivity. Severe sleep disturbance is common and vision and hearing can also be affected. Many children have seizures.
The age when symptoms start can vary, depending partly on the particular genetic disorder causing the dementia, but the average is around two years old. The symptoms are caused by significant, progressive brain damage.
Are there any treatments available?
Childhood dementia treatments currently under evaluation or approved are for a very limited number of disorders, and are only available in some parts of the world. These include gene replacement, gene-modified cell therapy and protein or enzyme replacement therapy. Enzyme replacement therapy is available in Australia for one form of childhood dementia. These therapies attempt to “fix” the problems causing the disease, and have shown promising results.
Other experimental therapies include ones that target faulty protein production or reduce inflammation in the brain.
Research attention is lacking
Death rates for Australian children with cancer nearly halved between 1997 and 2017 thanks to research that has enabled the development of multiple treatments. But over recent decades, nothing has changed for children with dementia.
In 2017–2023, research for childhood cancer received over four times more funding per patient compared to funding for childhood dementia. This is despite childhood dementia causing a similar number of deaths each year as childhood cancer.
The success for childhood cancer sufferers in recent decades demonstrates how adequately funding medical research can lead to improvements in patient outcomes.
Dementia is not just a disease of older people. Miljan Zivkovic/Shutterstock Another bottleneck for childhood dementia patients in Australia is the lack of access to clinical trials. An analysis published in March this year showed that in December 2023, only two clinical trials were recruiting patients with childhood dementia in Australia.
Worldwide however, 54 trials were recruiting, meaning Australian patients and their families are left watching patients in other parts of the world receive potentially lifesaving treatments, with no recourse themselves.
That said, we’ve seen a slowing in the establishment of clinical trials for childhood dementia across the world in recent years.
In addition, we know from consultation with families that current care and support systems are not meeting the needs of children with dementia and their families.
New research
Recently, we were awarded new funding for our research on childhood dementia. This will help us continue and expand studies that seek to develop lifesaving treatments.
More broadly, we need to see increased funding in Australia and around the world for research to develop and translate treatments for the broad spectrum of childhood dementia conditions.
Dr Kristina Elvidge, head of research at the Childhood Dementia Initiative, and Megan Maack, director and CEO, contributed to this article.
Kim Hemsley, Head, Childhood Dementia Research Group, Flinders Health and Medical Research Institute, College of Medicine and Public Health, Flinders University; Nicholas Smith, Head, Paediatric Neurodegenerative Diseases Research Group, University of Adelaide, and Siti Mubarokah, Research Associate, Childhood Dementia Research Group, Flinders Health and Medical Research Institute, College of Medicine and Public Health, Flinders University
This article is republished from The Conversation under a Creative Commons license. Read the original article.
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Type 2 Diabetic Foot Problems
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It’s Q&A Day!
Have a question or a request? You can always hit “reply” to any of our emails, or use the feedback widget at the bottom!
This newsletter has been growing a lot lately, and so have the questions/requests, and we love that! 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
Q: I’d like to know more about type 2 diabetic foot problems
You probably know that the “foot problems” thing has less to do with the feet and more to do with blood and nerves. So, why the feet?
The reason feet often get something like the worst of it, is because they are extremities, and in the case of blood sugars being too high for too long too often, they’re getting more damage as blood has to fight its way back up your body. Diabetic neuropathy happens when nerves are malnourished because the blood that should be keeping them healthy, is instead syrupy and sluggish.
We’ll definitely do a main feature sometime soon on keeping blood sugars healthy, for both types of diabetes plus pre-diabetes and just general advice for all.
In the meantime, here’s some very good advice on keeping your feet healthy in the context of diabetes. This one’s focussed on Type 1 Diabetes, but the advice goes for both:
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Treadmill vs Road
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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 😎
❝Why do I get tired much more quickly running outside, than I do on the treadmill? Every time I get worn out quickly but at home I can go for much longer!❞
Short answer: the reason is Newton’s laws of motion.
In other words: on a treadmill, you need only maintain your position in space relative the the Earth while the treadmill moves beneath you, whereas on the road, you need to push against the Earth with sufficient force to move it relative to your body.
Illustrative thought experiment to make that clearer: if you were to stand on a treadmill with roller skates, and hold onto the bar with even just one finger, you would maintain your speed as far as the treadmill’s computer is concerned—whereas to maintain your speed on a flat road, you’d still need to push with your back foot every few yards or so.
More interesting answer: it’s a qualitatively different exercise (i.e. not just quantitively different). This is because of all that pushing you’re having to do on the road, while on a treadmill, the only pushing you have to do is just enough to counteract gravity (i.e. to keep you upright).
As such, both forms of running are a cardio exercise (because simply moving your legs quickly, even without having to apply much force, is still something that requires oxygenated blood feeding the muscles), but road-running adds an extra element of resistance exercise for the muscles of your lower body. Thus, road-running will enable you to build-maintain muscle much more than treadmill-running will.
Some extra things to bear in mind, however:
1) You can increase the resistance work for either form of running, by adding weight (such as by wearing a weight vest):
Weight Vests Against Osteoporosis: Do They Really Build Bone?
…and while road-running will still be the superior form of resistance work (for the reasons we outlined above), adding a weight vest will still be improving your stabilization muscles, just as it would if you were standing still while holding the weight up.
2) Stationary cycling does not have the same physics differences as stationary running. By this we mean: an exercise bike will require your muscles to do just as much pushing as they would on a road. This makes stationary cycling an excellent choice for high intensity resistance training (HIRT):
3) The best form of exercise is the one that you will actually do. Thus, when it’s raining sidewise outside, a treadmill inside will get exercise done better than no running at all. Similarly, a treadmill exercise session takes a lot less preparation (“switch it on”) than a running session outside (“get dressed appropriately for the weather, apply sunscreen if necessary, remember to bring water, etc etc”), and thus is also much more likely to actually occur. The ability to stop whenever one wants is also a reassuring factor that makes one much more likely to start. See for example:
How To Do HIIT (Without Wrecking Your Body)
Take care!
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Apricots vs Oranges – Which is Healthier?
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Our Verdict
When comparing apricots to oranges, we picked the apricots.
Why?
Both are great, and it was close!
In terms of macros, apricots have more protein while oranges have more carbs and fiber, the ratio of of which means that apricots have the slightly lower glycemic index, though really, nobody is getting metabolic disease from eating whole fruit. All in all, we’ll call this category a tie.
In the category of vitamins, apricots have more of vitamins A, B3, E, and K, while oranges have more of vitamins B1, B9, C, and choline, meaning another tie in this category.
When it comes to minerals, apricots have more copper, iron, magnesium, manganese, phosphorus, potassium, and zinc, while oranges have more calcium and selenium. A win for apricots, then!
In terms of beneficial phytochemicals, apricots have more, and you can read about some of them in the link below.
Adding up the sections makes for an overall win for apricots, but by all means enjoy either or both; diversity is good!
Want to learn more?
You might like:
Top 8 Fruits That Prevent & Kill Cancer
Enjoy!
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