How To Make Disease Disappear – by Dr. Rangan Chatterjee
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We’ve previously reviewed a number of other books by Dr. Chatterjee, all of them good. This one’s perhaps his most generalized book that we’ve read, though it has a lot of overlap with his “Four Pillar Plan”, and indeed, each of those four pillars (relax, eat, move, sleep) gets a section in this book, each section getting 5 chapters on how to optimize the thing in question.
You may be wondering why “relax” and “sleep” don’t get one section between them; the idea of “relax” is about stress management, mindfulness (especially mindful eating), and so forth. Thus, it does connect to the other sections, but is very much its own topic also.
The premise is, as per the title, to “make disease disappear”. The way to do that, he argues, is through engaging in progressively healthy habits to accumulate chronic good health. With the 20 things you will be doing from the first four sections of 5 chapters each, you will be soon be well on your way, and he finishes up with “finding your balance”—because the trick, he says, is not to focus unduly on one, two, or even three of the pillar(s) as the expense of the other(s), but to ensure a good balance between them.
The style is light pop-science with a focus on readability; there are many personal accounts and examples, but nothing brash or self-serving, simply, illustrative. Indeed, he shows his mistakes as much as his successes, that we may learn from them.
Bottom line: this is, in essence, a rehash of his Four Pillar Plan, but tailored for an American audience. As such, American readers may find it more easily applicable than the previous book. Either way, the quality is just as good, so by all means take your pick between them.
Click here to check out How To Make Disease Disappear, and make disease disappear!
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GLP-1 Drugs Delay Alcohol’s Effects!
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GLP-1 drugs were designed as antidiabetic drugs, and took over the market as weight loss drugs.
Their usefulness to reduce cravings has been noted to also reduce non-food cravings, including for some addictive substances, and some compulsive behaviors.
See: Can a drug like Ozempic help treat addictions to alcohol, opioids or other substances?
But, there’s more to it than that…
It’s not just about drinking less
Researchers (Dr. Alexandra DiFeliceantonio et al.) have found that GLP-1 agonists such as semaglutide, tirzepatide, and liraglutide slow the rate at which alcohol enters the bloodstream, resulting in delayed (and weaker) intoxicating effects.
What they tested: in a randomized controlled trial, all participants fasted, ate a standardized snack, then consumed an alcoholic drink within 10 minutes. Breath alcohol, glucose, blood pressure, and pulse were then measured repeatedly over the next four hours.
What they found is that those on GLP-1 drugs had slower increases in breath alcohol concentration and consistently reported feeling less intoxicated than those not taking such.
How it works: the current hypothesis is that GLP-1 drugs likely reduce alcohol’s effects by slowing gastric emptying, delaying alcohol absorption, rather than directly affecting the brain. Because alcohol will then still be processed by the liver, it simply means the liver can process it little by little.
This is important, because it means that (so far as the data so far can tell us) it doesn’t run into the same problem as occurs when people take cannabis edibles, think “hmm, I don’t feel it”, and then take more, and then end up overdosing, because everything was just delayed batch-by-batch, rather than slowed down in a continuous process.
You can find the paper itself here: A preliminary study of the physiological and perceptual effects of GLP-1 receptor agonists during alcohol consumption in people with obesity
You may be thinking: “with obesity? Isn’t that protective against alcohol’s effects?”, and the answer is that in the case of adiposity (as opposed to being muscular) there’s a mixed effect that cancels itself out rather; yes, alcohol has a per-kg effect, but a kg of muscle is a lot more helpful metabolically than a kg of fat, which is in most cases more of a metabolic problem than a solution. Still, it cannot be said with certainty that the conclusions will applicable to all people of all body types; more research will be needed to make a definitive declaration about that.
GLP-1 drugs can protect the liver in one more way, too
It’s also known that GLP-1 drugs lower liver levels of an enzyme known by the snappy name of Cyp2e1, which normally breaks alcohol down into acetaldehyde, the highly toxic metabolite responsible for much of alcohol’s liver damage.
You can read more about this, here: GLP-1 receptor agonism results in reduction in hepatic ethanol metabolism
Want to learn more?
Here’s an unusually balanced overview of GLP-1 drugs when it comes to many aspects of life, rather than providing a glowing report or a terrible condemnation:
And if GLP-1 drugs aren’t your thing, then we cover some other approaches for those who wish to drink alcohol and minimize its harmful effects:
How To Make Drinking Less Harmful ← our main feature on such
Take care!
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Why Rheumatoid Arthritis Often Defies Drugs (& What Else you Can Try)
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Arthritis is the umbrella term for a cluster of joint diseases involving inflammation of the joints, hence “arthr-” (joint) “-itis” (suffix used to denote inflammation). These are mostly, but not all, autoimmune diseases, in which the body’s immune system mistakenly attacks our own joints.
Rheumatoid arthritis is one of those. Indeed, it’s the common of the autoimmune forms of arthritis. Some quick facts:
- Approximately one third of people stop work within two years of its onset, and this increases thereafter.
- It affects a little under 1% of the global population, but the older we get, the more likely it becomes
- Early onset of rheumatoid arthritis is most likely to show up around the age of 50 (but it can show up at any age)
- However, incidence (not onset) of rheumatoid arthritis peaks in the 70s age bracket
- It is 2–4 times more common in women than in men
When meds don’t work (and why)
There are three main kinds:
- Pain relief (always hit-and-miss, unless going for literal anaesthetic)
- Anti-inflammatory (can rarely go too far wrong, although some can give different problems)
- Arthritis-specific, which are usually also anti-inflammatory in their own way, but deserve a special mention
For example, a lot of arthritis medications act via the interleukin-17 pathways.
However, researchers (Dr. Martina Zoccheddu et al.) found that in rheumatoid arthritis, the immune cells that normally make IL-17 gradually stop producing it, which explains why IL-17-targeted drugs lose effectiveness as the disease progresses.
Even worse, once these cells stop making IL-17, they turn into aggressive forms that can still sustain joint inflammation independently of IL-17, meaning that the meds can end up doing more harm than good in the long-run!
To quote Dr. Joyce So when asked about this,
❝This important new insight contributes to shifting the paradigm of how we understand rheumatoid arthritis progression and why IL-17 treatments haven’t worked as well as expected. Only with a precise understanding of the biological mechanisms of disease can effective, precision therapies be developed.
In the meantime, clinicians can help patients in early or presymptomatic stages make the most of treatments that may lose effectiveness over time.❞
You can find the paper itself, here: TH17 cells converted into exTH17 cells sustain rheumatoid-like IL-17–independent inflammatory arthritis
About those early or presymptomatic stages…
Another team of researchers (Dr. Marla Glass et al.) recently found that rheumatoid arthritis begins long before pain, with people who carry a particular kind of antibodies showing body-wide inflammation, malfunctioning immune cells, and gene-regulation changes for at least seven years before symptoms show up.
In other words, the immune system is behaving as though rheumatoid arthritis is already active, and so, in a way, arguably it is already active.
This is all going on in ways that you wouldn’t see without doing blood tests, though.
For example (we will quote these key points directly):
- Widespread inflammation: The researchers observed that people at risk for RA already showed signs of systemic inflammation throughout the body. This inflammation was not limited to the joints. Instead, it resembled the body-wide inflammatory pattern commonly seen in individuals with active RA.
- Immune cell dysfunction: Multiple immune cell types showed unusual behavior.
- B cells, which normally create protective antibodies, were found in a heightened pro-inflammatory state.
- T helper cells, especially those similar to Tfh17 cells, had expanded far beyond typical levels. These cells help coordinate immune responses, including the creation of autoantibodies (antibodies that attack the body’s own tissues). Their expansion helps explain why the immune system begins targeting healthy tissue.
- Cellular reprogramming: One of the most striking discoveries was that even “naive” T cells, which have not yet encountered pathogens, showed epigenetic changes. Although their DNA sequence remained intact, the regulation of their genes had shifted. This altered gene activity suggests these cells were being reprogrammed before encountering any threats.
- Joint-like inflammation detected in blood: The team also found that monocytes (a type of white blood cell) circulating in the bloodstream were producing high amounts of inflammatory molecules. Remarkably, these cells closely resembled the macrophages typically found in the inflamed joints of RA patients, indicating that the immune system was already setting the stage for joint inflammation.
You can find this paper itself, here: Progression to rheumatoid arthritis in at-risk individuals is defined by systemic inflammation and by T and B cell dysregulation
What that means in practical terms
If you get a rheumatoid arthritis diagnosis, even if it feels like you got it quickly, chances are you’ve technically had it for a long time already.
So, if you don’t have such a diagnosis, it is good to behave as though you did (aside from the pain relief component, of course, if you have no pain), because honestly, the advice for managing arthritis is very good advice anyway, since it tends to target improving joint health and reducing chronic inflammation.
With that in mind, do check out:
And for a very deep dive into excellent exercise vs arthritis, see:
Yoga Therapy for Arthritis – by Dr. Steffany Moonaz & Erin Byron
…which is a particularly good book, much better than most of its kind, because:
- One of the problems with arthritis and exercise is that arthritis can often impede exercise.
- Another of the problems with arthritis and exercise is that some kinds of exercise can exacerbate arthritis.
This book deals with both of those issues, by providing yoga specifically tailored to living with arthritis. Indeed, the first-listed author’s PhD in public health was the result of 8 years of study developing an evidence-based yoga program for people with arthritis, including osteoarthritis and rheumatoid arthritis.
The authors take the view that arthritis is a whole-person disease (i.e. it affects all parts of you), and so addressing it requires a whole-person approach, which is what this book delivers, and so that’s why we highly recommend it.
And if you do have the pain component already…
We’ve written quite a bit about pain management, including:
- Before You Reach For That Tylenol…
- How To Stop Pain Spreading
- How To Dial Down Your Pain
- Managing Chronic Pain (Realistically!)
- Get The Right Help For Your Pain
- The 7 Approaches To Pain Management
- Science-Based Alternative Pain Relief (When Painkillers Aren’t Helping, These Things Might)
Take care!
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Sesame Oil vs Almond Oil – Which is Healthier?
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Our Verdict
When comparing sesame oil to almond oil, we picked the almond.
Why?
We were curious about this one! Were you, or were you confident? You see, almonds tend to blow away all the other nuts with their nutritional density, but they’re far from the oiliest of nuts, and their greatest strengths include their big dose of protein and fiber (which don’t make it into the oil), vitamins (most of which don’t make it into the oil) and minerals (which don’t make it into the oil). So, a lot will come down to the fat profile!
On which note, looking at the macros first, it’s 100% fat in both cases, but sesame oil has more saturated fat and polyunsaturated fat, while almond oil has more monounsaturated fat. Since the mono- and poly-unsaturated fats are both healthy and each oil has more of one or the other, the deciding factor here is which has the least saturated fat—and that’s the almond oil, which has close to half the saturated fat of sesame oil. As an aside, neither of them are a source of omega-3 fatty acids.
In terms of vitamins, there’s not a lot to say here, but “not a lot” is not nothing: sesame oil has nearly 2x the vitamin K, while almond oil has 28x the vitamin E*, and 2x the choline. So, another win for almond oil.
*which is worth noting, not least of all because seeds are more widely associated with vitamin E in popular culture, but it’s the almond oil that provide much more here. Not to get too distracted into looking at the values of the actual seeds and nuts, almonds themselves do have over 102x the vitamin E compared to sesame seeds.
Now, back to the oils:
In the category of minerals, there actually is nothing to say here, except you can’t get more than the barest trace of any mineral from either of these two oils. So it’s a tie on this one.
Adding up the categories makes for a clear win for almond oil!
Want to learn more?
You might like to read:
Avocado Oil vs Olive Oil – Which is Healthier?
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How Acetaminophen (Paracetamol) Suppresses Endocannabinoids
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…contrary to all expectations (and how this can lead to more effective acetaminophen-like pain relief, without the toxicity!
It’s well known that acetaminophen (international name: paracetamol, most well-known brand name in the US: Tylenol) is a mild painkiller and anti-fever agent; what’s not well understood is how it actually works.
Recently, a team of researchers (Dr. Michaela Dvorakova et al.) looked into this, and found something that was quite surprising, to understate it considerably.
That sounds like a clickbait headline (“and what they discovered will shock you!”) but well, we don’t do clickbait and our own headline covers it: acetaminophen suppresses endocannabinoids, when generally for painkilling purposes we want more endocannabinoids, not less.
Before we get into that, let’s take a moment to note some of the bad parts of acetaminophen’s safety profile, which is to say: it’s really not very safe.
Rather than repeat ourselves though, we’ll link to where we did a whole main feature about that, here: Before You Reach For That Tylenol…
Now, about acetaminophen and endocannabinoids
In the lead researcher’s words:
❝There are hypotheses, but we still don’t know precisely how it works. Up until now we thought that elevated endocannabinoids in our body meant less pain, but our study shows that in the case of 2-AG, it might be the opposite. Actually, reduced levels of 2-AG leads to decreased pain.❞
~ Dr. Michaela Dvorakova
You may be wondering: what’s 2-AG?
And the answer is that it’s 2-arachidonoyl glycerol, which is a cannabinoid naturally made by the human body (thus, endogenous cannabinoid, or usually written: endocannabinoid).
What the researchers found is that acetaminophen inhibits an enzyme that makes that endocannabinoid, namely, diacylglycerol lipase α (DAGLα) ← as in, this is the name of the enzyme that makes it.
Thus, inhibiting the enzyme means inhibiting endocannabinoid production. So, what gives, and why does this work as a painkiller, when it looks like it’s doing the opposite?
The researchers propose… Well, we’ll quote them:
❝This gives rise to the counterintuitive hypothesis that decreasing endocannabinoid production by DAGLα inhibition may be antinociceptive in certain settings.
Supporting this hypothesis, we find that diacylglycerol lipase (DAGL) inhibition by RHC80267 is antinociceptive in wild-type but not CB1 knockout mice in the hot-plate test.
We propose (1) that activation of DAGLα may exacerbate some forms of nociception and (2) a mechanism for the antinociceptive actions of acetaminophen, whereby acetaminophen inhibits a DAGLα/CB1-based circuit that plays a permissive role in at least one form of nociception.❞
Translating from sciencese: by stopping the endocannabinoid production, the body is triggered to engage a different, more effective method of killing pain.
You can read the paper in full here: Acetaminophen inhibits diacylglycerol lipase synthesis of 2-arachidonoyl glycerol: Implications for nociception
As for what the implications are? Per the researchers, it means that if we understand that inhibiting the enzyme DAGLα triggers a painkilling response, then new drugs can be designed to target DAGLα without the toxicity of acetaminophen.
So, keep an eye out for that, and you heard it hear first!
Want to learn more?
We’ve written quite a bit about pain management, including:
- How To Stop Pain Spreading
- How To Dial Down Your Pain
- Managing Chronic Pain (Realistically!)
- Get The Right Help For Your Pain
- The 7 Approaches To Pain Management
- Science-Based Alternative Pain Relief (When Painkillers Aren’t Helping, These Things Might)
Take care!
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What immunocompromised people want you to know
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While many people in the U.S. have abandoned COVID-19 mitigations like vaccines and masking, the virus remains dangerous for everyone, and some groups face higher risks than others. Immunocompromised people—whose immune systems don’t work as well as they should due to health conditions or medications—are more vulnerable to infection and severe symptoms from the virus.
Public Good News spoke with three immunocompromised people about the steps they take to protect themselves and what they want others to know about caring for each other.
[Editor’s note: The contents of these interviews have been condensed for length.]
PGN: What measures have you been taking to protect yourself since the COVID-19 pandemic began?
Tatum Spears, Virginia
From less than a year old, I had serious, chronic infections and have missed huge chunks of my life. In 2020, I quit my public job, and I have not worked publicly since.
I have a degree in vocal performance and have been singing my whole life, but I haven’t performed publicly since 2019. I feel like a bird without wings. I had to stop traveling. Since no one wears a mask anymore, I can’t go to the movies or social outings or any party.
All my friends live in my phone now. It’s a community of people—a lot of them are immunocompromised or disabled in some way.
There are a good portion of them who just take COVID-19 seriously and want to protect their health, who feel the existential abandonment and the burden of all of this. It’s really isolating having to step back from any sort of social life. I have to assess my risk every single time I leave the house.
Gwendolyn Alyse Bishop, Washington
I was hit by a car when I was very young. I woke up from surgery, and doctors told me I had lost almost all of my spleen. So, I was always the sickest kid in my school.
When COVID-19 hit, I started working from home. At first, I wore cloth masks. I didn’t really learn about KN95 masks until right around the time that COVID-19 disabled me. [Editor’s note: N95 and KN95 masks have been shown to be significantly more effective at preventing the transmission of viral particles than cloth masks.]
I actually don’t get out much anymore because I am disabled by long COVID now, but when I do leave, I wear a respirator in all shared air spaces. My roommate and I have HEPA filters going in every room.And then we test. I have a Pluslife testing dock, and so we keep a weekly testing schedule with that and then test if there are any symptoms. I got reinfected [with COVID-19] last winter, and a Pluslife test helped me catch it early and get Paxlovid. [Editor’s note: Pluslife is a brand of an at-home COVID-19 nucleic acid amplification test, which has been shown to be significantly more effective at detecting COVID-19 than at-home antigen rapid tests.]
Abby Mahler, California
I have lupus, and in 2016, I started taking the drug hydroxychloroquine, which is an immunomodulator. I’m not as immunocompromised as some people, but I certainly don’t have a normal immune system, which has resulted in long-term infections like C. diff.I started masking early. My roommates and I prioritize going outside. We don’t remove our masks inside in public places.
We are in a pod with one other household, and the pod has agreements on the way that we interact with public space. So, we will only unmask with people who have tested ahead of time. We use Metrix, an at-home nucleic acid amplification test.
While it’s not easy and it’s not the life that we had prior to COVID-19’s existence, it is a life that has provided us quite a lot of freedom, in the sense that we are not sick all the time. We are conscientiously making decisions that allow us to have a nice time without a monkey on our backs, which is freeing.
PGN: What do you want people who are not immunocompromised to know?
T.S.: Don’t be afraid to be the only person in a room wearing a mask. Your own health is worth it. And you have to realize how callous [people who don’t wear a mask are] by existing in spaces and breathing [their] air [on immunocompromised people].
People think that vaccines are magic, but vaccines alone are not enough. I would encourage people to look at the Swiss cheese model of risk assessment.
Each slice of Swiss cheese has holes in it in different places, and each layer represents a layer of virus mitigation. One layer is vaccines. Another layer is masks. Then there’s staying home when you’re sick and testing.
G.A.B.: I wish people were masking. I wish people understood how likely it is that they are also now immunocompromised and vulnerable because of the widespread immune dysregulation that COVID-19 is causing. [Editor’s note: Research shows that COVID-19 infections may cause long-term harm to the immune system in some people.]
I want people to be invested in being good community members, and part of that is understanding that COVID-19 hits the poorest the hardest—gig workers, underpaid employees, frontline service workers, people who were already disabled or immunocompromised.
If people want to be good community members, they not only need to protect immunocompromised and disabled people by wearing a mask when they leave their homes, but they also need to actually start taking care of their community members and participating in mutual aid. [Editor’s note: Mutual aid is the exchange of resources and services within a community, such as people sharing extra N95 masks.]
I spend pretty much all of my time working on LongCOVIDAidBot, which promotes mutual aid for people who have been harmed by COVID-19.
A.M.: An important thing to think about when you’re not disabled is that it becomes a state of being for all people, if they’re lucky. You will become disabled, or you will die.
It is a privilege, in my opinion, to become disabled because I can learn different ways of living my life. And being able to see yourself as a body that changes over time, I hope, opens up a way of looking at your body as the porous reality that it is.
Some people think of themselves as being willing to make concessions or change their behavior when immunocompromised people are around, but you don’t always know when someone is immunocompromised.
So, if you’re not willing to change the way that you think about yourself as a person who is susceptible [to illness], then you should change the way that you consider other people around you. Wearing a mask—at the very least in public indoor spaces—means considering the unknown realities of all the people who are interacting with that space.
This article first appeared on Public Good News and is republished here under a Creative Commons license.
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How To Nap Like A Pro (No More “Sleep Hangovers”!)
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How To Be An Expert Nap-Artist
There’s a lot of science to say that napping can bring us health benefits—but mistiming it can just make us more tired. So, how to get some refreshing shut-eye, without ending up with a case of the midday melatonin blues?
First, why do we want to nap?
Well, maybe we’re just tired, but there are specific benefits even if we’re not. For example:
- Increased alertness
- Helps with learning
- Improved memory
- Boost to immunity
- Enhance athletic performance
What can go wrong?
There are two main things that can go wrong, physiologically speaking:
- We can overdo it, and not sleep well at night
- We can awake groggy and confused and tired
The first is self-explanatory—it messes with the circadian rhythm. For this reason, we should not sleep more than 90 minutes during the day. If that seems like a lot, and maybe you’ve heard that we shouldn’t sleep more than half an hour, there is science here, so read on…
The second is a matter of sleep cycles. Our brain naturally organizes our sleep into multiples of 20-minute segments, with a slight break of a few minutes between each. Consequently, naps should be:
- 25ish minutes
- 40–45 minutes
- 90ish minutes
If you wake up mid-cycle—for example, because your alarm went off, or someone disturbed you, or even because you needed to pee, you will be groggy, disoriented, and exhausted.
For this reason, a nap of one hour (a common choice, since people like “round” numbers) is a recipe for disaster, and will only work if you take 15 minutes to fall asleep. In which case, it’d really be a nap of 45 minutes, made up of two 20-minute sleep cycles.
Some interruptions are better/worse than others
If you’re in light or REM sleep, a disruption will leave you not very refreshed, but not wiped out either. And as a bonus, if you’re interrupted during a REM cycle, you’re more likely to remember your dreams.
If you’re in deep sleep, a disruption will leave you with what feels like an incredible hangover, minus the headache, and you’ll be far more tired than you were before you started the nap.
The best way to nap
Taking these factors into account, one of the “safest” ways to nap is to set your alarm for the top end of the time-bracket above the one you actually want to nap for (e.g., if you want to nap for 25ish minutes, set your alarm for 45).
Unless you’re very sleep-deprived, you’ll probably wake up briefly after 20–25 minutes of sleep. This may seem like nearer 30 minutes, if it took you some minutes to fall asleep!
If you don’t wake up then, or otherwise fail to get up, your alarm will catch you later at what will hopefully be between your next sleep cycles, or at the very least not right in the middle of one.
When you wake up from a nap before your alarm, get up. This is not the time for “5 more minutes” because “5 more minutes” will never, ever, be refreshing.
Rest well!
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