Should Men Over 50 Get PSA?
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As ever: if the question/request can be answered briefly, we’ll do it here in our Q&A Thursday edition. If not, we’ll make a main feature of it shortly afterwards!
So, no question/request too big or small
❝Loved the information on prostate cancer. Do recommend your readers get a PSA or equivalent test annually for over 50 yr old men.❞
(This is about: Prostate Health: What You Should Know)
Yep, or best yet, the much more accurate PSE test! But if PSA test is what’s available, it’s a lot better than nothing. And, much as it’s rarely the highlight of anyone’s day, a prostate exam by a suitably qualified professional is also a good idea.
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The Kitchen Doctor
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Dr. Rupy Aujla: The Kitchen Doctor
This is Dr. Rupy Aujla, and he’s a medical doctor. He didn’t set out to become a “health influencer”.
But then, a significant heart condition changed his life. Having a stronger motivation to learn more about nutritional medicine, he did a deep dive into the scientific literature, because that’s what you do when your life is on the line, especially if you’re a doctor!
Using what he learned, he was able to reverse his condition using a food and lifestyle approach. Now, he devotes himself to sharing what he learned—and what he continues to learn as he goes along.
One important thing he learned because of what happened to him, was that he hadn’t been paying enough attention to what his body was trying to tell him.
He wants us to know about interoception—which isn’t a Chris Nolan movie. Rather, interoception is the sense of what is going on inside one’s own body.
The counterpart of this is exteroception: our ability to perceive the outside world by means of our various senses.
Interoception is still using the senses, but is sensing internal body sensations. Effectively, the brain interprets and integrates what happens in our organs.
When interoception goes wrong, researchers found, it can lead to a greater likelihood of mental health problems. Having an anxiety disorder, depression, mood disorder, or an eating disorder often comes with difficulties in sensing what is going on inside the body.
Improving our awareness of body cues
Those same researchers suggested therapies and strategies aimed at improving awareness of mind-body connections. For example, mindfulness-based stress reduction, yoga, meditation and movement-based treatments. They could improve awareness of body cues by attending to sensations of breathing, cognitions and other body states.
But where Dr. Aujla puts his focus is “the heart of the home”, the kitchen.
The pleasure of food
❝Eating is not simply ingesting a mixture of nutrients. Otherwise, we would all be eating astronaut food. But food is not only a tool for health. It’s also an important pleasure in life, allowing us to connect to others, the present moment and nature.❞
Dr. Rupy Aujla
Dr. Aujla wants to help shift any idea of a separation between health and pleasure, because he believes in food as a positive route to well-being, joy and health. For him, it starts with self-awareness and acceptance of the sensory pleasures of eating and nourishing our bodies, instead of focusing externally on avoiding perceived temptations.
Most importantly:
We can use the pleasure of food as an ally to healthy eating.
Instead of spending our time and energy fighting the urge to eat unhealthy things that may present a “quick fix” to some cravings but aren’t what our body actually wants, needs, Dr. Aujla advises us to pay just a little more attention, to make sure the body’s real needs are met.
His top tips for such are:
- Create an enjoyable relaxing eating environment
To help cultivate positive emotions around food and signal to the nervous system a shift to food-processing time. Try setting the table with nothing else on it beyond what’s relevant to the dinner, putting away distractions, using your favorite plates, tablecloth, etc.
- Take 3 deep abdominal breaths before eating
To help you relax and ground yourself in the present moment, which in turn is to prepare your digestive system to receive and digest food.
- Pay attention to the way you sit
Take some time to sit comfortably with your feet grounded on the floor, not slouching, to give your stomach space to digest the food.
- Appreciate what it took to bring this food to your plate
Who was involved in the growing process and production, the weather and soil it took to grow the food, and where in the world it came from.
- Enjoy the sensations
When you’re cooking, serving, and eating your food, be attentive to color, texture, aroma and even sound. Taste the individual ingredients and seasonings along the way, when safe and convenient to do so.
- Journal
If you like journaling, you can try adding a mindful eating section to that. Ask questions such as: “how did I feel before, during, and after the meal?”
In closing…
Remember that this is a process, not only on an individual level but as a society too.
Oftentimes it’s hard to eat healthily… We can be given to wonder even “what is healthy, after all?”, and we can be limited by what is available, what is affordable, and what we have time to prepare.
But if we make a conscious commitment to make the best choices we reasonably can as we go along, then small changes can soon add up.
Interested in what kind of recipes Dr. Aujla goes for?
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The Biological Mind – by Dr. Alan Jasanoff
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How special is our brain? According to Dr. Alan Jasanoff, it’s not nearly as special as we think it is.
In this work, he outlines the case for how we have collectively overstated the brain’s importance. That it’s just another organ like a heart or a kidney, and that who we are is as much a matter of other factors, as what goes on in our brain.
In this reviewer’s opinion, he overcorrects a bit. The heart and kidneys are very simple organs, as organs go. The brain is not. And while everything from our gut microbiota to our environment to our hormones may indeed contribute to what is us, our brain is one thing that can’t just be swapped out.
Nevertheless, this very well-written book can teach us a lot about everything else that makes us us, including many biological factors that many people don’t know about or consider.
Towards the end of the book, he switches into futurist speculation, and his speculation can be summed up as “we cannot achieve anything worthwhile in the future”.
Bottom line: if you’ve an interest in such things as how transplanting glial cells can give a 30% cognitive enhancement, and how a brain transplant wouldn’t result in the same us in a different body, this is the book for you.
Click here to check out The Biological Mind, and learn about yours!
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The Sucralose News: Scaremongering Or Serious?
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What’s the news on sucralose?
These past days the press has been abuzz with frightening tales:
- This Common Artificial Sweetener Can Break Down DNA, Scientists Warn
- Sucralose Damages DNA, Linked to Leaky Gut
- Chemical found in common sweetener damages DNA
- Chemical found in widely used sweetener breaks up DNA
- Chemical from Splenda breaks up DNA
How true and/or serious is this?
Firstly, let’s manage expectations. Pineapple juice also breaks down DNA, but is not generally considered a health risk. So let’s keep that in mind, while we look into the science.
Is sucralose as scary as pineapple juice, or is it something actually dangerous?
The new study (that sparked off these headlines)
The much-referenced study is publicly available to read in full—here it is:
You may notice that this doesn’t have quite the snappy punchiness of some of the headlines, but let’s break this down, if you’ll pardon the turn of phrase:
- Toxicological: pertaining to whether or not it has toxic qualities
- Pharmacokinetic: the science of asking, of chemicals in bodies, “where did it come from; where did it go; what could it do there; what can we know?”
- Sucralose-6-acetate: an impurity that can be found in sucralose. For perspective, the study found that the sucralose in Splenda contained “up to” 0.67% sucralose-6-acetate.
- Sucralose: a modified form of sucrose, that makes it hundreds of times sweeter, and non-caloric because the body cannot break it down so it’s treated as a dietary fiber and just passes through
- In vitro: things are happening in petri dishes, not in animals (human or otherwise), which would be called “in vivo”
- Screening assays: “we set up a very closed-parameters chemical test, to see what happens when we add this to this” ⇽ oversimplification, but this is the basic format of a screening assay
Great, now we understand the title, but what about the study?
Researchers looked primarily at the effects of sucralose-6-acetate and sucralose (together and separately) on epithelial cells (these are very simple cells that are easy to study; conveniently, they are also most of what makes up our intestinal walls). For this, they used a fancy way of replicating human intestinal walls, that’s actually quite fascinating but beyond the scope of today’s newsletter. Suffice it to say: it’s quite good, and/but has its limitations too. They also looked at some in vivo rat studies.
What they found was…
Based on samples from the rat feces (somehow this didn’t make it into the headlines), it appears that sucralose may be acetylated in the intestines. What that means is that we, if we are like the rats (definitely not a given, but a reasonable hypothesis), might convert up to 10% of sucralose into sucralose-6-acetate inside us. Iff we do, the next part of the findings become more serious.
Based on the in vitro simulations, both sucralose and sucralose-6-acetate reduced intestinal barrier integrity at least a little, but sucralose-6-acetate was the kicker when it came to most of the effects—at least, so we (reasonably!) suppose.
Basically, there’s a lot of supposition going on here but the suppositions are reasonable. That’s how science works; there’s usually little we can know for sure from a single study; it’s when more studies roll in that we start to get a more complete picture.
What was sucralose-6-acetate found to do? It increased the expression of genes associated with inflammation, oxidative stress, and cancer (granted those three things generally go together). So that’s a “this probably has this end result” supposition.
More concretely, and which most of the headlines latched onto, it was found (in vitro) to induce cytogenic damage, specifically, of the clastogenic variety (produces DNA strand breaks—so this is different than pineapple’s bromelain and DNA-helicase’s relatively harmless unzipping of genes).
The dose makes the poison
So, how much is too much and is that 0.67% something to worry about?
- Remembering the rat study, it may be more like 10% once our intestines have done their thing. Iff we’re like rats.
- But, even if it’s only 0.67%, this will still be above the “threshold of toxicological concern for genotoxicity”, of 0.15µg/person/day.
- On the other hand, the fact that these were in vitro studies is a serious limitation.
- Sometimes something is very dangerous in vitro, because it’s being put directly onto cells, whereas in vivo we may have mechanisms for dealing with that.
We won’t know for sure until we get in vivo studies in human subjects, and that may not happen any time soon, if ever, depending on the technical limitations and ethical considerations that sometimes preclude doing certain studies in humans.
Bottom line:
- The headlines are written to be scary, but aren’t wrong; their claims are fundamentally true
- What that means for us as actual humans may not be the same, however; we don’t know yet
- For now, it is probably reasonable to avoid sucralose just in case
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The Emperor’s New Klotho, Or Something More?
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Unzipping The Genes Of Aging?
Klotho is an enzyme encoded in humans’ genes—specifically, in the KL gene.
It’s found throughout all living parts of the human body (and can even circulate about in its hormonal form, or come to rest in its membranaceous form), and its subgroups are especially found:
- α-klotho: in the brain
- β-klotho: in the liver
- γ-klotho: in the kidneys
Great! Why do we care?
Klotho, its varieties and variants, its presence or absence, are very important in aging.
Almost every biological manifestation of aging in humans has some klotho-related indicator; usually the decrease or mutation of some kind of klotho.
Which way around the cause and effect go has been the subject of much debate and research: do we get old because we don’t have enough klotho, or do we make less klotho because we’re getting old?
Of course, everything has to be tested per variant and per system, so that can take a while (punctuated by research scientists begging for more grants to do the next one). Given that it’s about aging, testing in humans would take an incredibly long while, so most studies so far have been rodent studies.
The general gist of the results of rodent studies is “reduced klotho hastens aging; increased klotho slows it”.
(this can be known by artificially increasing or decreasing the level of klotho expression, again something easier in mice as it is harder to arrange transgenic humans for the studies)
Here’s one example of many, of that vast set of rodent studies:
Suppression of Aging in Mice by the Hormone Klotho
Relevance for Alzheimer’s, and a science-based advice
A few years ago (2020), an Alzheimer’s study was undertaken; they noted that the famous apolipoprotein E4 (apoE4) allele is the strongest genetic risk factor for Alzheimer’s, and that klotho may be another. FGF21 (secreted by the liver, mostly during fasting) binds to its own receptor (FGFR1) and its co-receptor β-klotho. Since this is a known neuroprotective factor, they wondered whether klotho itself may interact with β-amyloid (Aβ), and found:
❝Aβ can enhance the ability of klotho to draw FGF21 to regions of incipient neurodegeneration in AD❞
In other words: β-amyloid, the substance whose accumulation is associated with neurodegeneration in Alzheimer’s disease, is a mediator in klotho bringing a known neuroprotective factor, FGF21, to the areas of neurodegeneration
In fewer words: klotho calls the firefighters to the scene of the fire
Read more: Alignment of Alzheimer’s disease amyloid β-peptide and klotho
The advice based on this? Consider practicing intermittent fasting, if that is viable for you, as it will give your liver more FGF21-secreting time, and the more FGF21, the more firefighters arrive when klotho sounds the alarm.
See also: Intermittent Fasting: What’s the truth?
…and while you’re at it:
Does intermittent fasting have benefits for our brain?
A more recent (2023) study with a slightly different (but connected) purpose, found results consistent with this:
Longevity factor klotho enhances cognition in aged nonhuman primates
…and, for that matter this (2023) study that found:
Associations between klotho and telomere biology in high stress caregivers
…which looks promising, but we’d like to see it repeated with a sounder method (they sorted caregiving into “high-stress” and “low-stress” depending on whether a child was diagnosed with ASD or not, which is by no means a reliable way of sorting this). They did ask for reported subjective stress levels, but to be more objective, we’d like to see clinical markers of stress (e.g. cortisol levels, blood pressure, heart rate changes, etc).
A very recent (April 2024) study found that it has implications for more aspects of aging—and this time, in humans (but using a population-based cohort study, rather than lab conditions):
Can I get it as a supplement?
Not with today’s technology and today’s paucity of clinical trials, you can’t. Maybe in the future!
However… The presence of senescent (old, badly copied, stumbling and staggering onwards when they should have been killed and eaten and recycled already) cells actively reduces klotho levels, which means that taking supplements that are senolytic (i.e., that kill those senescent cells) can increase serum klotho levels:
Orally-active, clinically-translatable senolytics restore α-Klotho in mice and humans
Ok, what can I take for that?
We wrote about a senolytic supplement that you might enjoy, recently:
Fisetin: The Anti-Aging Assassin
Want to know more?
If you have the time, Dr. Peter Attia interviews Dr. Dena Dubal (researcher in several of the above studies) here:
Click Here If The Embedded Video Doesn’t Load Automatically
Enjoy!
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No, taking drugs like Ozempic isn’t ‘cheating’ at weight loss or the ‘easy way out’
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Hundreds of thousands of people worldwide are taking drugs like Ozempic to lose weight. But what do we actually know about them? This month, The Conversation’s experts explore their rise, impact and potential consequences.
Obesity medication that is effective has been a long time coming. Enter semaglutide (sold as Ozempic and Wegovy), which is helping people improve weight-related health, including lowering the risk of a having a heart attack or stroke, while also silencing “food noise”.
As demand for semaglutide increases, so are claims that taking it is “cheating” at weight loss or the “easy way out”.
We don’t tell people who need statin medication to treat high cholesterol or drugs to manage high blood pressure they’re cheating or taking the easy way out.
Nor should we shame people taking semaglutide. It’s a drug used to treat diabetes and obesity which needs to be taken long term and comes with risks and side effects, as well as benefits. When prescribed for obesity, it’s given alongside advice about diet and exercise.
How does it work?
Semaglutide is a glucagon-like peptide-1 receptor agonist (GLP-1RA). This means it makes your body’s own glucagon-like peptide-1 hormone, called GLP-1 for short, work better.
GLP-1 gets secreted by cells in your gut when it detects increased nutrient levels after eating. This stimulates insulin production, which lowers blood sugars.
GLP-1 also slows gastric emptying, which makes you feel full, and reduces hunger and feelings of reward after eating.
GLP-1 receptor agonist (GLP-1RA) medications like Ozempic help the body’s own GLP-1 work better by mimicking and extending its action.
Some studies have found less GLP-1 gets released after meals in adults with obesity or type 2 diabetes mellitus compared to adults with normal glucose tolerance. So having less GLP-1 circulating in your blood means you don’t feel as full after eating and get hungry again sooner compared to people who produce more.
GLP-1 has a very short half-life of about two minutes. So GLP-1RA medications were designed to have a very long half-life of about seven days. That’s why semaglutide is given as a weekly injection.
What can users expect? What does the research say?
Higher doses of semaglutide are prescribed to treat obesity compared to type 2 diabetes management (up to 2.4mg versus 2.0mg weekly).
A large group of randomised controlled trials, called STEP trials, all tested weekly 2.4mg semaglutide injections versus different interventions or placebo drugs.
Trials lasting 1.3–2 years consistently found weekly 2.4 mg semaglutide injections led to 6–12% greater weight loss compared to placebo or alternative interventions. The average weight change depended on how long medication treatment lasted and length of follow-up.
Higher doses of semaglutide are prescribed for obesity than for type 2 diabetes. fcm82/Shutterstock Weight reduction due to semaglutide also leads to a reduction in systolic and diastolic blood pressure of about 4.8 mmHg and 2.5 mmHg respectively, a reduction in triglyceride levels (a type of blood fat) and improved physical function.
Another recent trial in adults with pre-existing heart disease and obesity, but without type 2 diabetes, found adults receiving weekly 2.4mg semaglutide injections had a 20% lower risk of specific cardiovascular events, including having a non-fatal heart attack, a stroke or dying from cardiovascular disease, after three years follow-up.
Who is eligible for semaglutide?
Australia’s regulator, the Therapeutic Goods Administration (TGA), has approved semaglutide, sold as Ozempic, for treating type 2 diabetes.
However, due to shortages, the TGA had advised doctors not to start new Ozempic prescriptions for “off-label use” such as obesity treatment and the Pharmaceutical Benefits Scheme doesn’t currently subsidise off-label use.
The TGA has approved Wegovy to treat obesity but it’s not currently available in Australia.
When it’s available, doctors will be able to prescribe semaglutide to treat obesity in conjunction with lifestyle interventions (including diet, physical activity and psychological support) in adults with obesity (a BMI of 30 or above) or those with a BMI of 27 or above who also have weight-related medical complications.
What else do you need to do during Ozempic treatment?
Checking details of the STEP trial intervention components, it’s clear participants invested a lot of time and effort. In addition to taking medication, people had brief lifestyle counselling sessions with dietitians or other health professionals every four weeks as a minimum in most trials.
Support sessions were designed to help people stick with consuming 2,000 kilojoules (500 calories) less daily compared to their energy needs, and performing 150 minutes of moderate-to-vigorous physical activity, like brisk walking, dancing and gardening each week.
STEP trials varied in other components, with follow-up time periods varying from 68 to 104 weeks. The aim of these trials was to show the effect of adding the medication on top of other lifestyle counselling.
Trial participants also exercised for 150 minutes a week. Elena Nichizhenova/Shutterstock A review of obesity medication trials found people reported they needed less cognitive behaviour training to help them stick with the reduced energy intake. This is one aspect where drug treatment may make adherence a little easier. Not feeling as hungry and having environmental food cues “switched off” may mean less support is required for goal-setting, self-monitoring food intake and avoiding things that trigger eating.
But what are the side effects?
Semaglutide’s side-effects include nausea, diarrhoea, vomiting, constipation, indigestion and abdominal pain.
In one study these led to discontinuation of medication in 6% of people, but interestingly also in 3% of people taking placebos.
More severe side-effects included gallbladder disease, acute pancreatitis, hypoglycaemia, acute kidney disease and injection site reactions.
To reduce risk or severity of side-effects, medication doses are increased very slowly over months. Once the full dose and response are achieved, research indicates you need to take it long term.
Given this long-term commitment, and associated high out-of-pocket cost of medication, when it comes to taking semaglutide to treat obesity, there is no way it can be considered “cheating”.
Read the other articles in The Conversation’s Ozempic series here.
Clare Collins, Laureate Professor in Nutrition and Dietetics, University of Newcastle
This article is republished from The Conversation under a Creative Commons license. Read the original article.
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Nine Pints – by Rose George
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Rose George is not a scientist, but an investigative journalist. As such, she’s a leave-no-stone-unturned researcher, and that shows here.
The style throughout is, as one might expect, journalistic. But, she’s unafraid of diving into the science of it, interviewing many medical professionals as part of her work. She also looks to people living with various blood-related conditions, ranging from hemophilia to HIV.
Speakling of highly-stigmatized yet very manageable conditions, there’s also a fair section devoted to menstruation, menstrual blood, and societies’ responses to such, from shunning to active support.
We also learn about the industrialization of blood—from blood banks to plasma labs to leech farms. You probably knew leeches are still used as a medical tool in even the most high-tech of hospitals, but you’ll doubtlessly learn a fascinating thing or two from the “insider views” along the way.
Bottom line: if you’d like to know more about the red stuff in all its marvelous aspects, with neither sensationalization nor sanitization (the topic needs neither!), this is the book for you.
Click here to check out Nine Pints, and learn more about yours!
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