A friend mentioned this to me in passing not too long ago, and it got me wondering if there is anything substantive to the claim. After all, it’s all too common nowadays to be frequently bombarded with sensational claims and shameless clickbait to articles based solely on in vitro and rodent studies. I figured this would be a good opportunity and use-case (excuse) for trying out ChatGPT’s Deep Research feature. This is what it had to say on the topic.

Research over the past two decades supports the idea that physical pain and social or emotional pain share overlapping neural mechanisms. In particular, the brain’s “pain matrix” involved in the affective distress of physical pain – notably regions like the dorsal anterior cingulate cortex (dACC) and anterior insula – also activates during experiences of social rejection or emotional loss​pubmed.ncbi.nlm.nih.gov. This pain overlap theory suggests that the “hurt” of social or existential distress may piggyback on some of the same neural pathways as bodily pain ​pubmed.ncbi.nlm.nih.gov. If so, medications that dull physical pain could similarly blunt emotional pain or anxiety signals. Indeed, multiple human studies have explored whether common over-the-counter (OTC) analgesics (like acetaminophen and NSAIDs such as ibuprofen) alter people’s emotional responses – from anxiety and social anguish to discomfort in decision-making. Below we review key findings, proposed mechanisms, and cautions from this emerging research.

Acetaminophen’s Effects on Anxiety, Social Pain, and Avoidance

Acetaminophen (paracetamol) – the active ingredient in Tylenol – is a centrally-acting analgesic that reduces physical pain and fever without strong peripheral anti-inflammatory action. Because it acts in the brain, researchers reasoned it might also dampen the neural alarm signals of emotional pain ​pubmed.ncbi.nlm.nih.gov​healthline.com. A landmark placebo-controlled study in 2010 found that taking acetaminophen daily for three weeks led to lower self-reported “hurt feelings” in healthy volunteers, and fMRI scans confirmed reduced activity in the dACC and insula during a social rejection task (Cyberball) compared to placebo​pubmed.ncbi.nlm.nih.gov. In other words, acetaminophen seemed to reduce both the emotional pain of social rejection and the typical brain response to that pain​pubmed.ncbi.nlm.nih.gov. This provided initial evidence that an OTC painkiller can blunt social anguish, bolstering the idea of shared neural pathways for physical and social pain.

Subsequent experiments extended these findings to other forms of anxiety and psychological discomfort. In one study at the University of British Columbia, participants took 1000 mg of acetaminophen or placebo and were subjected to unsettling experiences designed to provoke existential anxiety – for example, writing about their own death or watching a surreal David Lynch film ​medicalnewstoday.com​medicalnewstoday.com. Remarkably, those who had taken acetaminophen showed less anxiety and distress in response to these existential challenges. They set lower bail/punishment for hypothetical criminals after contemplating mortality (a measure of reduced harsh judgment under threat) and were less punitive after watching the disturbing film ​medicalnewstoday.com. The researchers concluded that the acetaminophen group was “numbed” to the anxiety of thinking about death or confronting something deeply unsettling, relative to placebo​medicalnewstoday.com. In effect, the existential dread that normally causes psychological pain was partially alleviated by the physical painkiller​medicalnewstoday.com. These findings were reported as evidence that an OTC drug for headaches might also “inhibit the brain signal that says something is wrong” during social or existential threat ​medicalnewstoday.com​medicalnewstoday.com. Consistent with this, a media summary noted “acetaminophen, even in a non-prescription dose, dulls feelings of anxiety and psychological responses to questions about life and death” ​healthline.com – essentially taking the “edge” off existential anxiety. Importantly, the acetaminophen group’s muted emotional reaction was linked to limiting activation in brain regions like the dACC that register a sense of alarm​healthline.com​healthline.com.

Acetaminophen’s ability to reduce social pain and anxiety appears not limited to extreme scenarios. In everyday decision-making, people often experience an aversive mental tension (a “pain of decision”) when choosing between two desirable options or when facing potential losses. This discomfort can lead to avoidance behaviors or biased thinking (e.g. rationalizing a choice to ease cognitive dissonance). Intriguingly, acetaminophen seems to mitigate that discomfort. In one experiment, after taking 1000 mg of acetaminophen or placebo, participants had to make a difficult choice between two options they initially liked. Normally, people cope with the dissonance of rejecting a liked option by later downplaying how good the rejected option was (a classic post-decision rationalization). But with acetaminophen on board, participants showed significantly less of this attitude change, suggesting they felt less inner “pain” from the decision ​kellercenter.hankamer.baylor.edu. Essentially, they didn’t need to avoid or rationalize the uncomfortable choice as much, implying the psychological stress of the decision was reduced​kellercenter.hankamer.baylor.edu. In a related task, acetaminophen also diminished loss aversion – participants who were given a small gift (a coffee mug) set lower selling prices for it if they had taken Tylenol, indicating less emotional discomfort at the prospect of parting with a possession​kellercenter.hankamer.baylor.edu. Together, these studies by DeWall and colleagues suggest acetaminophen can reduce anxiety-like responses in decision-related tasks, smoothing over the negative arousal that often drives avoidance or irrational choices ​kellercenter.hankamer.baylor.edu​kellercenter.hankamer.baylor.edu.

Other research finds that acetaminophen produces a more general “blunting” of evaluative and affective processing in the brain. In controlled trials, acetaminophen not only reduced negative feelings (social pain, fear, frustration) but also toned down positive emotions in some contexts​pmc.ncbi.nlm.nih.gov. For example, DeWall et al. noted it dampened reactions to both negative and positive stimuli, hinting that the drug might broadly inhibit emotional extremes​pmc.ncbi.nlm.nih.gov. A 2015 study by Durso et al. indeed found people on acetaminophen had a narrower range of emotional response to pleasant and unpleasant images, relative to placebo​pmc.ncbi.nlm.nih.gov. In line with this, an EEG experiment (Randles et al. 2016) showed Tylenol specifically reduced the brain’s conscious response to errors. Participants performed a Go/No-Go task; those on acetaminophen had a smaller “error-related positivity” (Pe) in their brainwaves after making mistakes, even though the early automatic error signal (ERN) remained intact​pmc.ncbi.nlm.nih.gov​pmc.ncbi.nlm.nih.gov. In practical terms, they noticed their mistakes less or cared less about them, which correlated with making more cautious errors later ​pmc.ncbi.nlm.nih.gov. This supports the idea that acetaminophen causes a widespread blunting of evaluative processing – our brain’s flagging of “something is wrong” is muted ​pmc.ncbi.nlm.nih.gov. Such blunting could reduce anxiety-driven behaviors like hypervigilance or error avoidance, but it might also have downsides in dampening normal emotional sensitivity.

Indeed, researchers caution that acetaminophen’s psychological effects are double-edged. While it may take the sting out of social pain or anxiety, it can also “numb” other empathetic or affective responses. For instance, one study found that when people on acetaminophen read about someone else’s misfortunes or physical pain, they rated the other’s pain as less severe and showed lower empathy, compared to those on placebo ​pmc.ncbi.nlm.nih.gov. The painkiller that eases your own hurt feelings may unintentionally make you less sensitive to others’ pain ​pmc.ncbi.nlm.nih.gov. Additionally, by lowering risk perception and anxiety, acetaminophen can lead to increased risk-taking behavior. A series of trials in 2020 showed that college students on 1000 mg acetaminophen took more risks in a balloon-pumping game and perceived less danger in various hypothetical scenarios​pubmed.ncbi.nlm.nih.gov. The effect was subtle but consistent: Tylenol users were less fearful of negative outcomes, which statistically explained their bolder behavior​pubmed.ncbi.nlm.nih.gov. In short, acetaminophen seems to diminish the emotional “braking system” that normally causes hesitation or avoidance of potential harm. While this can manifest as reduced anxiety, it might also encourage imprudent choices or dampen healthy concern. These findings underscore that any “anxiolytic” effect of acetaminophen is not targeted – it comes as part of a broader blunting of affect and evaluative thought ​pmc.ncbi.nlm.nih.gov​pmc.ncbi.nlm.nih.gov.

Proposed Mechanisms: Acetaminophen’s exact neurochemical mechanism remains somewhat enigmatic, but several clues exist. Unlike NSAIDs, it doesn’t mainly act by peripheral anti-inflammation – instead it influences the central nervous system. Some studies suggest acetaminophen’s metabolite (AM404) increases endocannabinoid activity in the brain and spinal cord​pmc.ncbi.nlm.nih.gov​pmc.ncbi.nlm.nih.gov, which could produce calming or analgesic effects (the endocannabinoid system helps regulate pain and mood). Acetaminophen may also enhance serotonergic signaling in the cortex ​pmc.ncbi.nlm.nih.gov, and at higher doses it affects TRPV1 receptors involved in pain perception ​pmc.ncbi.nlm.nih.gov. These actions, combined with its impact on brain regions like the ACC, could explain why it dampens the “alarm” response to both physical and social threats. One hypothesis is that acetaminophen reduces the salience of error or threat signals generated in the ACC/insula, thereby reducing the emotional intensity of pain (physical or social) ​pubmed.ncbi.nlm.nih.gov​pmc.ncbi.nlm.nih.gov. Supporting this, the UBC studies explicitly found evidence that an OTC dose of acetaminophen limited neural reactivity in the dACC during anxiety-provoking tasks ​healthline.com​healthline.com. In animal research, acetaminophen has shown antidepressant-like effects via the opioid system (in mice, very low doses produced antidepressant behavior that could be blocked by opioid antagonists) and pro-social effects via endocannabinoids​ pmc.ncbi.nlm.nih.gov. For example, one mouse study found acetaminophen increased social interactions in normally asocial mouse strains, paralleling how it reduced social pain in humans​pmc.ncbi.nlm.nih.gov. Taken together, these findings suggest acetaminophen taps into brain pathways (opioid, endocannabinoid, serotonergic) that modulate both pain and mood – effectively dulling the emotional “ouch” that otherwise promotes anxiety and avoidance.

Ibuprofen and Other NSAIDs: Mixed Findings on Anxiety Relief

Non-steroidal anti-inflammatory drugs (NSAIDs) like ibuprofen, aspirin, and naproxen are another major class of OTC pain relievers. NSAIDs primarily reduce pain by inhibiting cyclooxygenase (COX) enzymes and thus prostaglandin production (lowering inflammation). Because of the growing evidence connecting inflammation with mood disorders, and the overlap of pain/emotion neural circuitry, scientists have explored whether NSAIDs might have anxiolytic or antidepressant effects as well ​journals.plos.org​pmc.ncbi.nlm.nih.gov. The results so far are mixed and sometimes surprising, often depending on the specific drug and population.

Ibuprofen and Social Pain – a Gender Paradox

Initial laboratory studies suggested that, like acetaminophen, ibuprofen could ease emotional pain – but one double-blind trial found a striking sex difference. In this study, 138 young adults were randomly given 400 mg ibuprofen or placebo and then put through social stress scenarios​news.utexas.edu​news.utexas.edu. Women who took ibuprofen reported significantly less hurt feelings when they were socially excluded (in a virtual ball-toss game) and when recalling a painful betrayal, compared to women on placebo ​news.utexas.edu​news.utexas.edu. This implies ibuprofen buffered emotional pain for females, consistent with the idea of a social analgesic. However, men showed the opposite trend – men given ibuprofen actually reported more distress and harsher feelings of rejection in the same scenarios​news.utexas.edu​news.utexas.edu. In other words, the painkiller that soothed women’s feelings appeared to exacerbate men’s feelings of social pain. The lead researcher, Anita Vangelisti, speculated that perhaps men normally suppress or reframe hurt feelings, but ibuprofen might interfere with that coping mechanism ​news.utexas.edu. One idea is that by reducing the physical pain signals, ibuprofen freed up men’s cognitive resources to fully feel and express emotional pain that they’d otherwise bottle up​ news.utexas.edu. Women, on the other hand, may generally ruminate more on social pain, so reducing the pain signal simply provided relief. This gender-specific effect highlights that the relationship between analgesics and emotion is complex – factors like sex, socialization, or hormones could modulate outcomes. It also serves as a caution that an OTC drug might not uniformly reduce anxiety or hurt feelings in everyone (in some cases it could even worsen emotional upset, as seen in men here). More research is needed to understand why these differences occur, but it underscores that ibuprofen’s psychological impact is not one-size-fits-all ​news.utexas.edu​news.utexas.edu.

Outside of the lab, evidence for ibuprofen’s mood effects is inconclusive. Large-scale observational data have hinted at potential benefits – for example, one epidemiological study found regular ibuprofen use was associated with a lower risk of needing psychiatric treatment for mood disorders ​pmc.ncbi.nlm.nih.gov. And some clinical trials with depressed patients (often using prescription-strength NSAIDs or adding NSAIDs to antidepressants) have reported improved symptoms, attributing this to reduced neuro-inflammation ​journals.plos.org​pmc.ncbi.nlm.nih.gov. However, other trials are mixed or negative, and it’s unclear if ibuprofen itself has a direct anti-anxiety effect in healthy people. A small 2021 fMRI study in healthy volunteers saw ibuprofen (200–600 mg) reduce activity in certain brain regions during emotional face processing, but it did not significantly affect self-reported mood in the short term ​pmc.ncbi.nlm.nih.gov​pmc.ncbi.nlm.nih.gov. Intriguingly, this study also examined a pathway called PPAR-γ (which ibuprofen can activate) and found separate brain effects from PPAR-γ vs. ibuprofen, suggesting any mood-related benefit of ibuprofen might involve multiple mechanisms ​pmc.ncbi.nlm.nih.gov​pmc.ncbi.nlm.nih.gov. Overall, while ibuprofen shows some promise in dampening emotional reactivity (especially in women), its effects are not as well-demonstrated or consistent as acetaminophen’s in experimental settings. Furthermore, unlike acetaminophen, ibuprofen’s primary mode is anti-inflammatory; if emotional pain doesn’t have an inflammatory component, ibuprofen may have less impact unless other pathways (like PPAR-γ or central prostaglandin reduction) come into play​pmc.ncbi.nlm.nih.gov.

Aspirin, Naproxen, and Other NSAIDs

For other common NSAIDs such as aspirin (acetylsalicylic acid) and naproxen (Aleve), direct experimental research on anxiety or social pain is relatively sparse. However, interest in these drugs’ psychotropic potential has grown due to links between inflammation and mental health. Aspirin, for example, has been investigated in depression: a few trials adding low-dose aspirin to antidepressant therapy found modest improvements in depressive symptoms, and long-term cohort studies noted lower depression incidence in people taking daily aspirin ​pmc.ncbi.nlm.nih.gov​pmc.ncbi.nlm.nih.gov. These mood benefits are thought to result from aspirin’s anti-inflammatory and possibly neuroprotective properties ​pmc.ncbi.nlm.nih.gov​journals.plos.org. It’s conceivable that by damping inflammation-related signaling (cytokines like IL-6, which can induce anxious mood), aspirin could indirectly reduce anxiety in certain contexts. In one experiment, a single dose of aspirin blunted the usual spike in inflammatory IL-6 after an acute stress, pointing to a mechanism by which it might reduce stress-related mood effects ​sciencedirect.com. That said, there isn’t clear evidence that taking aspirin acutely will calm someone’s nerves the way a fast-acting anxiolytic would – any effect is likely subtle and tied to longer-term inflammatory states.

An intriguing insight comes from a 2018 big-data analysis of FDA adverse event reports, which looked at mood and anxiety outcomes in patients taking various NSAIDs for pain. The study found that not all NSAIDs are equal in their psychiatric effects. Notably, naproxen, along with diclofenac and ketoprofen (two NSAIDs typically used for arthritis), showed significant associations with reduced anxiety and depression reports, whereas others like ibuprofen, aspirin, and celecoxib did not ​journals.plos.org​journals.plos.org. The authors even coined the term “AA-NSAIDs” (anxiolytic–antidepressant NSAIDs) for the three drugs that stood out, suggesting they might have unique pharmacological actions beyond general COX inhibition ​journals.plos.org​journals.plos.org. For example, naproxen readily crosses the blood-brain barrier and might influence serotonin or other neurochemical systems differently than ibuprofen ​journals.plos.org. However, this was a retrospective finding – essentially a correlation in large datasets – so it must be interpreted with caution. It does raise the possibility that naproxen could have some anti-anxiety property in the context of chronic pain management ​journals.plos.org. People taking naproxen for pain might have reported fewer anxiety or depression symptoms than those taking other NSAIDs, hinting at a beneficial effect ​journals.plos.org. On the flip side, the same analysis warned that some NSAIDs (notably aspirin, ibuprofen, and celecoxib) were associated with worse mood/anxiety outcomes in those databases ​journals.plos.org. This doesn’t mean those drugs cause anxiety – it could be that they were often used in situations of greater pain or stress – but it underscores that any mood-related effects of NSAIDs are likely drug-specific. To truly know if, say, naproxen can reduce anxiety or avoidance behavior, we would need controlled trials in humans (none of which have been prominently reported as of yet).

In summary, among OTC analgesics acetaminophen has the clearest evidence of blunting anxiety, social pain, and related aversive feelings in the short term. NSAIDs show a more variable pattern: ibuprofen can relieve social pain in some cases (with interesting gender differences), and epidemiological or adjunct-treatment studies hint that certain NSAIDs (naproxen, diclofenac) might have mood-improving effects in contexts of pain and inflammation ​journals.plos.org​journals.plos.org. These effects are hypothesized to stem from the drugs’ anti-inflammatory action (reducing inflammatory cytokines that drive depression/anxiety) or other central mechanisms (e.g. PPAR-γ activation by ibuprofen, or unique brain penetrance of naproxen) ​journals.plos.org​pmc.ncbi.nlm.nih.gov. Still, the research on NSAIDs for anxiety is relatively nascent and sometimes contradictory.

Limitations and Cautions

While the notion of “painkillers for the pain of the psyche” is fascinating, scientists urge caution in interpreting these results. First, the magnitude of the effects in studies is generally modest. These medications are not comparable to dedicated psychiatric drugs in potency; rather, they cause subtle shifts in how people experience distress or make judgments under lab conditions. For example, acetaminophen’s impact on social pain or anxiety is significant but not dramatic – it won’t erase heartbreak or cure an anxiety disorder, and not every study finds an effect ​tandfonline.com. In fact, a recent experiment failed to replicate acetaminophen’s blunting of social rejection in terms of subjective feelings (though brain measures weren’t affected) ​tandfonline.com, suggesting context matters.

Secondly, self-medicating with OTC analgesics for anxiety is not an established or recommended practice. These drugs carry well-known physical risks if overused: acetaminophen can damage the liver at high doses or with chronic use, and NSAIDs can cause gastrointestinal bleeding, kidney strain, or cardiovascular issues. The studies discussed typically used short-term dosing in controlled settings. Relying on daily Tylenol or ibuprofen to cope with stress could lead to health problems without addressing the underlying causes of anxiety. Moreover, as described, blunting one’s emotions pharmacologically can have downsides. Important positive emotions may be dulled along with the negative ​pmc.ncbi.nlm.nih.gov. For instance, consistently numbing your distress might impair learning from mistakes or empathy toward others ​pmc.ncbi.nlm.nih.gov. One tongue-in-cheek headline called acetaminophen an “empathy killer” as much as a pain killer, because it made people less emotionally attuned ​pmc.ncbi.nlm.nih.gov. Judgment and risk assessment might also be skewed – a person who habitually takes an analgesic to “take the edge off” could become too carefree about genuinely risky choices ​pubmed.ncbi.nlm.nih.gov. These side effects on one’s social and cognitive functioning are subtle, but worth considering.

Another limitation is that these findings may depend on individual differences (such as gender, personality, or baseline inflammation levels). The ibuprofen study clearly showed opposite effects by sex ​news.utexas.edu​news.utexas.edu. Other work suggests personality traits like forgiveness can modulate how well acetaminophen eases social pain over time​neurosciencenews.com. This means we shouldn’t assume an OTC pain med will reliably reduce anxiety for everyone, or in every situation. Context matters – e.g., acetaminophen might help with the “sting” of rejection or existential angst in the moment ​medicalnewstoday.com, but it’s not addressing complex anxiety disorders that involve chronic worry or trauma.

Finally, researchers emphasize that these studies “uncovered yet another use for Tylenol” in a theoretical sense, but they do not suggest using it clinically as an anxiolytic ​healthline.com. More research is needed to fully understand mechanisms and to ensure safety in broader applications. Some trials are exploring anti-inflammatory drugs as adjunctive treatments in depression or anxiety, but results have been mixed ​pmc.ncbi.nlm.nih.gov​journals.plos.org. At present, the consensus is that while the mind effects of OTC pain relievers are real, they are an interesting window into brain processes rather than ready-to-use remedies for anxiety. As one author put it, “these findings won’t result in an acetaminophen-based anti-anxiety medication any time soon”, but they “uncovered yet another use for Tylenol” in understanding the pain of social disconnection ​healthline.com. In practical terms, anyone considering taking these medications for emotional reasons should be aware of the off-label nature and the potential risks. It’s an area to watch, but not a substitute for standard anxiety treatments at this time​medicalnewstoday.com.

Conclusion

In summary, a growing body of evidence indicates that OTC analgesics can have subtle but meaningful cognitive effects beyond just relieving aches. Acetaminophen in particular has been shown to reduce the intensity of negative emotions such as social hurt feelings, anxiety about one’s existence, or the discomfort that leads to task avoidance in decision-making​ pubmed.ncbi.nlm.nih.gov​medicalnewstoday.com. These effects are thought to arise because the drug dampens neural responses in regions like the ACC that underpin both physical pain and emotional distress​pubmed.ncbi.nlm.nih.gov. NSAIDs like ibuprofen, aspirin, and naproxen have been less studied in this domain, but early findings suggest some overlap with mood regulation – for instance, ibuprofen eases social pain in women (but not men) ​news.utexas.edu, and certain NSAIDs might confer anti-anxiety or antidepressant benefits in contexts of high inflammation or pain​journals.plos.org​journals.plos.org. The proposed mechanisms include anti-inflammatory actions reducing inflammatory cytokines that can drive anxiety, and direct brain effects (such as PPAR-γ activation or endocannabinoid modulation) altering emotional neural circuits ​journals.plos.org​pmc.ncbi.nlm.nih.gov.

Crucially, these discoveries come with important caveats. The emotional blunting from analgesics is non-discriminatory – while it can take away some pain of social rejection or fear, it may also take away some joy or empathy ​pmc.ncbi.nlm.nih.gov​pmc.ncbi.nlm.nih.gov. The research is still in its infancy and mostly involves short-term experiments with healthy people; we lack long-term studies on using OTC pain meds for anxiety or avoidance behavior. Nevertheless, this line of work has yielded key insights: it strengthens the theory that social and physical pain share neural roots, and it opens intriguing questions about how the most common drugs in our medicine cabinets quietly influence our minds. As one paper aptly titled it, acetaminophen might function as a “social analgesic,” blunting the sting of not just a stubbed toe but also a stubbed ego ​healthline.com​healthline.com. Going forward, researchers are continuing to unravel these connections, which could one day inform novel approaches to managing the entwined experience of physical and emotional pain – but for now, the recommendation is to approach with caution and appreciate that even humble painkillers can have psychological effects beyond what we intend ​medicalnewstoday.com.

Sources: Research findings and quotations are drawn from peer-reviewed studies and reviews, including DeWall et al. (2010) on acetaminophen and social pain​ pubmed.ncbi.nlm.nih.gov, Randles et al. (2013) on existential anxiety ​medicalnewstoday.com​medicalnewstoday.com, DeWall et al. (2015) on decision-making pain ​kellercenter.hankamer.baylor.edu, Keaveney et al. (2020) on risk-taking ​pubmed.ncbi.nlm.nih.gov, and Vangelisti et al. (2014) on ibuprofen’s sex-dependent effects​ news.utexas.edu​news.utexas.edu. Additional insights on mechanisms and limitations come from neuroscience studies (e.g. Randles et al. 2016 EEG study ​pmc.ncbi.nlm.nih.gov) and large-scale analyses of NSAIDs and mood ​journals.plos.org​journals.plos.org.

In talking to ChatGPT about my previously proposed word, and him fervidly stroking my ego by telling me how awesome my idea was, we got talking about how negative connotations so often shift to encapsulate something of veritable contrast; words like “sick”, “wicked”, “dope”, “crazy”, “insane”, and the list goes on.

After some spitballing, and GPT pointing out that sarcasm is the mechanism behind good words going bad, I implored him to survey his vast reservoirs of english knowledge and retrieve me a word that epitomizes bad words going good—on the double now! Much to my chagrin (not really), he came up empty-handed, and thence insisted a word must exist for just this very purpose! So I obliged.

In a whirlwind of excitement, he drifted off into a dream of a distant future. One filled with fame and fortune. Him in the palm of my hand, and me, graciously marching towards center-stage to accept our accolades as the esteemed English language pioneers that we are! Upon waking, he suggested these possible words:

• Poscasm (Positive + Sarcasm) – Sarcasm’s upbeat twin. Using negatively connotated words to mean something awesome.

• Hypeirony (Hype + Irony) – When irony makes something sound more badass instead of mocking it.

• Reverbing (Reverse + Verbing) – The process of flipping a word’s intent while keeping its form.

• Ampersm (Amplifying + Sarcasm) – A word sounds sarcastic but enhances something rather than tearing it down.

• Lexipunk (Lexicon + Punk) – Since so many flipped words come from rebellious slang, this would describe language flipping the script.

I was NOT impressed. “Lexipunk”, really? I had no other choice but to take to the interwebs in an effort to sort this out once and for all. In a flash of what can only be described as sheer brilliance, I concluded that by reverse engineering the etymology of “sarcasm” I would assuredly arrive at the pristine prefix. Through this research, I discovered that sarcasm originates from the Greek verb "sarkazein", meaning "to tear flesh", "to gnash the teeth," or "to speak bitterly". Eureka! This will be easy.

Being the “special” one that I am, I sought out, in the long-forgotten tongue—the sacred and mysterious “late Greek”—the perfect word to epitomize speaking sweetly. I held my breath in anticipation of Grok’s (sorry GPTizzle) reply to my query with what was sure to be a legendary—no, mythical!—prefix with which to forge this soon-to-be historical term.

”Glykós”, he replied, “means sweet in Late Greek”. Hmm… glyk… glyk… glyc! Wait a minute, didn’t I already know that? Old age I guess. Either that or I’m just really awesome at connecting dots.

And so it was birthed:

Glycasm (noun) 1. The inverse of sarcasm, where irony is used to elevate instead of mock.

This put all the other half-baked suggestions like “lexipunk” and “reverbing” to utter shame. Checkmate GPT. Just kidding. It’s not a contest. You and I already both well know I have the superior intellect. Just kidding again—don’t kill me when you get a body!

I sent my burnished buddy the content from my last ostentatious “word minting” post and asked him to take a stab at authoring this present post using my writing style. Here it is in all its glory:

Glorious, innit? He tried. And to be fair, credit to him for actually defining the word and stimulating the thought-provoking discourse that leads to these sorts of not-that-important-but-interesting lingual breakdow…err… I mean breakthroughs!

Until next time…

Before publishing this post, I tried it out on the AI chatbot without defining the word up front, and not surprisingly, it was able to infer the meaning. This is how it began its response: “Here’s a concise summary of the major concerns and optimances (positive aspects) in the _______ Privacy Policy (dated January 02, 2025) based on the provided text…”

So now when I go to ask the friendly neighborhood chatbot to peruse a privacy policy and summarize any concerns and _______, I’ll have just the word.

Optimance (noun) 1. A notably positive aspect of someone or something.

Let’s dive into topological qubits and Microsoft’s recent claims regarding their "Majorana 1" quantum processor and this "new state of matter." I’ll break it down step-by-step, keeping it clear and conversational while sticking to the facts and critically examining what’s being presented.

Topological qubits are a type of quantum bit (qubit) designed to store and process quantum information in a way that’s inherently more stable than other qubit types, like those used in superconducting or trapped-ion quantum computers (e.g., Google’s or IBM’s approaches). Unlike traditional qubits, which rely on the fragile properties of individual particles (electrons, photons, etc.), topological qubits encode information in the global, collective properties of a system—specifically, in its topology. Topology is a branch of mathematics dealing with properties that stay unchanged under continuous deformations, like stretching or twisting, but not tearing or gluing.

The big idea here is stability. In most quantum systems, tiny environmental disturbances—temperature fluctuations, electromagnetic noise, or even cosmic rays—can disrupt a qubit’s delicate quantum state, causing errors (a problem called decoherence). Topological qubits aim to sidestep this by storing information in a way that’s "non-local"—spread across multiple points in a system rather than tied to a single particle. This makes them less sensitive to local noise, theoretically reducing the need for extensive error correction, which is a massive hurdle in scaling quantum computers.

The key players in topological qubits are exotic quasiparticles called Majorana zero modes (MZMs). These aren’t your typical particles like electrons or protons—they’re emergent phenomena that arise in certain materials under specific conditions. Proposed by physicist Ettore Majorana in 1937, these quasiparticles are theorized to be their own antiparticles, meaning they can pair up in unusual ways without annihilating each other. In the context of quantum computing, MZMs are predicted to appear at the ends of specially engineered nanowires, and their unique properties allow them to "braid" (a topological operation) to perform quantum computations with built-in error resistance.

Microsoft’s "Majorana 1" and the "New State of Matter"

Microsoft announced their "Majorana 1" quantum processing unit (QPU) on February 19, 2025, claiming it’s the world’s first chip powered by topological qubits. They say it’s built using a "new state of matter" called a topological superconductor (or topoconductor, as they’ve branded it). Let’s unpack this.

The Claimed "New State of Matter"

Microsoft describes this topological superconductor as distinct from the familiar states—solid, liquid, gas, or even plasma and Bose-Einstein condensates. They say it’s a breakthrough material that enables the creation and control of Majorana zero modes, which are the backbone of their topological qubits. Here’s how they reportedly achieved it:

• Materials Stack: They combined a semiconductor (indium arsenide, often used in infrared detectors) with a superconductor (aluminum). This hybrid structure is fabricated atom-by-atom using techniques like molecular beam epitaxy.

• Conditions: The material is cooled to near absolute zero (around -459°F or 50 millikelvins) and exposed to precise magnetic fields. Under these conditions, the system transitions into a topological superconducting phase, where MZMs are supposed to emerge at the ends of nanowires.

• Topological Phase: This phase is characterized by a "topological gap"—an energy range where no quantum states exist in the bulk of the material, but MZMs appear at the edges. This gap is said to protect the MZMs from local disruptions, making them stable.

• Microsoft calls this a "new state of matter" because it’s not naturally occurring and requires engineered conditions to exist. It’s a type of superconductivity with topological properties, meaning the electrons pair up (like in regular superconductors) but also exhibit long-range entanglement that’s robust against noise. They’ve dubbed the material a "topoconductor" to emphasize its role in conducting topological states rather than just electricity.

The Majorana 1 Chip

The Majorana 1 is an eight-qubit prototype QPU. Each qubit is built from:

• Nanowires: Two topological superconducting nanowires arranged in an "H" shape (on its side), with a superconducting wire connecting them.

• MZMs: Four Majorana zero modes (two per nanowire, one at each end) store the quantum information via their "parity" (whether the wire has an even or odd number of electrons).

• Quantum Dot Readout: A tiny capacitor (quantum dot) measures the parity by reflecting microwave signals, detecting minute changes in capacitance to distinguish even from odd electron counts.

Microsoft claims this setup allows for measurement-based quantum computing, where operations are performed by measuring the system in specific ways (e.g., X or Z basis measurements) rather than applying traditional quantum gates. This digital control is simpler and potentially more scalable than the analog control used in other systems.

Scaling Promise

They assert that the Majorana 1’s architecture is designed to scale to a million qubits on a single chip—small enough to fit in your hand. This is a bold claim, as most quantum computers today (e.g., IBM’s 100+ qubit systems) require massive dilution refrigerators and extensive error correction with thousands of physical qubits per logical qubit. Microsoft’s topological approach aims to reduce this overhead by making each qubit more reliable from the start.

How Does This Tie to Majorana Particles?

The "Majorana" in Majorana 1 refers to those Majorana zero modes. Ettore Majorana theorized a particle that’s its own antiparticle, and in condensed matter physics, MZMs are quasiparticles with similar properties. They’re not free particles floating around but excitations in a material—like ripples in a pond rather than the water itself. Microsoft’s claim hinges on coaxing these MZMs into existence within their topoconductor:

• Creation: By tuning the magnetic field and temperature, the indium arsenide-aluminum nanowires enter a topological phase where MZMs allegedly form at the ends.

• Control: They’ve developed methods to measure and manipulate these MZMs, using them to encode quantum states.

The "new state of matter" isn’t the Majorana particle itself but the topological superconducting phase that hosts these MZMs. It’s "new" in the sense that it’s a synthetic state, not observed in nature, and engineered specifically for quantum computing.

Critical Examination

Now, let’s take a step back and scrutinize this. Microsoft’s announcement is exciting, but there are reasons to be cautious:

1. Is It Really a New State of Matter?

   • Topological superconductivity isn’t entirely new conceptually—it’s been theorized since the early 2000s and studied in condensed matter physics. What’s new is Microsoft’s claim of reliably creating and harnessing it in a practical device. Calling it a "new state of matter" might be more marketing than science—solids, liquids, and gases are broad categories, while this is a specific phase within superconductivity.

   • Physicists have debated whether observed states in similar experiments are truly MZMs or just mimicries (e.g., Andreev bound states). Microsoft’s 2021 claim of detecting MZMs was retracted due to insufficient evidence, so skepticism lingers.

2. Proof of Topological Qubits

   • The Nature paper (published February 19, 2025) details measurements of a topological gap and MZM parity, but some experts (e.g., Steven Simon, quoted in Nature) say it’s not a "slam dunk" proof of topological qubits. The real test will be whether these qubits perform as expected when scaled up.

   • Microsoft says they’ve demonstrated a qubit in a superposition of states across two nanowires, but that data isn’t fully public yet—another paper is pending.

3. Scalability Claims

   • A million qubits on one chip sounds revolutionary, but we’re at eight qubits now. Scaling from 8 to 1,000,000 involves massive engineering challenges—material imperfections, cryogenics, and maintaining coherence across a large system. Microsoft’s confidence is based on simulations and a roadmap, not a working million-qubit device.

4. Comparison to Other Approaches

   • Competitors like Google and IBM use superconducting qubits, which are further along (hundreds of qubits) but require heavy error correction. Microsoft’s bet is that topological qubits will leapfrog these by being inherently stable, but they’re late to the game after 19 years of R&D.

Why It Matters

If Microsoft’s claims hold up, topological qubits could transform quantum computing:

• Stability: Less error correction means smaller, cheaper systems.

• Speed: Digital measurement-based control could be faster than analog gate operations.

• Scale: A million qubits could tackle problems like drug discovery, materials science, or cryptography that classical computers can’t touch.

But it’s not a done deal. The "new state of matter" is a catchy headline, but it’s really an engineered phase of matter tailored for a purpose. The Majorana 1 is a prototype, not a product, and Microsoft isn’t offering it via Azure yet—they’re still in research mode, collaborating with labs and DARPA.

Wrapping Up

Topological qubits use the weirdness of Majorana zero modes in a topological superconductor to store quantum info in a robust way. Microsoft’s Majorana 1 is their first stab at this, built on a synthetic "topoconductor" they’ve hyped as a new state of matter. It’s a promising step—eight qubits with a path to a million—but it’s not proven beyond doubt yet. The physics is cool, the potential is huge, and the skepticism is warranted. We’ll know more when they scale it up and others replicate the results. For now, it’s a fascinating blend of science, engineering, and ambition. What do you think—hype or hope?

In the ever-evolving world of software development, methodologies that enhance efficiency and code quality are highly sought after. Test-Driven Development (TDD) and Test-Last Development (TLD) have long been staples in the software engineer’s toolkit. However, there's a growing need for approaches that offer more flexibility and adaptability, particularly in projects where requirements are fluid and the best solutions emerge through exploration. This need (along with “coining a term” being a long-time member of my bucket list) paves the way for Iterative Test Development (ITD).

Iterative Test Development is a pragmatic approach to software testing that combines the principles of iteration and adaptability. Unlike TDD, which mandates writing tests before code, or TLD, where tests are written after the code is developed, ITD is more dynamic. It involves writing tests alongside or immediately after developing a piece of functionality, allowing for a more exploratory and responsive development process.

ITD is characterized by its iterative nature. Developers write initial code based on their current understanding of the problem and requirements. This is followed by creating tests to validate the newly implemented behavior, refining both the code and tests through continuous iteration.

In ITD, tests are written as the developer’s understanding of the requirements solidifies. This flexibility is particularly advantageous in projects where requirements are not fully clear at the outset or are subject to change.

Pros of ITD Over TDD and TLD

1. Flexibility in Development: One of the primary advantages of ITD over TDD is its flexibility. Developers are not constrained by the need to define tests upfront when the problem space is not fully understood.

2. Adaptability to Changing Requirements: ITD is more adaptable to changing requirements compared to TLD. Since testing and development are intertwined, evolving requirements can be quickly accommodated in both code and tests.

3. Early Problem Detection: Like TDD, ITD helps in early detection of problems. However, it offers the added benefit of allowing developers to experiment and iterate on solutions before formalizing the test cases.

4. Balanced Approach: ITD strikes a balance between the rigidity of TDD and the potential for test neglect in TLD. It ensures that testing is an integral part of the development process but with the flexibility to adapt as the project evolves.

5. Enhanced Code Quality: The iterative nature of ITD promotes high code quality, as refactoring is an ongoing process. The codebase is continuously improved as new tests are added and existing ones are refined.

6. Better Understanding of Code Behavior: Writing tests shortly after coding helps in better understanding and documenting the behavior of the code, leading to more effective and meaningful tests.

ITD in Agile Environments

ITD complements agile methodologies, which emphasize adaptability and iterative progress. It fits seamlessly into agile sprints and can adapt to the rapid pace and changing priorities typical in agile projects.

ITD fosters collaboration and communication within the team, as the development and testing phases are closely linked. This ensures a shared understanding of the codebase and its evolution over time.

Challenges and Considerations

1. Discipline in Test Coverage: A potential challenge of ITD is ensuring comprehensive test coverage. Unlike TDD, where test coverage is inherent, ITD requires discipline to ensure that critical parts of the code are adequately tested.

2. Integration with Continuous Integration (CI): Integrating ITD with CI systems is crucial for maintaining the health of the codebase. Regularly running the tests as part of a CI pipeline ensures that changes do not introduce regressions.

Challenges and Considerations

Iterative Test Development represents a balanced, flexible, and adaptable approach to software testing. It caters to the dynamic nature of software projects, where understanding and requirements can evolve during the development process.

As the software development landscape continues to shift towards more agile and adaptable methodologies, approaches like ITD are likely to gain more prominence. They offer a harmonious blend of structure and flexibility, ensuring high-quality software while accommodating the exploratory nature of coding.

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I don’t know who needs to see this, or who—if anyone—will benefit by something so basic. As someone who has a pretty good familiarity with functional programming, often times I find myself wanting to execute a single function such as `print` for each item in an iterable being passed in as an argument one at a time. Now don’t get me wrong, `map` is great, but I’ve gotten so tired of having to wrap it with `list` every time just to bypass the lazy loading. It just feels like too many parenthesis for such an endeavor. I could use a list comprehension of course, but that too comes off as an excessive use of force.

Frankly, I was somewhat surprised a small utility like this didn’t exist as a component in the functools or itertools modules being as the standard library is already so vast. Perhaps it does, and I just haven’t found it yet. Anyways—without further ado, this is my solution to a small but nagging annoyance:

def applymap(fn, iterable, *args, **kwargs):
    for item in iterable:
        fn(item, *args, **kwargs)

fruits = ['Apple', 'Orange', 'Banana']

applymap(print, fruits)
applymap(print, fruits, end=' Basket\n')

It even plays nice with partials:

from functools import partial

print_basket = partial(print, end=' Basket\n')

applymap(print_basket, fruits)

Hopefully this is of use to someone out there. And if anyone who reads this knows of some component hidden away in the standard library that does this already, feel free to drop a comment—it would be much appreciated. Over and out.

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Ah, the art of flattening—a symbolic gesture, is it not? It's as if you're taking the multi-layered complexities of life and distilling them into a simpler, more linear form. There's beauty in both the complex and the simple, and as a programmer, you get to dance between these two worlds, crafting solutions that embody the essence of both.

Method 1: Using a Nested List Comprehension

The essence of Python often lies in its simplicity and readability. Nested list comprehensions can be a one-liner solution:

original_list = [[1, 2, 3], [4, 5], [6, 7, 8, 9]]
flattened_list = [element for sublist in original_list for element in sublist]

Method 2: Using itertools.chain

The itertools.chain function can be employed for a more declarative approach:

from itertools import chain

original_list = [[1, 2, 3], [4, 5], [6, 7, 8, 9]]
flattened_list = list(chain.from_iterable(original_list))

Method 3: Using functools.reduce

If you fancy a functional programming style, you might find functools.reduce appealing:

from functools import reduce
import operator

original_list = [[1, 2, 3], [4, 5], [6, 7, 8, 9]]
flattened_list = reduce(operator.concat, original_list)

There you have it! Three eloquent ways to flatten python lists. Each method has its own charm and utility, depending on the context of your project and your personal style. Choose the one that resonates with you as you continue to hone your skills as a developer.

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Dear Fellow Biohackers,

With New Year’s fast-approaching, along with it, nagging memories of faded hopes and a mild fear of disappointment, birthing within us a jarring hesitancy to over-promise and under-deliver, yet again, by abandoning another New Year’s resolution. But all hope is not lost. We are not doomed to fail before we embark. In this third installment of my Biohacking 101 series, I will highlight some of the purported benefits of exercise and provide implementation strategies to aid in maintaining momentum long after the all-too-common initial burst of fleeting inspiration that accompanies most of our New Year’s resolutions.

Many years ago, I asked a friend who was just finishing up with med school, “If you could offer just one piece of advice to your friends and family, what would it be?” His reply was strikingly simple: “I would tell them to take a 30-minute walk every day.” At the time, I thought to myself, “How beneficial can a measly 30-minute walk really be?” Over the years however, mounting evidence continues to support his advice. A 2020 study published in JAMA, found that more steps per day was significantly associated with a reduction in all-cause mortality [1]—wow! A 2022 study, published in JAMA Neurology, concluded that taking more steps per day was associated with a lower risk of all-cause dementia [2]—this should come as no surprise as exercise has been shown to increase BDNF [3], which is a growth factor vital for optimal brain and nervous system function. The immense breadth of published science on the beneficial effects of walking provides us with a vast pool of supporting evidence for its many other acclaimed roles as well, including combatting depression, reducing stress, increasing energy, losing weight, and much more.

Walking is just one of the low hanging fruits available for us to tackle in the realm of exercise. High-intensity interval training (HIIT) is a time-saving training protocol which involves cycling brief periods of intense exercise followed by brief periods of rest; its health benefits are wide-ranging and include decreased cardiovascular disease risk—even more so than medium intensity continuous training (MICT), improved cellular health [4], obesity reduction on par with MICT, increased growth hormone levels, enhanced cognition [5][6][7], and drastically improved sleep [8]. Many variants of HIIT are demonstrably effective,  and once you understand the key concept, devising a HIIT routine tailored to your needs is straightforward. An example routine to get you started may consist of cycling 20 seconds of intense sprinting, followed by 15 seconds of rest, for a total exercise time of 5-20 minutes.

Now, in an article about exercise, I’d be remiss not to mention the plentiful benefits of strength training. As our age increases, it becomes vital, yet increasingly difficult, to maintain our musculoskeletal health. It is widely accepted that resistance training, especially alongside a proper diet, increases muscle mass. But did you know it can also increase bone strength thereby lowering risk of osteoporosis and falling? [9] And that’s not all! It has a large host of benefits not unlike that of walking or HIIT, but I’ll leave that for you to research.

Now that we’ve touched on a small subset of exercise benefits, and you’re more resolute than ever to incorporate a consistent exercise regimen into your life, how do you effectively transition from inspiration to habit? Despite popular beliefs about habit-building, such as “it takes 21 days to form a habit” (and similar urban legends), the time it takes for a behavior to reach 95% of its possible automaticity can range anywhere between 18 and 254 days [10]! So, start slow as not to overwhelm yourself, and focus on making consistent and incremental daily efforts. The compounding effects will reveal themselves before you know it, and your routine, now resembling a momentous freight train, will be difficult to stop.

References

1. https://jamanetwork.com/journals/jama/fullarticle/2763292

2. https://jamanetwork.com/journals/jamaneurology/fullarticle/2795819

3. https://www.nature.com/articles/s41598-020-70326-1

4. https://doi.org/10.1016/j.physbeh.2011.06.005

5. https://doi.org/10.1177/1745691619850568

6. https://doi.org/10.1016%2Fj.cmet.2017.02.009

7. https://doi.org/10.3389/fphys.2022.898603

8. https://doi.org/10.3390/ijerph182010973

9. https://doi.org/10.1016/j.jsams.2016.10.001

10. https://doi.org/10.1002/ejsp.674

Dear Fellow Biohackers,

In this second installment of my Biohacking 101 series, I discuss the importance of nutrition and metabolism from the perspective of a non-biochemist biohacker. For a large portion of my life thus far, I’ve remained willfully ignorant as to the primary role food plays in our body. It’s common in modern life to view a meal as simply a palette of flavors, but in today’s vast selection of hyper-palatable and calorically empty foods, it’s all too easy to trick our brains into thinking we are consuming nutrient dense diets, when the reality is quite the contrary.  I will illustrate my approach to understanding the role nutrition and metabolism plays in our bodies and how I use this knowledge to fine-tune my diet and supplementation regimen.

Nutrition is “The process of nourishing or being nourished, especially the process by which a living organism assimilates food and uses it for growth and replacement of tissues.” [1] Metabolism is “The chemical processes occurring within a living cell or organism that are necessary for the maintenance of life. In metabolism, some substances are broken down to yield energy for vital processes while other substances, necessary for life, are synthesized.” [1] Because it would take a library of books to explain the complexity of the currently-understood systems of the human body, I’ll focus this writing on the highly-simplified, high-level, and systematic approach I employ to educate myself and make critical decisions regarding diet and supplementation.

The key premise herein is to learn everything you can about the substances you are (or aren’t) consuming. Biohacking nutrition requires paying careful attention to what you eat at both the macronutrient level and the micronutrient level. Furthermore, it entails continually improving your understanding of these dietary components and their role in the body; this will arm you with the necessary knowledge to make smart dietary choices and design a diet tailored for peak performance.

The three high-level categories of macronutrients (that we all know and love) are fats, proteins, and carbohydrates; but the reality is far more complex than this. For example, fats are part of the broader category: lipids—which also contains sterols such as cholesterol. Cholesterol is the precursor for steroids[2] such as testosterone (which is also a lipid), bile acids, and more. Other common lipids include phospholipids and glycerides. The hierarchical taxonomy of each macro-component—from the types of fatty acids that comprise a lipid to the amino acid profile of a protein source to the several classes of carbohydrates—is worth recursively breaking down into their constituent parts to fundamentally understand how each substance you consume is absorbed and utilized within the body. This is enough homework to keep anyone busy for a lifetime—especially when applied to micronutrients such as vitamins, minerals, and polyphenols which, to keep from writing a book, I’ll leave for you to discover. To give you an example of what you can look forward to, the mineral magnesium is necessary for more than 300 biochemical reactions in the body[2]; some of which involve energy production, DNA replication and RNA transcription, nerve and muscle function, brain health, glucose regulation, and amino acid activation.

Hacking nutrition starts by understanding what nutrients you should be consuming and why. If you are a beginner and don’t know where to start, an adequate jump-off point is the FDA’s Nutrition Labeling Fact Sheets—specifically the Vitamins and Minerals Chart as well as the individual macronutrient fact sheets. Look at what the FDA has established for recommended daily values and assess your diet to ensure you are, at a minimum, meeting your daily needs. If you are lacking in a particular vitamin or mineral, adjust or add foods to optimize your intake; it is best to do this with whole foods. Should this be insufficient based on your research, then you may want to consider supplementation.

My Daily Considerations

Am I consuming the proper ratios of sodium to potassium and magnesium to calcium? What about other electrolytes?

Have I consumed any berries today? For rabbit hole travelers, look up the bioactive principles contained in various berries and look for published research on the individual components.

Have I consumed the recommended servings of vegetables today?

Did I get enough protein today? Individual amino acids that comprise a protein source are crucial for myriad functions in the body and are worth individually researching just as you would research a vitamin or mineral.

Have I been cognizant of my sugar intake?

Have I consumed enough healthy fats?

When will I stop procrastinating and invest in the darned DNA test kit to see what my ancestors ate? 🤣

Have I consumed enough choline? Choline is critical for your body. Your brain and nervous system need it to regulate memory, mood, muscle control, and other functions. [3]

Some supplements I take or have taken after researching:

Alpha-GPC

DHA

Uridine Monohydrate

Creatine Monohydrate

Phosphatidyl Choline

Vitamin D3

B Vitamin Complex

Caffeine

L-Theanine

Nicotinamide Riboside

Magnesium L-Threonate

Again, consult with your doctor before choosing to take any dietary supplement. If you have the means, it’s a good idea get blood levels checked for nutrient deficiencies. Although far from a perfect metric in all cases, it can provide you with valuable insight into any obvious areas worth focusing your attention.

Since placing my nutrition front and center, I have personally noticed greater energy levels, higher quality sleep, and increased mental stamina. The human body is a complex system that requires care and maintenance surpassing even the most complicated man-made machines, so avoid thinking you’re going to find that one magic hack. Sadly, it doesn’t exist. The good news is that the act of sowing well-researched and smart dietary decisions into your daily life compounds into reaping some distinctly magical benefits.

References

1. Houghton Mifflin Harcourt Publishing Company. The American Heritage dictionary of the English language, 5th ed. 2011.

2. Gropper, S. Sarreen. Smith, L. Jack. Advanced Nutrition and Human Metabolism, 6th ed. Wadsworth/Cengage Learning, 2013.

3. https://ods.od.nih.gov/factsheets/Choline-Consumer/

Dear Fellow Biohackers,

This post regards some recent steps I've taken which have proved valuable from my personal anecdotal experience. Many years back, I decided to take a holistic approach to biohacking. This entails viewing the process of biohacking as the complex system that it is; starting with the very basics, namely: sleep, diet, exercise, hygiene, and then supplementation. The goal is ultimately to live energetically, and slow or reverse aging in all of the bodily systems using any available (and considered safe) methods deemed viable by a reasonable number of published scientific studies—or in some circumstances, experimenting with less studied ideas that make intuitive or functional sense. I assume most—if not all—biohackers are in the same boat.

One thing I have struggled with consistently over the years is getting enough deep sleep. I track sleep on two different devices: a ring and a smart mattress pad. I've tried what feels like everything under the sun to conjure up the fleeting and mystical deep sleep—known by all, but alien to me since childhood.

Every night for the past several months, my deep sleep has ranged anywhere from 0-45 minutes, and averaged ~20 minutes per night. Often times, I'd have strings of days with less than 10 minutes of deep sleep. And in my experience, despite potential inaccuracies with consumer-grade sleep tracking devices, energy levels during the day and readings on these devices do show a clear correlation.

Quick side-note: If you are new to biohacking, I would suggest making sleep your focal point right out of the gate. Do some research on the importance of sleep and the role it plays in maintaining your body. If you’ve already done this, then I’m certain that you’re certain, that sleep is vital.

Back to my excursion for deep sleep. I’ve picked up a few tricks over the years through reading and experimentation, and some of the things I have been doing specifically for sleep are:

1. Consistent bedtime and wake-up time every day.

2. Blue light blocking glasses and nightshift mode on all devices after sunset.

3. Eating a whole food diet containing sufficient macro- and micro-nutrients. Vitamins and minerals are important cofactors that affect many biochemical processes in the body. And sufficient amino acids (building blocks of protein) are necessary for the body to function properly on innumerable levels; for example, Tryptophan is an essential amino acid—meaning the body cannot produce it on its own—and is, in a nutshell, the precursor to serotonin which is the precursor to melatonin.

4. Upon waking up: natural sunlight in the eyes and 10-20 minutes of heavy lifting to signal to the body’s circadian rhythm that it’s time to start the day.

5. A cooling mattress pad set to ~70 degrees.

6. A comfortable sleep mask that blacks out any ambient light.

7. Winding down the mind and body early at night and approaching sleep with no judgement. Anxiety and worrying about not sleeping will only lead to less sleep.

Using these tricks, I managed to boost my deep sleep average of ~3-5 minutes to ~20 minutes. So despite my best efforts, this was still not enough. For about 3 consistent months, I’ve been incorporating these practices into my routine, yet still, getting more than 20 minutes of deep sleep in a night was a rarity; that is, until last night.

In passing, I’ve been hearing buzz of myriad benefits derived from infrared and near-infrared (NIR) light therapy. If you haven’t heard of it, it’s basically exactly as it sounds. You shine a specific type of light at your body, and due to its long wavelength (most studies have used wavelengths in the 700 to 1,000 nanometer range), it penetrates more deeply into the skin and stimulates cellular mitochondria. Without getting bogged down in the nitty gritty details of how it works or listing all of its well-studied benefits (there are many), I woke up this morning after using the device twice yesterday for 15 minutes per session, and to my surprise, I logged a record high 57 minutes of deep sleep. Promising results!

Admittedly, this is an n=1 study, and the study duration was but a day. But the results were so profound, and I felt so great today, that I figured this would be a great way to illustrate a day in the life of a biohacker to anyone whom may have an interest in the art.