
Beta-Blockers: Useless vs Heart Attacks & Worse For Women?
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Currently, more than 80% of uncomplicated heart attack patients are discharged on beta-blockers—this has been the go-to standard of care for the past 40 years—notwithstanding that there are common side effects such as bradycardia (slow heart rate), and resultant fatigue and sexual dysfunction.
However, researchers (Dr. Borja Ibanez et al.) have turned that on its head with a sweeping study involving 8,505 patients enrolled across 109 hospitals in Spain and Italy, randomized to receive or not receive beta-blockers, with a median follow-up of a little under 4 years.
What they found
In few words: overall, there was no significant differences between groups in death, recurrent heart attack, or hospitalization for heart failure.
However, for women specifically, they did find that there was (in the beta-blocker group), a slightly higher absolute risk of death over 3.7 years, plus higher rates of heart attack or heart failure hospitalization—specifically, they more often had heart attacks without obstructive coronary arteries.
Some of this disparity may be explained by the fact that women were less often prescribed recommended secondary prevention therapies (e.g. antiplatelet therapies, ACE inhibitors/ARBs, and cardiac rehabilitation) despite high overall prescription rates, but not all of it, because those receiving higher beta-blocker doses also saw a correspondingly higher risk.
You can find the paper itself here: Beta-Blockers after Myocardial Infarction without Reduced Ejection Fraction
And further modelling of more or less the same data here: Beta-blockers after myocardial infarction: effects according to sex in the REBOOT trial
You may be wondering: why “more or else”? Because they are both running numbers from the same trial, but the latter used only the intention-to-treat population, which was 8,438 out of the 8,505 patients.
One more thing…
While beta-blockers are generally considered “calming” (indeed, historically they’ve sometimes been prescribed for anxiety; less so nowadays), hence the bradycardia we mentioned in the introduction, this does mean that they can also promote depression—without actually alleviating anxiety:
❝At baseline, 27% of patients were possible cases of anxiety (m, 5.6; SD, 3.9) and 14% were possible cases of depression (m, 3.9; SD, 3.2). Beta-blocker treatment had a [worsening] effect on depressive symptoms at both follow-ups 1 (β = 0.48; 95% CI 09–0.86; P = 0.015) and 2 (β = 0.41; 95% CI = 0.01–0.81; P = 0.047), but no effect on anxiety.❞
Want to learn more?
For more on sex differences in this matter, see:
- Statins: His & Hers ← for women, statins are (in most cases) less useful and more potentially harmful
- Heart Attacks: His & Hers
And for why a lot of this kind of medical disparity occurs when it comes to outcomes:
Unwell Women: Misdiagnosis and Myth in a Man-Made World – by Elinor Cleghorn
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Squat Variations for Painful Knees (No More Pain!)
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Having bad knees can be a bit of a catch-22; you want to squat to make them stronger, but you can’t do that because your knees are not good. But, there are ways to do it!
Dr. Alyssa Kuhn, a doctor of physical therapy, advises:
Gently does it
Ten ways to choose from:
- Pool Squats: performed in a pool for joint-friendly support. Can use both hands, one hand, or no support. Focus on sitting back and standing up, aiming for 10–20 reps.
- Supported Squats: use a sink, rings, or handles for support. Stand a distance away and sit back while keeping your knees behind your heels. Perform 10–20 reps for 2–3 sets.
- Chair Loop Squats: use a resistance band around your knees while sitting on a chair. Press your knees outward as you stand and sit to strengthen hip and knee stability. Do 8–12 reps for 2–3 sets.
- Heel Elevated Squats: place your heels on dumbbells to shift emphasis to thighs and reduce knee strain. Ideal for stiff ankles or back tightness. Perform 10–15 reps for 2–3 sets.
- Sumo Squats: a wide stance squat, good for hip strength and reducing knee stress. Adjust your foot positioning for comfort. Perform 15–20 reps for 2–3 sets.
- Chair Squats: hold a weight close to your chest while sitting and standing from a chair. Can use kettlebells or dumbbells. Do 8–10 reps for 2–3 sets.
- Band Squats: use a resistance band secured behind your knees to provide support and encourage proper squat mechanics. Perform 5–12 reps for 2–3 sets.
- Modified Single Leg Squat: sit-to-stand using one leg with the other as a kickstand. Adjust your foot position for difficulty. Perform 8–12 reps per side for 2–3 sets.
- Weighted Squats: add weight using dumbbells or a barbell. Maintain an upright torso. Adjust the weight and reps based on difficulty, and do 5–10 reps for 2–4 sets.
- Split Squat: a stationary lunge, keeping your feet in place and lowering straight down. Focus on your front leg while keeping balance. Can add weight if you want. Perform 5–12 reps per side based on difficulty.
For more on each of these plus visual demonstrations, enjoy:
Click Here If The Embedded Video Doesn’t Load Automatically!
Want to learn more?
You might also like to read:
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Huperzine A: A Natural Nootropic
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Huperzine A: A Natural Nootropic
Huperzine A is a compound, specifically a naturally occurring sesquiterpene alkaloid, that functions as an acetylcholinesterase inhibitor. If that seems like a bunch of big words, don’t worry, we’ll translate in a moment.
First, a nod to its origins: it is found in certain kinds of firmoss, especially the “toothed clubmoss”, Huperzia serrata, which grows in many Asian countries.
What’s an acetylcholinesterase inhibitor?
Let’s do this step-by-step:
- An acetylcholinesterase inhibitor is a compound that inhibits acetylcholinesterase.
- Acetylcholinesterase is an enzyme that catalyzes (speeds up) the breakdown of acetylcholine.
- Acetylcholine is a neurotransmitter; it’s an ester of acetic acid and choline.
- This is the main neurotransmitter of the parasympathetic nervous system, and is also heavily involved in cognitive functions including memory and creative thinking.
What this means: if you take an acetylcholinesterase inhibitor like huperzine A, it will inhibit acetylcholinesterase, meaning you will have more acetylcholine to work with. That’s good.
What can I expect from it?
Huperzine A has been well-studied for a while, mostly for the prevention and treatment of Alzheimer’s disease:
- New insights into huperzine A for the treatment of Alzheimer’s disease
- Huperzine A: Is it an Effective Disease-Modifying Drug for Alzheimer’s Disease?
- Huperzine A and Its Neuroprotective Molecular Signaling in Alzheimer’s Disease
However, research has suggested that huperzine A is much better as a prevention than a treatment:
❝A central event in the pathogenesis of Alzheimer’s disease (AD) is the accumulation of senile plaques composed of aggregated amyloid-β (Aβ) peptides.
Ex vivo electrophysiological experiments showed that 10 μM of Aβ1-40 significantly decreased the effect of the AChE inhibitor huperzine A on the synaptic potential parameters. ❞
~ Dr. Irina Zueva
In other words: the answer to the titular question is “Yes, yes it can”
And, to translate Dr. Zueva’s words into simple English:
- People with Alzheimer’s have amyloid-β plaque in their brains
- That plaque reduces the effectiveness of huperzine A
So, what if we take it in advance? That works much better:
❝Pre-treatment with [huperzine A] at concentrations of 50, 100, and 150 µg/mL completely inhibited the secretion of PGE2, TNF-α, IL-6, and IL-1β compared to post-treatment with [huperzine A].
This suggests that prophylactic treatment is better than post-inflammation treatment. ❞
~ Dr. Thu Kim Dang
Source: Anti-neuroinflammatory effects of alkaloid-enriched extract from Huperzia serrata
As you may know, neuroinflammation is a big part of Alzheimer’s pathology, so we want to keep that down. The above research suggests we should do that sooner rather than later.
Aside from holding off dementia, can it improve memory now, too?
There’s been a lot less research done into this (medicine is generally more concerned with preventing/treating disease, than improving the health of healthy people), but there is some:
^This is a small (n=68) old (1999) study for which the full paper has mysteriously disappeared and we only get to see the abstract. It gave favorable results, though.
The effects of huperzine A and IDRA 21 on visual recognition memory in young macaques
^This, like most non-dementia research into HupA, is an animal study. But we chose to spotlight this one because, unlike most of the studies, it did not chemically lobotomize the animals first; they were and remained healthy. That said, huperzine A improved the memory scores most for the monkeys that performed worst without it initially.
Where can I get it?
As ever, we don’t sell it, but here’s an example product on Amazon for your convenience
Enjoy!
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Recognize The Early Symptoms Of Parkinson’s Disease
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Parkinson’s disease is a degenerative condition with wide-reaching implications for health. While there is currently no known cure, there are treatments, so knowing about it sooner rather than later is important.
Spot The Signs
There are two main kinds of symptoms, motor and non-motor.
Motor symptoms include:
- trembling that occurs when muscles are relaxed; often especially visible in the fingers
- handwriting changes—not just because of the above, but also often getting smaller
- blank expression, on account of fewer instruction signals getting through to the face
- frozen gait—especially difficulty starting walking, and a reduced arm swing
Non-motor symptoms include:
- loss of sense of smell—complete, or a persistent reduction of
- sleepwalking, or sleep-talking, or generally acting out dreams while asleep
- constipation—on an ongoing basis
- depression/anxiety, especially if there was no prior history of these conditions
For more detail on each of these, as well as what steps you might want to take, check out what Dr. Luis Zayas has to say:
Click Here If The Embedded Video Doesn’t Load Automatically!
Want to learn more?
You might also like to read:
Citicoline vs Parkinson’s (And More)
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‘Disease X’: What it is (and isn’t)
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What you need to know
- In January 2024, the World Economic Forum hosted an event called Preparing for Disease X to discuss strategies to improve international pandemic response.
- Disease X is a term used in epidemiology to refer to potential disease threats. It is not a real disease or a global conspiracy.
- Preparation to prevent and respond to future pandemics is a necessary part of global health to keep us all safer.
During the World Economic Forum’s 54th annual meeting in Davos, Switzerland, global health experts discussed ways to strengthen health care systems in preparation for future pandemics. Conspiracy theories quickly began circulating posts about the event and the fictional disease at its center, so-called Disease X.
What is Disease X?
In 2018, the World Health Organization added Disease X to its list of Blueprint Priority Diseases that are public health risks. But, unlike the other diseases on the list, Disease X doesn’t exist. The term represents a hypothetical human disease capable of causing a pandemic. Although experts don’t know what the next Disease X will be, they can make educated guesses about where and how it may emerge—and how we can prepare for it.
Why are we hearing about Disease X now?
COVID-19 has been the deadliest infectious disease outbreak of the 21st century. It’s also an example of a Disease X: a previously unknown pathogen that spreads rapidly around the world, claiming millions of lives.
When the WEF hosted a panel of experts to discuss Disease X, it was the first exposure that many people had to a concept that global health experts have been discussing since 2018.
Even before the routine pandemic preparedness event took place, online conspiracy theorists began circulating false claims that those discussing and preparing for Disease X had sinister motives, underscoring how widespread distrust of global health entities has become in the wake of the COVID-19 pandemic.
Why does Disease X matter?
Epidemiologists use concepts like Disease X to plan for future outbreaks and avoid the mistakes of past outbreaks. The COVID-19 pandemic and the recent non-endemic outbreak of mpox highlight the importance of global coordination to efficiently prevent and respond to disease outbreaks.
Pandemics are inevitable, but the scale of their destruction doesn’t have to be. Major disease outbreaks are likely to become more frequent due to the impacts of climate change. Preparing for a pandemic now helps ensure that the world is better equipped to handle the next one.
This article first appeared on Public Good News and is republished here under a Creative Commons license.
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Fermenting Everything – by Andy Hamilton
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This is not justanother pickling book! This is, instead, what it says on the front cover, “fermenting everything”.
Ok, maybe not literally everything, but every kind of thing that can reasonably be fermented, and it’s probably a lot more things than you might think.
From habanero chutney to lacto-lemonade, aioli to kombucha, Ukrainian fermented tomatoes to kvass. We could go on, but we’d soon run out of space. You get the idea. If it’s a fermented product (food, drink, condiment) and you’ve heard of it, there’s probably a recipe in here.
All in all, this is a great way to get in your gut-healthy daily dose of fermented products!
He does also talk safety, and troubleshooting too. And so long as you have a collection of big jars and a fairly normally-furnished kitchen, you shouldn’t need any more special equipment than that, unless you decide to you your fermentation skills for making beer (which does need some extra equipment, and he offers advice on that—our advice as a health science publication is “don’t drink beer”, though).
Bottom line: with this in hand, you can create a lot of amazing foods/drinks/condiments that are not only delicious, but also great for gut health.
Click here to check out Fermenting Everything, and widen your culinary horizons!
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Uric Acid’s Extensive Health Impact (And How To Lower It)
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Uric Acid’s Extensive Health Impact (And How To Lower It)
This is Dr. David Perlmutter. He’s a medical doctor, and a Fellow of the American College of Nutrition. He’s a member of the Editorial Board for the Journal of Alzheimer’s Disease, and has been widely published in many other peer-reviewed journals.
What does he want us to know?
He wants us to know about the health risks of uric acid (not something popularly talked about so much!), and how to reduce it.
First: what is it? Uric acid is a substance we make in our own body. However, unlike most substances we make in our body, we have negligible use for it—it’s largely a waste product, usually excreted in urine.
However, if we get too much, it can build up (and crystallize), becoming such things as kidney stones, or causing painful inflammation if it shows up in the joints, as in gout.
More seriously (unpleasant as kidney stones and gout may be), this inflammation can have a knock-on effect triggering (or worsening) other inflammatory conditions, ranging from non-alcoholic fatty liver disease, to arthritis, to dementia, and even heart problems. See for example:
- David Perlmutter | Uric Acid and Cognitive Decline
- American Heart Association | Uric acid linked to later risk for irregular heart rhythm
- World Journal of Gastroenterology | The role of uric acid in non-alcoholic steatohepatitis development
How can we reduce our uric acid levels?
Uric acid is produced when we metabolize purine nucleotides, which are found in many kinds of food. We can therefore reduce our uric acid levels by reducing our purine intake, as well as things that mess up our liver’s ability to detoxify things. Offsetting the values for confounding variables (such as fiber content, or phytochemicals that mitigate the harm), the worst offenders include…
Liver-debilitating things:
- Alcohol (especially beer)
- High-fructose corn syrup (and other fructose-containing things that aren’t actual fruit)
- Other refined sugars
- Wheat / white flour products (this is why beer is worse than wine, for example; it’s a double-vector hit)
Purine-rich things:
- Red meats and game
- Organ meats
- Oily fish, and seafood (great for some things; not great for this)
Some beans and legumes are also high in purines, but much like real fruit has a neutral or positive effect on blood sugar health despite its fructose content, the beans and legumes that are high in purines, also contain phytochemicals that help lower uric acid levels, so have a beneficial effect.
Eggs (consumed in moderation) and tart cherries have a uric-acid lowering effect.
Water is important for all aspects of health, and doubly important for this.
Hydrate well!
Lifestyle matters beyond diet
The main key here is metabolic health, so Dr. Perlmutter advises the uncontroversial lifestyle choices of moderate exercise and good sleep, as well as (more critically) intermittent fasting. We wrote previously on other things that can benefit liver health:
…in this case, that means the liver gets a break to recuperate (something it’s very good at, but does need to get a chance to do), which means that while you’re not giving it something new to do, it can quickly catch up on any backlog, and then tackle any new things fresh, next time you start eating.
Want to know more about this from Dr. Perlmutter?
You might like his article:
An Integrated Plan for Lowering Uric Acid ← more than we had room for here; he also talks about extra things to include in your diet/supplementation regime for beneficial effects!
And/or his book:
…on which much of today’s main feature was based.
Take care!
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