No, COVID-19 vaccines don’t cause ‘turbo cancer’

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What you need to know

  • COVID-19 vaccines do not cause “turbo cancer” or contain SV40, a virus that has been suspected of causing cancer.
  • There is no link between rising cancer rates and COVID-19 vaccines.
  • Staying up to date on COVID-19 vaccines is a safe, free way to support long-term health.

Myths that COVID-19 vaccines cause cancer have been circulating since the vaccines were first developed. These false claims resurfaced last month after Princess Kate Middleton announced that she is undergoing cancer treatment, with some vaccine opponents falsely claiming Middleton has a “turbo cancer” caused by COVID-19 vaccines.

Here’s what we know: “Turbo cancer” is a made-up term for a fake phenomenon, and there is strong evidence that COVID-19 vaccines do not cause cancer or increase cancer risk.

Read on to learn how to recognize false claims about COVID-19 vaccines and cancer.


Do COVID-19 vaccines contain cancer-causing ingredients?

No. Some vaccine opponents claim that COVID-19 vaccines contain SV40, a virus that has been suspected of causing cancer. This claim is false.

A piece of SV40’s DNA sequence—called a “promoter”—was used as starting material to develop COVID-19 vaccines, but the virus itself is not present in the vaccines. The promoter does not contain the part of the virus that enters the cell nucleus, so it poses no risk.

COVID-19 vaccines and their ingredients have been rigorously studied in millions of people worldwide and have been determined to be safe. The National Cancer Institute and the American Cancer Society agree that COVID-19 vaccines do not increase cancer risk or accelerate cancer growth.

Why are cancer rates rising in the U.S.?

Since the 1990s, cancer rates have been on the rise globally and in the U.S., most notably in people under 50. Increased cancer screening may partially explain the rising number of cancer diagnoses. Exposure to air pollution and lifestyle factors like tobacco use, alcohol use, and diet may also be contributing factors.

What are the benefits of staying up to date on COVID-19 vaccines?

Staying up to date on COVID-19 vaccines is a safe way to protect our long-term health. COVID-19 vaccines prevent severe illness, hospitalization, death, and long COVID.

The CDC says staying up to date on COVID-19 vaccines is a safer and more reliable way to build protection against COVID-19 than getting sick from COVID-19.

For more information, talk to your health care provider.

This article first appeared on Public Good News and is republished here under a Creative Commons license.

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  • An Accessible New Development Against Alzheimer’s

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    Dopamine vs Alzheimer’s

    One of the key hallmarks of Alzheimer’s disease is the formation of hardened beta-amyloid plaques around neurons. The beta-amyloid peptides themselves are supposed to be in the brain, but the hardened pieces of them that form the plaques are not.

    While the full nature of the relationship between those plaques and Alzheimer’s disease is not known for sure (there are likely other factors involved, and “the amyloid hypothesis” is at this stage nominally just that, a hypothesis), one thing that has been observed is that increasing or reducing the plaques increases or reduces (respectively) Alzheimer’s symptoms such as memory loss.

    Neprilysin

    There is an enzyme, neprilysin, that can break down those plaques.

    Neprilysin is made naturally in the brain, and/but we cannot take it as a supplement or medication, because it’s too big to pass through the blood-brain barrier.

    A team of researchers led by Dr. Takaomi Saido genetically manipulated mice to produce more neprilysin, and those mice resultantly experienced fewer beta-amyloid plaques and better memory in their old age.

    However wonderful for the mice (and a great proof of principle) the above approach is not useful as a treatment for humans whose genomes weren’t modified at our conception in a lab.

    Since (as mentioned before) we also can’t take it as a medication/supplement, that leaves one remaining option: find a way to make our already-existing brains produce more of it.

    The team’s previous research allowed them to narrow this down to “there is probably a hormone made in the hypothalamus that modulates this”, so they began experimenting with making the mice produce more hormones there.

    The DREADD switch

    DREADDs, or Designer Receptors Exclusively Activated by Designer Drugs, were the next tool in the toolbox. The scientists attached these designer receptors to dopamine-producing neurons in the mice, so that they could be activated by the appropriate designer drugs—basically, allowing for a “make more dopamine” button, without having to literally wire up the brains with electrodes. The “button” gets triggered instead by a chemical trigger, the designer drug. You can read more about them here:

    DREADDs for Neuroscientists: A Primer

    The result was positive; when the mice made more dopamine, the result was that they also made more neprilysin. So far, the hypothesis is that the presence of dopamine upregulates the production of neprilysin. In other words, the increased neprilysin levels were caused by the increased dopamine levels (the alternatives would have been: they were both caused by the same thing—in this case that’d be the DREADD activation—or the increase was caused by something else entirely that hadn’t been controlled for).

    As to how the causal relationship was determined…

    “But I don’t have (or want) a DREADD switch in my head”

    Happily for us (and probably happily for the mice too, because dopamine causes feelings of happiness), the experiments continued.

    This time, instead of using the DREADD system, they tried simply supplementing the mouse food with l-dopa, a dopamine precursor. L-dopa is often used in the treatment of Parkinson’s disease, because the molecules are small enough to pass through the blood-brain barrier, and can be converted to full dopamine inside the brain itself. So, taking l-dopa normally raises dopamine levels.

    The results? The mice who were given l-dopa enjoyed:

    • higher dopamine levels
    • higher neprilysin levels
    • lower beta-amyloid plaque levels
    • better memory in tests

    The next step for the researchers is to investigate how exactly dopamine regulates neprilysin in the brain, but for now, the relationship between l-dopa consumption and the reduction of Alzheimer’s symptoms seems clear.

    You can read about the study here:

    The dopaminergic system promotes neprilysin-mediated degradation of amyloid-β in the brain

    Is there a catch?

    L-dopa has common side effects that are not pleasant; the list begins with nausea and vomiting, and continues with things that one might expect from having “too much of a good thing” when it comes to dopamine, such as dyskinesia (extra movements) and hallucinations.

    You can read about it more here at the Parkinson’s Foundation:

    Parkinson’s Foundation | Levodopa

    However! All is not lost. Rather than reaching for the heavy guns by taking l-dopa unnecessarily, there are other dopamine precursors that don’t have those side effects (and are consequently less restricted, to the point they can be purchased as supplements, or indeed, enjoyed where they occur naturally in some foods).

    Top of the list of such safe* and readily-available dopamine precursors is…

    N-Acetyl L-Tyrosine (NALT): The Dopamine Precursor & More

    If you’d like to try that, here’s an example product on Amazon… Or you could eat fish, white beans, tofu, natto, or pumpkin seeds 😉

    *Quick note on safety: “safe” is a relative term and may vary from person to person. Please speak with your own doctor to be sure, check with your pharmacist in case of any meds interactions, and be especially careful taking anything that increases dopamine levels if you have bipolar disorder or are otherwise prone to psychosis of any kind. For most people, this shouldn’t be an issue as our brains have a built-in mechanism for scrubbing excess dopamine and ensuring we don’t end up with too much, but for some people whose dopamine regulation is not so good in that regard, it can cause problems. So again, speak with your doctor to be sure, because we are not doctors, let alone your doctor.

    Lastly…

    If you’d like an entirely drug-free approach, that’s skipping even the “nutraceuticals”, you might enjoy:

    Short On Dopamine? Science Has The Answer

    Take care!

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  • Visceral Belly Fat & How To Lose It

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    Visceral Belly Fat & How To Lose It

    We’ve talked before about how waist circumference is a much more useful indicator of metabolic health than BMI.

    So, let’s say you’ve a bit more around the middle than you’d like, but it stubbornly stays there. What’s going on underneath what you can see, why is it going on, and how can you get it to change?

    What is visceral fat?

    First, let’s talk about subcutaneous fat. That’s the fat directly under your skin. Women usually have more than men, and that’s perfectly healthy (up to a point); it’s supposed to be that way. We (women) will tend to accumulate this mostly in places such as our breasts, hips, and butt, and work outwards from there. Men will tend to put it on more to the belly and face.

    Side-note: if you’re undergoing (untreated) menopause, the changes in your hormone levels will tend to result in more subcutaneous fat to the belly and face too. That’s normal, and/but normal is not always good, and treatment options are great (with hormone replacement therapy, HRT, topping the list).

    Visceral fat (also called visceral adipose tissue), on the other hand, is the fat of the viscera—the internal organs of the abdomen.

    So, this is fat that goes under your abdominal muscles—you can’t squeeze this (directly).

    So what can we do?

    Famously “you can’t do spot reduction” (lose fat from a particular part of your body by focusing exercises on that area), but that’s about subcutaneous fat. There are things you can do that will reduce your visceral fat in particular.

    Some of these advices you may think “that’s just good advice for losing fat in general” and it is, yes. But these are things that have the biggest impact on visceral fat.

    Cut alcohol use

    This is the biggie. By numerous mechanisms, some of which we’ve talked about before, alcohol causes weight gain in general yes, but especially for visceral fat.

    Get better sleep

    You might think that hitting the gym is most important, but this one ranks higher. Yes, you can trim visceral fat without leaving your bed (and even without getting athletic in bed, for that matter). Not convinced?

    So, the verdict is clear: you snooze, you lose (visceral fat)!

    Tweak your diet

    You don’t have to do a complete overhaul (unless you want to), but a few changes can make a big difference, especially:

    If you’d like to learn more and enjoy videos, here’s an informative one to get you going!

    Click Here If The Embedded Video Doesn’t Load Automatically!

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  • Laziness Does Not Exist – by Dr. Devon Price

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    Some cultures prize productivity as an ideal above most other things, and it’s certainly so in the US. Not only is this not great for mental health in general, but also—as Dr. Price explains—it’s based on a lie.

    Generally speaking, when a person appears lazy there is something stopping them/you from doing better, and it’s not some mystical unseen force of laziness, not a set character trait, not a moral failing. Rather, the root cause may be physical, psychological, socioeconomic, or something else entirely.

    Those causes can in some cases be overcome (for example, a little CBT can often set aside perfectionist anxiety that results in procrastination), and in some cases they can’t, at least on an individual level (disabilities often stubbornly remain disabling, and societal problems require societal solutions).

    This matters for our mental health in areas well beyond the labor marketplace, of course, and these ideas extend to personal projects and even personal relationships. Whatever it is, if it’s leaving you exhausted, then probably something needs to be changed (even if the something is just “expectations”).

    The book does offer practical solutions to all manner of such situations, improving what can be improved, making easier what can be made easier, and accepting what just needs to be accepted.

    The style of this book is casual yet insightful and deep, easy-reading yet with all the acumen of an accomplished social psychologist.

    Bottom line: if life leaves you exhausted, this book can be the antidote and cure

    Click here to check out Laziness Does Not Exist, and break free!

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  • Why is cancer called cancer? We need to go back to Greco-Roman times for the answer

    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.

    One of the earliest descriptions of someone with cancer comes from the fourth century BC. Satyrus, tyrant of the city of Heracleia on the Black Sea, developed a cancer between his groin and scrotum. As the cancer spread, Satyrus had ever greater pains. He was unable to sleep and had convulsions.

    Advanced cancers in that part of the body were regarded as inoperable, and there were no drugs strong enough to alleviate the agony. So doctors could do nothing. Eventually, the cancer took Satyrus’ life at the age of 65.

    Cancer was already well known in this period. A text written in the late fifth or early fourth century BC, called Diseases of Women, described how breast cancer develops:

    hard growths form […] out of them hidden cancers develop […] pains shoot up from the patients’ breasts to their throats, and around their shoulder blades […] such patients become thin through their whole body […] breathing decreases, the sense of smell is lost […]

    Other medical works of this period describe different sorts of cancers. A woman from the Greek city of Abdera died from a cancer of the chest; a man with throat cancer survived after his doctor burned away the tumour.

    Where does the word ‘cancer’ come from?

    Galen, the physician
    Why does the word ‘cancer’ have its roots in the ancient Greek and Latin words for crab? The physician Galen offers one explanation. Pierre Roche Vigneron/Wikimedia

    The word cancer comes from the same era. In the late fifth and early fourth century BC, doctors were using the word karkinos – the ancient Greek word for crab – to describe malignant tumours. Later, when Latin-speaking doctors described the same disease, they used the Latin word for crab: cancer. So, the name stuck.

    Even in ancient times, people wondered why doctors named the disease after an animal. One explanation was the crab is an aggressive animal, just as cancer can be an aggressive disease; another explanation was the crab can grip one part of a person’s body with its claws and be difficult to remove, just as cancer can be difficult to remove once it has developed. Others thought it was because of the appearance of the tumour.

    The physician Galen (129-216 AD) described breast cancer in his work A Method of Medicine to Glaucon, and compared the form of the tumour to the form of a crab:

    We have often seen in the breasts a tumour exactly like a crab. Just as that animal has feet on either side of its body, so too in this disease the veins of the unnatural swelling are stretched out on either side, creating a form similar to a crab.

    Not everyone agreed what caused cancer

    Bust of physician Erasistratus
    The physician Erasistratus didn’t think black bile was to blame. Didier Descouens/Musée Ingres-Bourdelle/Wikimedia, CC BY-SA

    In the Greco-Roman period, there were different opinions about the cause of cancer.

    According to a widespread ancient medical theory, the body has four humours: blood, yellow bile, phlegm and black bile. These four humours need to be kept in a state of balance, otherwise a person becomes sick. If a person suffered from an excess of black bile, it was thought this would eventually lead to cancer.

    The physician Erasistratus, who lived from around 315 to 240 BC, disagreed. However, so far as we know, he did not offer an alternative explanation.

    How was cancer treated?

    Cancer was treated in a range of different ways. It was thought that cancers in their early stages could be cured using medications.

    These included drugs derived from plants (such as cucumber, narcissus bulb, castor bean, bitter vetch, cabbage); animals (such as the ash of a crab); and metals (such as arsenic).

    Galen claimed that by using this sort of medication, and repeatedly purging his patients with emetics or enemas, he was sometimes successful at making emerging cancers disappear. He said the same treatment sometimes prevented more advanced cancers from continuing to grow. However, he also said surgery is necessary if these medications do not work.

    Surgery was usually avoided as patients tended to die from blood loss. The most successful operations were on cancers of the tip of the breast. Leonidas, a physician who lived in the second and third century AD, described his method, which involved cauterising (burning):

    I usually operate in cases where the tumours do not extend into the chest […] When the patient has been placed on her back, I incise the healthy area of the breast above the tumour and then cauterize the incision until scabs form and the bleeding is stanched. Then I incise again, marking out the area as I cut deeply into the breast, and again I cauterize. I do this [incising and cauterizing] quite often […] This way the bleeding is not dangerous. After the excision is complete I again cauterize the entire area until it is dessicated.

    Cancer was generally regarded as an incurable disease, and so it was feared. Some people with cancer, such as the poet Silius Italicus (26-102 AD), died by suicide to end the torment.

    Patients would also pray to the gods for hope of a cure. An example of this is Innocentia, an aristocratic lady who lived in Carthage (in modern-day Tunisia) in the fifth century AD. She told her doctor divine intervention had cured her breast cancer, though her doctor did not believe her.

    Ancient city of Carthage
    Innocentia from Carthage, in modern-day Tunisia, believed divine intervention cured her breast cancer. Valery Bareta/Shutterstock

    From the past into the future

    We began with Satyrus, a tyrant in the fourth century BC. In the 2,400 years or so since then, much has changed in our knowledge of what causes cancer, how to prevent it and how to treat it. We also know there are more than 200 different types of cancer. Some people’s cancers are so successfully managed, they go on to live long lives.

    But there is still no general “cure for cancer”, a disease that about one in five people develop in their lifetime. In 2022 alone, there were about 20 million new cancer cases and 9.7 million cancer deaths globally. We clearly have a long way to go.

    Konstantine Panegyres, McKenzie Postdoctoral Fellow, Historical and Philosophical Studies, The University of Melbourne

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

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  • The Dopa-Bean

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    Mucuna pruriens, also called the “magic velvet bean”, is an established herbal drug used for the management of male infertility, nervous disorders, and also as an aphrodisiac:

    The Magic Velvet Bean of Mucuna pruriens

    How it works is more interesting than that, though.

    It’s about the dopamine

    M. pruriens contains levodopa (L-dopa). That’s right, the same as the dopaminergic medication most often prescribed for Parkinson’s disease. Furthermore, it might even be better than synthetic L-dopa, because:

    M. pruriens seed extract demonstrated acetylcholinesterase inhibitory activity, while synthetic L-dopa enhanced the activity of the enzyme. It can be concluded that the administration of M. pruriens seed might be effective in protecting the brain against neurodegenerative disorders such as Parkinson’s and Alzheimer’s diseases.

    M. pruriens seed extract containing L-dopa has shown less acetylcholinesterase activity stimulation compared with L-dopa, suggesting that the extract might have a superior benefit for use in the treatment of Parkinson’s disease.❞

    ~ Dr. Narisa Kamkaen et al.

    Read in full: Mucuna pruriens Seed Aqueous Extract Improved Neuroprotective and Acetylcholinesterase Inhibitory Effects Compared with Synthetic L-Dopa

    Indeed, it has been tested specifically in (human!) Parkinson’s disease patients, which RCT found:

    ❝The rapid onset of action and longer on time without concomitant increase in dyskinesias on mucuna seed powder formulation suggest that this natural source of l-dopa might possess advantages over conventional l-dopa preparations in the long term management of Parkinson’s disease❞

    ~ Dr. Regina Katzenschlager et al.

    Read more: Mucuna pruriens in Parkinson’s disease: a double-blind clinical and pharmacological study

    Beyond Parkinson’s disease

    M. pruriens has also been tested and found beneficial in cases of disease other than Parkinson’s, thus:

    Mucuna pruriens in Parkinson’s and in some other diseases: recent advancement and future prospective

    …but the science is less well-established for things not generally considered related to dopamine, such as cancer, diabetes, and cardiometabolic disorders.

    Note, however, that the science for it being neuroprotective is rather stronger.

    Against depression

    Depression can have many causes, and (especially on a neurological level) diverse presentations. As such, sometimes what works for one person’s depression won’t touch another person’s, because the disease and treatment are about completely different neurotransmitter dysregulations. So, if a person’s depression is due to a shortage of serotonin, for example, then perking up the dopamine won’t help much, and vice versa. See also:

    Antidepressants: Personalization Is Key!

    When it comes to M. pruriens and antidepressant activity, then predictably it will be more likely to help if your depression is due to too little dopamine. Note that this means that even if your depression is dopamine-based, but the problem is with your dopamine receptors and not the actual levels of dopamine, then this may not help so much, depending on what else you have going on in there.

    The science for M. pruriens and depression is young, and we only found non-human animal studies so far, for example:

    Dopamine mediated antidepressant effect of Mucuna pruriens seeds in various experimental models of depression

    In summary

    It’s good against Parkinson’s in particular and is good against neurodegeneration in general.

    It may be good against depression, depending on the kind of depression you have.

    Is it safe?

    That’s a great question! And the answer is: it depends. For most people, in moderation, it should be fine (but, see our usual legal/medical disclaimer). Definitely don’t take it if you have bipolar disorder or any kind of schizoid/psychotic disorder; it is likely to trigger a manic/psychotic episode if you do.

    For more on this, we discussed it (pertaining to L-dopa in general, not M. pruriens specifically) at greater length here:

    An Accessible New Development Against Alzheimer’s ← scroll down to the heading that reads “Is there a catch?”

    Want to try some?

    We don’t sell it, but here for your convenience is an example product on Amazon 😎

    Enjoy!

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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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