Caramelized Caraway Cabbage

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Cabbage is an underrated vegetable for its many nutrients and its culinary potential—here’s a great way to make it a delectable starter or respectable side.

You will need

  • 1 medium white cabbage, sliced into 1″ thick slabs
  • 1 tbsp extra-virgin olive oil
  • 1 tbsp caraway seeds
  • 1 tsp black pepper
  • ½ tsp turmeric
  • ¼ tsp MSG or ½ tsp low-sodium salt

Method

(we suggest you read everything at least once before doing anything)

1) Preheat the oven to 400℉ / 200℃.

2) Combine the non-cabbage ingredients in a small bowl, whisking to mix thoroughly—with a tiny whisk if you have one, but a fork will work if necessary.

3) Arrange the cabbage slices on a lined baking tray and brush the seasoning-and-oil mixture over both sides of each slice.

4) Roast for 20–25 minutes until the cabbage is tender and beginning to caramelize.

5) Serve warm.

Enjoy!

Want to learn more?

For those interested in some of the science of what we have going on today:

Take care!

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  • The first pig kidney has been transplanted into a living person. But we’re still a long way from solving organ shortages

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    In a world first, we heard last week that US surgeons had transplanted a kidney from a gene-edited pig into a living human. News reports said the procedure was a breakthrough in xenotransplantation – when an organ, cells or tissues are transplanted from one species to another. https://www.youtube.com/embed/cisOFfBPZk0?wmode=transparent&start=0 The world’s first transplant of a gene-edited pig kidney into a live human was announced last week.

    Champions of xenotransplantation regard it as the solution to organ shortages across the world. In December 2023, 1,445 people in Australia were on the waiting list for donor kidneys. In the United States, more than 89,000 are waiting for kidneys.

    One biotech CEO says gene-edited pigs promise “an unlimited supply of transplantable organs”.

    Not, everyone, though, is convinced transplanting animal organs into humans is really the answer to organ shortages, or even if it’s right to use organs from other animals this way.

    There are two critical barriers to the procedure’s success: organ rejection and the transmission of animal viruses to recipients.

    But in the past decade, a new platform and technique known as CRISPR/Cas9 – often shortened to CRISPR – has promised to mitigate these issues.

    What is CRISPR?

    CRISPR gene editing takes advantage of a system already found in nature. CRISPR’s “genetic scissors” evolved in bacteria and other microbes to help them fend off viruses. Their cellular machinery allows them to integrate and ultimately destroy viral DNA by cutting it.

    In 2012, two teams of scientists discovered how to harness this bacterial immune system. This is made up of repeating arrays of DNA and associated proteins, known as “Cas” (CRISPR-associated) proteins.

    When they used a particular Cas protein (Cas9) with a “guide RNA” made up of a singular molecule, they found they could program the CRISPR/Cas9 complex to break and repair DNA at precise locations as they desired. The system could even “knock in” new genes at the repair site.

    In 2020, the two scientists leading these teams were awarded a Nobel prize for their work.

    In the case of the latest xenotransplantation, CRISPR technology was used to edit 69 genes in the donor pig to inactivate viral genes, “humanise” the pig with human genes, and knock out harmful pig genes. https://www.youtube.com/embed/UKbrwPL3wXE?wmode=transparent&start=0 How does CRISPR work?

    A busy time for gene-edited xenotransplantation

    While CRISPR editing has brought new hope to the possibility of xenotransplantation, even recent trials show great caution is still warranted.

    In 2022 and 2023, two patients with terminal heart diseases, who were ineligible for traditional heart transplants, were granted regulatory permission to receive a gene-edited pig heart. These pig hearts had ten genome edits to make them more suitable for transplanting into humans. However, both patients died within several weeks of the procedures.

    Earlier this month, we heard a team of surgeons in China transplanted a gene-edited pig liver into a clinically dead man (with family consent). The liver functioned well up until the ten-day limit of the trial.

    How is this latest example different?

    The gene-edited pig kidney was transplanted into a relatively young, living, legally competent and consenting adult.

    The total number of gene edits edits made to the donor pig is very high. The researchers report making 69 edits to inactivate viral genes, “humanise” the pig with human genes, and to knockout harmful pig genes.

    Clearly, the race to transform these organs into viable products for transplantation is ramping up.

    From biotech dream to clinical reality

    Only a few months ago, CRISPR gene editing made its debut in mainstream medicine.

    In November, drug regulators in the United Kingdom and US approved the world’s first CRISPR-based genome-editing therapy for human use – a treatment for life-threatening forms of sickle-cell disease.

    The treatment, known as Casgevy, uses CRISPR/Cas-9 to edit the patient’s own blood (bone-marrow) stem cells. By disrupting the unhealthy gene that gives red blood cells their “sickle” shape, the aim is to produce red blood cells with a healthy spherical shape.

    Although the treatment uses the patient’s own cells, the same underlying principle applies to recent clinical xenotransplants: unsuitable cellular materials may be edited to make them therapeutically beneficial in the patient.

    Sickle cells have a different shape to healthy round red blood cells
    CRISPR technology is aiming to restore diseased red blood cells to their healthy round shape. Sebastian Kaulitzki/Shutterstock

    We’ll be talking more about gene-editing

    Medicine and gene technology regulators are increasingly asked to approve new experimental trials using gene editing and CRISPR.

    However, neither xenotransplantation nor the therapeutic applications of this technology lead to changes to the genome that can be inherited.

    For this to occur, CRISPR edits would need to be applied to the cells at the earliest stages of their life, such as to early-stage embryonic cells in vitro (in the lab).

    In Australia, intentionally creating heritable alterations to the human genome is a criminal offence carrying 15 years’ imprisonment.

    No jurisdiction in the world has laws that expressly permits heritable human genome editing. However, some countries lack specific regulations about the procedure.

    Is this the future?

    Even without creating inheritable gene changes, however, xenotransplantation using CRISPR is in its infancy.

    For all the promise of the headlines, there is not yet one example of a stable xenotransplantation in a living human lasting beyond seven months.

    While authorisation for this recent US transplant has been granted under the so-called “compassionate use” exemption, conventional clinical trials of pig-human xenotransplantation have yet to commence.

    But the prospect of such trials would likely require significant improvements in current outcomes to gain regulatory approval in the US or elsewhere.

    By the same token, regulatory approval of any “off-the-shelf” xenotransplantation organs, including gene-edited kidneys, would seem some way off.

    Christopher Rudge, Law lecturer, University of Sydney

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

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  • Topping Up Testosterone?

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    The Testosterone Drop

    Testosterone levels decline amongst men over a certain age. Exactly when depends on the individual and also how we measure it, but the age of 45 is a commonly-given waypoint for the start of this decline.

    (the actual start is usually more like 20, but it’s a very small decline then, and speeds up a couple of decades later)

    This has been called “the male menopause”, or “the andropause”.

    Both terms are a little misleading, but for lack of a better term, “andropause” is perhaps not terrible.

    Why “the male menopause” is misleading:

    To call it “the male menopause” suggests that this is when men’s menstruation stops. Which for cis men at the very least, is simply not a thing they ever had in the first place, to stop (and for trans men it’s complicated, depending on age, hormones, surgeries, etc).

    Why “the andropause” is misleading:

    It’s not a pause, and unlike the menopause, it’s not even a stop. It’s just a decline. It’s more of an andro-pitter-patter-puttering-petering-out.

    Is there a better clinical term?

    Objectively, there is “late-onset hypogonadism” but that is unlikely to be taken up for cultural reasons—people stigmatize what they see as a loss of virility.

    Terms aside, what are the symptoms?

    ❝Andropause or late-onset hypogonadism is a common disorder which increases in prevalence with advancing age. Diagnosis of late-onset of hypogonadism is based on presence of symptoms suggestive of testosterone deficiency – prominent among them are sexual symptoms like…❞

    (Read more)

    …and there we’d like to continue the quotation, but if we list the symptoms here, it won’t get past a lot of filters because of the words used. So instead, please feel free to click through:

    Source: Andropause: Current concepts

    Can it be safely ignored?

    If you don’t mind the sexual symptoms, then mostly, yes!

    However, there are a few symptoms we can mention here that are not so subjective in their potential for harm:

    • Depression
    • Loss of muscle mass
    • Increased body fat

    Depression kills, so this does need to be taken seriously. See also:

    The Mental Health First-Aid That You’ll Hopefully Never Need

    (the above is a guide to managing depression, in yourself or a loved one)

    Loss of muscle mass means being less robust against knocks and falls later in life

    Loss of muscle mass also means weaker bones (because the body won’t make bones stronger than it thinks they need to be, so bone will follow muscle in this regard—in either direction)

    See also:

    Increased body fat means increased risk of diabetes and heart disease, as a general rule of thumb, amongst other problems.

    Will testosterone therapy help?

    That’s something to discuss with your endocrinologist, but for most men whose testosterone levels are lower than is ideal for them, then yes, taking testosterone to bring them [back] to “normal” levels can make you happier and healthier (though it’s certainly not a cure-all).

    See for example:

    Testosterone Therapy Improves […] and […] in Hypogonadal Men

    (Sorry, we’re not trying to be clickbaity, there are just some words we can’t use without encountering software problems)

    Here’s a more comprehensive study that looked at 790 men aged 65 or older, with testosterone levels below a certain level. It looked at the things we can’t mention here, as well as physical function and general vitality:

    ❝The increase in testosterone levels was associated with significantly increased […] activity, as assessed by the Psychosexual Daily Questionnaire (P<0.001), as well as significantly increased […] desire and […] function.

    The percentage of men who had an increase of at least 50 m in the 6-minute walking distance did not differ significantly between the two study groups in the Physical Function Trial but did differ significantly when men in all three trials were included (20.5% of men who received testosterone vs. 12.6% of men who received placebo, P=0.003).

    Testosterone had no significant benefit with respect to vitality, as assessed by the Functional Assessment of Chronic Illness Therapy–Fatigue scale, but men who received testosterone reported slightly better mood and lower severity of depressive symptoms than those who received placebo❞

    Source: Effects of Testosterone Treatment in Older Men

    We strongly recommend, by the way, when a topic is of interest to you to read the paper itself, because even the extract above contains some subjectivity, for example what is “slightly better”, and what is “no significant benefit”.

    That “slightly better mood and lower severity of depressive symptoms”, for example, has a P value of 0.004 in their data, which is an order of magnitude more significant than the usual baseline for significance (P<0.05).

    And furthermore, that “no significant benefit with respect to vitality” is only looking at either the primary outcome aggregated goal or the secondary FACIT score whose secondary outcome had a P value of 0.06, which just missed the cut-off for significance, and neglects to mention that all the other secondary outcome metrics for men involved in the vitality trial were very significant (ranging from P=0.04 to P=0.001)

    Click here to see the results table for the vitality trial

    Will it turn me into a musclebound angry ragey ‘roidmonster?

    Were you that kind of person before your testosterone levels declined? If not, then no.

    Testosterone therapy seeks only to return your testosterone levels to where they were, and this is done through careful monitoring and adjustment. It’d take a lot more than (responsible) endocrinologist-guided hormonal therapy to turn you into Marvel’s “Wolverine”.

    Is testosterone therapy safe?

    A question to take to your endocrinologist because everyone’s physiology is different, but a lot of studies do support its general safety for most people who are prescribed it.

    As with anything, there are risks to be aware of, though. Perhaps the most critical risk is prostate cancer, and…

    ❝In a large meta-analysis of 18 prospective studies that included over 3500 men, there was no association between serum androgen levels and the risk of prostate cancer development

    For men with untreated prostate cancer on active surveillance, TRT remains controversial. However, several studies have shown that TRT is not associated with progression of prostate cancer as evidenced by either PSA progression or gleason grade upstaging on repeat biopsy.

    Men on TRT should have frequent PSA monitoring; any major change in PSA (>1 ng/mL) within the first 3-6 months may reflect the presence of a pre-existing cancer and warrants cessation of therapy❞

    Those are some select extracts, but any of this may apply to you or your loved one, we recommend to read in full about this and other risks:

    Risks of testosterone replacement therapy in men

    See also: Prostate Health: What You Should Know

    Beyond that… If you are prone to baldness, then taking testosterone will increase that tendency. If that’s a problem for you, then it’s something to know about. There are other things you can take/use for that in turn, so maybe we’ll do a feature on those one of these days!

    For now, take care!

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  • Hair Growth: Caffeine and Minoxidil Strategies

    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.

    Questions and Answers 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!

    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

    Hair growth strategies for men combing caffeine and minoxidil?

    Well, the strategy for that is to use caffeine and minoxidil! Some more specific tips, though:

    • Both of those things need to be massaged (gently!) into your scalp especially around your hairline.
      • In the case of caffeine, that boosts hair growth. No extra thought or care needed for that one.
      • In the case of minoxidil, it reboots the hair growth cycle, so if you’ve only recently started, don’t be surprised (or worried) if you see more shedding in the first three months. It’s jettisoning your old hairs because new ones were just prompted (by the minoxidil) to start growing behind them. So: it will get briefly worse before it gets better, but then it’ll stay better… provided you keep using it.
    • If you’d like other options besides minoxidil, finasteride is a commonly prescribed oral drug that blocks the conversion of testosterone to DHT, which latter is what tells your hairline to recede.
    • If you’d like other options besides prescription drugs, saw palmetto performs comparably to finasteride (and works the same way).
      • You may also want to consider biotin supplementation if you don’t already enjoy that
    • Consider also using a dermaroller on your scalp. If you’re unfamiliar, this is a device that looks like a tiny lawn aerator, with many tiny needles, and you roll it gently across your skin.
      • It can be used for promoting hair growth, as well as for reducing wrinkles and (more slowly) healing scars.
      • It works by breaking up the sebum that may be blocking new hair growth, and also makes the skin healthier by stimulating production of collagen and elastin (in response to the thousands of microscopic wounds that the needles make).
      • Sounds drastic, but it doesn’t hurt and doesn’t leave any visible marks—the needles are that tiny. Still, practise good sterilization and ensure your skin is clean when using it.

    See: How To Use A Dermaroller ← also explains more of the science of it

    PS: this question was asked in the context of men, but the information goes the same for women suffering from androgenic alepoceia—which is a lot more common than most people think!

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  • Daily Activity Levels & The Measurable Difference They Make To Brain Health

    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.

    Most studies into the difference that exercise makes to cognitive decline are retrospective, i.e. they look backwards in time, asking participants what their exercise habits were like in the past [so many] years, and tallying that against their cognitive health in the present.

    Some studies are interventional, and those are most often 3, 6, or 12 months, depending on funding. In those cases, they make a hypothesis (e.g. this intervention will boost this measure of brain health) and then test it.

    However, humans aren’t generally great at making short term decisions for long term gains. In other words: if it’s rainy out, or you’re a little pushed for time, you’re likely to take the car over walking regardless of what data point this adjusts in an overarching pattern that will affect your brain’s amyloid-β clean-up rates in 5–20 years time.

    Nine days

    The study we’re going to look at today was a 9-day observational study, using smartphone-based tracking with check-ins every 3½ hours, with participants reporting their physical activity as light, moderate, or intense (these terms were defined and exemplified, so that everyone involved was singing from the same songsheet in terms of what activities constitute what intensity).

    The sample size was reasonable (n=204) and was generally heterogenous sample (i.e. varied in terms of sex, racial background, and fitness level) of New Yorkers aged 40–65.

    So, the input variable was activity level, and the output variable was cognitive fitness.

    As to how they measured the output, two brain games assessed:

    1. cognitive processing speed, and
    2. working memory (a proxy for executive function).

    What they found:

    1. participants active within the last 3½ hours had faster processing speed, equivalent to being four years younger
    2. response times in the working memory (for: executive function) task reflected similar processing speed improvements, for participants active in the last 3½ hours

    And, which is important to note,

    ❝This benefit was observed regardless of whether the activities they reported were higher intensity (e.g., running/jogging) or lower intensity (e.g., walking, chores).❞

    ~ Dr. Lizbeth Benson et al.

    Source: Cognitive Health Benefits of Everyday Physical Activity in a Diverse Sample of Middle-Aged Adults

    Practical take-away:

    Move more often! At least every couple of hours (when not sleeping)!

    The benefits will benefit you in the now, as well as down the line.

    See also:

    The Doctor Who Wants Us To Exercise Less, & Move More

    and, for that matter:

    Do You Love To Go To The Gym? No? Enjoy These “No-Exercise Exercises”!

    Take care!

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  • The Surprising Link Between Type 2 Diabetes & Alzheimer’s

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    The Surprising Link Between Type 2 Diabetes & Alzheimer’s

    This is Dr. Rhonda Patrick. She’s a biomedical scientist with expertise in the areas of aging, cancer, and nutrition. In the past five years she has expanded her research of aging to focus more on Alzheimer’s and Parkinson’s, as she has a genetic predisposition to both.

    What does that genetic predisposition look like? People who (like her) have the APOE-ε4 allele have a twofold increased risk of Alzheimer’s disease—and if you have two copies (i.e., one from each of two parents), the risk can be up to tenfold. Globally, 13.7% of people have at least one copy of this allele.

    So while getting Alzheimer’s or not is not, per se, hereditary… The predisposition to it can be passed on.

    What’s on her mind?

    Dr. Patrick has noted that, while we don’t know for sure the causes of Alzheimer’s disease, and can make educated guesses only from correlations, the majority of current science seems to be focusing on just one: amyloid plaques in the brain.

    This is a worthy area of research, but ignores the fact that there are many potential Alzheimer’s disease mechanisms to explore, including (to count only mainstream scientific ideas):

    • The amyloid hypothesis
    • The tau hypothesis
    • The inflammatory hypothesis
    • The cholinergic hypothesis
    • The cholesterol hypothesis
    • The Reelin hypothesis
    • The large gene instability hypothesis

    …as well as other strongly correlated factors such as glucose hypometabolism, insulin signalling, and oxidative stress.

    If you lost your keys and were looking for them, and knew at least half a dozen places they might be, how often would you check the same place without paying any attention to the others?

    To this end, she notes about those latter-mentioned correlated factors:

    ❝50–80% of people with Alzheimer’s disease have type 2 diabetes; there is definitely something going on❞

    There’s another “smoking gun” for this too, because dysfunction in the blood vessels and capillaries that line the blood-brain barrier seem to be a very early event that is common between all types of dementia (including Alzheimer’s) and between type 2 diabetes and APOE-ε4.

    Research is ongoing, and Dr. Patrick is at the forefront of that. However, there’s a practical take-away here meanwhile…

    What can we do about it?

    Dr. Patrick hypothesizes that if we can reduce the risk of type 2 diabetes, we may reduce the risk of Alzheimer’s with it.

    Obviously, avoiding diabetes if possible is a good thing to do anyway, but if we’re aware of an added risk factor for Alzheimer’s, it becomes yet more important.

    Of course, all the usual advices apply here, including a Mediterranean diet and regular moderate exercise.

    Three other things Dr. Patrick specifically recommends (to reduce both type 2 diabetes risk and to reduce Alzheimer’s risk) include:

    (links are to her blog, with lots of relevant science for each)

    You can also hear more from Dr. Patrick personally, as a guest on Dr. Peter Attia’s podcast recently. She discusses these topics in much greater detail than we have room for in our newsletter:

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  • What’s the difference between ‘man flu’ and flu? Hint: men may not be exaggerating

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    What’s the difference? is a new editorial product that explains the similarities and differences between commonly confused health and medical terms, and why they matter.

    The term “man flu” takes a humorous poke at men with minor respiratory infections, such as colds, who supposedly exaggerate their symptoms.

    According to the stereotype, a man lies on the sofa with a box of tissues. Meanwhile his female partner, also with a snotty nose, carries on working from home, doing the chores and looking after him.

    But is man flu real? Is there a valid biological reason behind men’s symptoms or are men just malingering? And how does man flu differ from flu?

    baranq/Shutterstock

    What are the similarities?

    Man flu could refer to a number of respiratory infections – a cold, flu, even a mild case of COVID. So it’s difficult to compare man flu with flu.

    But for simplicity, let’s say man flu is actually a cold. If that’s the case, man flu and flu have some similar features.

    Both are caused by viruses (but different ones). Both are improved with rest, fluids, and if needed painkillers, throat lozenges or decongestants to manage symptoms.

    Both can share similar symptoms. Typically, more severe symptoms such as fever, body aches, violent shivering and headaches are more common in flu (but sometimes occur in colds). Meanwhile sore throats, runny noses, congestion and sneezing are more common in colds. A cough is common in both.

    What are the differences?

    Flu is a more serious and sometimes fatal respiratory infection caused by the influenza virus. Colds are caused by various viruses such as rhinoviruses, adenoviruses, and common cold coronaviruses, and are rarely serious.
    Colds tend to start gradually while flu tends to start abruptly.

    Flu can be detected with laboratory or at-home tests. Man flu is not an official diagnosis.

    Severe flu symptoms may be prevented with a vaccine, while cold symptoms cannot.

    Serious flu infections may also be prevented or treated with antiviral drugs such as Tamiflu. There are no antivirals for colds.

    OK, but is man flu real?

    Again, let’s assume man flu is a cold. Do men really have worse colds than women? The picture is complicated.

    One study, with the title “Man flu is not a thing”, did in fact show there were differences in men’s and women’s symptoms.

    This study looked at symptoms of acute rhinosinusitis. That’s inflammation of the nasal passages and sinuses, which would explain a runny or stuffy nose, a sinus headache or face pain.

    When researchers assessed participants at the start of the study, men and women had similar symptoms. But by days five and eight of the study, women had fewer or less-severe symptoms. In other words, women had recovered faster.

    But when participants rated their own symptoms, we saw a somewhat different picture. Women rated their symptoms worse than how the researchers rated them at the start, but said they recovered more quickly.

    All this suggests men were not exaggerating their symptoms and did indeed recover more slowly. It also suggests women feel their symptoms more strongly at the start.

    Why is this happening?

    It’s not straightforward to tease out what’s going on biologically.

    There are differences in immune responses between men and women that provide a plausible reason for worse symptoms in men.

    For instance, women generally produce antibodies more efficiently, so they respond more effectively to vaccination. Other aspects of women’s immune system also appear to work more strongly.

    So why do women tend to have stronger immune responses overall? That’s probably partly because women have two X chromosomes while men have one. X chromosomes carry important immune function genes. This gives women the benefit of immune-related genes from two different chromosomes.

    XX female chromosomes
    X chromosomes carry important immune function genes. Rost9/Shutterstock

    Oestrogen (the female sex hormone) also seems to strengthen the immune response, and as levels vary throughout the lifespan, so does the strength of women’s immune systems.

    Men are certainly more likely to die from some infectious diseases, such as COVID. But the picture is less clear with other infections such as the flu, where the incidence and mortality between men and women varies widely between countries and particular flu subtypes and outbreaks.

    Infection rates and outcomes in men and women can also depend on the way a virus is transmitted, the person’s age, and social and behavioural factors.

    For instance, women seem to be more likely to practice protective behaviours such as washing their hands, wearing masks or avoiding crowded indoor spaces. Women are also more likely to seek medical care when ill.

    So men aren’t faking it?

    Some evidence suggests men are not over-reporting symptoms, and may take longer to clear an infection. So they may experience man flu more harshly than women with a cold.

    So cut the men in your life some slack. If they are sick, gender stereotyping is unhelpful, and may discourage men from seeking medical advice.

    Thea van de Mortel, Professor, Nursing, School of Nursing and Midwifery, Griffith University

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

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