
Undoing The Damage Of Life’s Hard Knocks
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Sometimes, What Doesn’t Kill Us Makes Us Insecure
We’ve written before about Complex PTSD, which is much more common than the more popularly understood kind:
Given that C-PTSD affects so many people (around 1 in 5, but really, do read the article above! It explains it better than we have room to repeat today), it seems like a good idea to share tips for managing it.
(Last time, we took all the space for explaining it, so we just linked to some external resources at the end)
What happened to you?
PTSD has (as a necessity, as part of its diagnostic criteria) a clear event that caused it, which makes the above question easy to answer.
C-PTSD often takes more examination to figure out what tapestry of circumstances (and likely but not necessarily: treatment by other people) caused it.
Often it will feel like “but it can’t be that; that’s not that bad”, or “everyone has things like that” (in which case, you’re probably one of the one in five).
The deeper questions
Start by asking yourself: what are you most afraid of, and why? What are you most ashamed of? What do you fear that other people might say about you?
Often there is a core pattern of insecurity that can be summed up in a simple, harmful, I-message, e.g:
- I am a bad person
- I am unloveable
- I am a fake
- I am easy to hurt
- I cannot keep my loved ones safe
…and so forth.
For a bigger list of common insecurities to see what resonates, check out:
Basic Fears/Insecurities, And Their Corresponding Needs/Desires
Find where they came from
You probably learned bad beliefs, and consequently bad coping strategies, because of bad circumstances, and/or bad advice.
- When a parent exclaimed in anger about how stupid you are
- When a partner exclaimed in frustration that always mess everything up
- When an employer told you you weren’t good enough
…or maybe they told you one thing, and showed you the opposite. Or maybe it was entirely non-verbal circumstances:
- When you gambled on a good idea and lost everything
- When you tried so hard at some important endeavour and failed
- When you thought someone could be trusted, and learned the hard way that you were wrong
These are “life’s difficult bits”, but when we’ve lived through a whole stack of them, it’s less like a single shattering hammer-blow of PTSD, and more like the consistent non-stop tap tap tap that ends up doing just as much damage in the long run.
Resolve them
That may sound a bit like a “and quickly create world peace” level of task, but we have tools:
Ask yourself: what if…
…it had been different? Take some time and indulge in a full-blown fantasy of a life that was better. Explore it. How would those different life lessons, different messages, have impacted who you are, your personality, your behaviour?
This is useful, because the brain is famously bad at telling real memories from false ones. Consciously, you’ll know that one was an exploratory fantasy, but to your brain, it’s still doing the appropriate rewiring. So, little by little, neuroplasticity will do its thing.
Tell yourself a better lie
We borrowed this one from the title of a very good book which we’ve reviewed previously.
This idea is not about self-delusion, but rather that we already express our own experiences as a sort of narrative, and that narrative tends to contain value judgements that are often not useful, e.g. “I am stupid”, “I am useless”, and all the other insecurities we mentioned earlier. Some simple examples might be:
- “I had a terrible childhood” → “I have come so far”
- “I should have known better” → “I am wiser now”
- “I have lost so much” → “I have experienced so much”
So, replacing that self-talk can go a long way to re-writing how secure we feel, and therefore how much trauma-response (ideally: none!) we have to stimuli that are not really as threatening as we sometimes feel they are (a hallmark of PTSD in general).
Here’s a guide to more ways:
How To Get Your Brain On A More Positive Track (Without Toxic Positivity)
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The Polyvagal Theory – by Dr. Stephen Porges
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Do you ever find that your feelings (or occasionally: lack thereof) sometimes can seem mismatched with the observed facts of your situation? This book unravels that mystery—or rather, that stack of mysteries.
Dr. Porges’ work on this topic is, by the way, the culmination of 40 years of research. While he’s not exactly a household name to the layperson, he’s very respected in his field, and this book is his magnum opus.
Here he explains the disparate roles of the two branches of the vagus nerve (hence: polyvagal theory). At least, the two branches that we mammals have; non-mammalian vertebrates have only one. This makes a big difference, because of the cascade of inhibitions that this allows.
The answer to the very general question “What stops you from…?” is usually found somewhere down this line of cascade of inhibitions.
These range from “what stops you from quitting your job/relationship/etc” to “what stops you from freaking out” to “what stops you from relaxing” to “what stops you from reacting quickly” to “what stop you from giving up” to “what stops you from gnawing your arm off” and many many more.
And because sometimes we wish we could do something that we can’t, or wish we wouldn’t do something that we do, understanding this process can be something of a cheat code to life.
A quick note on style: the book is quite dense and can be quite technical, but should be comprehensible to any layperson who is content to take their time, because everything is explained as we go along.
Bottom line: if you’d like to better understand the mysteries of how you feel vs how you actually are, and what that means for what you can or cannot wilfully do, this is a top-tier book
Click here to check out Polyvagal Theory, and take control of your responses!
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Cardio vs Strength Training: Which Is Better For Brain Health?
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Dr. Tracey Marks, psychiatrist, explains:
It depends on which kind of brain health
Here at 10almonds, often say “what’s good for your heart is good for your brain” and it’s true, largely because the blood is what nourishes the brain (with oxygen and nutrients), and ultimately takes away detritus that shouldn’t be there (including α-synuclein and β-amyloid clearance, to protect you from Parkinson’s and Alzheimer’s, respectively).
And obviously, having good vasculature will have a protective effect against vascular dementia and stroke.
So, this is a hands-down win for cardio, right? Cardio also has further specific brain benefits in the short- and long-term:
- Short-term: within one exercise session (and certainly within 30 minutes of such), cardio exercise increases levels of the neurotransmitters dopamine, serotonin, and norepinephrine, resulting in an immediate mood boost.
- Long-term: if you do it consistently over time, it strengthens connections between the prefrontal cortex and amygdala, improving emotional regulation and stress resilience, and also reducing the risk of depression and anxiety.
However, strength-training also has its place, including for brain health.
Specifically, it boosts brain growth factors, which is as good as it sounds (and promotes healthy brain cell survival and synaptic plasticity, both of which are good things). It also helps regulate cortisol and, consequently, reduces chronic brain inflammation, as measurable by the reduced prevalence of inflammatory markers like CRP and TNF-Alpha. In terms of results we can see without lab equipment, it also improves executive function and memory, especially in older adults.
For more on all of this plus Dr. Marks’ recommendation of how to combine the two, enjoy:
Click Here If The Embedded Video Doesn’t Load Automatically!
Want to learn more?
You might also like:
How Your Exercise Today Gives A Brain Boost Tomorrow
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Finally! Chronic Fatigue Syndrome Biomarkers Identified
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And other items from this week’s health news:
Good news for Chronic Fatigue Syndrome sufferers
Historically considered a syndrome that has no observable signs (only symptoms reported by the sufferer), chronic fatigue syndrome (CFS) now has some biomarkers identified, achieving 90% diagnostic accuracy—offering objective proof for a disease often dismissed due to a lack of lab evidence.
How it was done: researchers (Dr. Julia Oh et al.) showed how the gut microbiome, immune cells, and metabolites correlate with symptoms like fatigue, pain, and sleep disturbances. ME/CFS patients had reduced butyrate (a gut-beneficial fatty acid), elevated tryptophan and benzoate (indicators of microbial imbalance), and increased inflammatory responses, especially in cells linked to gut health. In terms of which parts did what, immune cell data best predicted overall symptom severity, while gut microbiome data correlated most with gastrointestinal, emotional, and sleep-related symptoms. Meanwhile, symptoms like dizziness, sleep disturbances, and headaches were linked directly to disruptions in gut-immune-metabolic networks, offering a systems-level disease view.
In other words, a lot of data.
It was also worthy of note that biological disruptions were less extensive in patients ill for under four years compared to those ill over a decade, implying worsening dysregulation over time.
Which makes it all the more important that we now have ways to categorically identify and thus usefully diagnose it:
Read in full: Previously undetectable biomarkers in gut microbiome may predict “invisible” chronic fatigue syndrome, long COVID
Related: How To Be 7.5x More Likely To Develop Chronic Fatigue Syndrome
Texas is taking the lead!
But not in good ways, unfortunately. This time it’s not about measles, though, and rather is about STI rates, especially on a county level. For example, Dallas county ranked 7th (in the US), with 1,314.5 STI cases per 100,000 people.
You might be wondering what STIs specifically, and: chlamydia and gonorrhea dominate case numbers, but syphilis and HIV are steadily rising, particularly in urban areas.
The report identified the following factors as being the main reasons the rates are rising so much:
- inadequate sex education
- limited access to affordable care and regular testing
- high infection rates among youth lacking primary care
- stigma and misinformation
- racial and economic disparities (impacting accessibility of testing and treatment)
In Texas, people aged 15–29 represent the largest portion of new infections, but before you write that off as “young people nowadays” who cannot contain their hormones, note that that’s new infections—the only reason older demographics score lower is because each instance of infection is less likely to be one’s first, the further one goes through life. Overall infection rates (i.e., not just “new infections”) are rising the highest in adults over 50.
Read in full: Texas counties have some of the highest STD rates in US, new report says
Related: Why STIs Are On The Rise In Older Adults
The change
Prostate cancer is one of the major killers of men, the top cancer for men by prevalence, and affects over 60% of men over the age of 60 (with that percentage then rising each year thereafter). Note that this means “if something else doesn’t kill you first, you are more likely to get this than not”.
Prostate cancer is also something where the early stages of it are often described “nothing to worry about for now; let’s keep an eye on it”.
Happily, researchers have now discovered how prostate cancer evolves into its most lethal form, neuroendocrine prostate cancer (NEPC). This was a win for medical AI (while both are called “AI”, this is incredibly different from ChatGPT et al.), and specifically, it was a 3d genome mapping breakthrough; using advanced genomic tools, they created the first 3D map of how prostate cancer cells rewire their DNA structure to enable and promote the aforementioned shift to NEPC.
Some technical bits for those who want it:
- The key proteins involved have been identified: FOXA2 and NKX2-1 drive the transformation by reprogramming the cancer cells; FOXA2 opens inaccessible DNA regions, allowing NKX2-1 to activate NEPC-related genes.
- The role of cbp and p300 enzymes have been identified: these enzymes help activate oncogenes crucial to the NEPC transformation, acting as co-drivers of the aggressive cancer form.
- A potential treatment has been identified: the drug CCS1477, a CBP/p300 inhibitor in clinical trials, successfully halted NEPC tumor growth in lab studies.
The latter is particularly important, as it allows for new treatment avenues for prostate cancers that become resistant to hormone therapy, by preventing or reversing the NEPC transition.
Read in full: Study uncovers how prostate cancer becomes deadly, offers hope for new treatments
Related: Prostate Health: What You Should Know
Take care!
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Demystifying C-Reactive Protein (CRP)!
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Most people over a certain age who are at least somewhat invested in their health know that c-reactive protein (CRP) is a blood biomarker that’s considered an indicator of cardiovascular health (or: illness, as the case may be), but often know little more than that.
So, what is it and what does it mean?
Oh, CRP
CRP is produced by the liver in response to immune activation from infections, tissue damage, autoimmune disease, obesity, and diabetes.
As for what its actual job is (because the body does produce it for reasons other than for its usefulness as a biomarker in blood tests),
❝Similar to immunoglobulin (Ig)G, it activates complement, binds to Fc receptors and acts as an opsonin for various pathogens. Interaction of CRP with Fc receptors leads to the generation of proinflammatory cytokines that enhance the inflammatory response. Unlike IgG, which specifically recognizes distinct antigenic epitopes, CRP recognizes altered self and foreign molecules based on pattern recognition. Thus, CRP is though to act as a surveillance molecule for altered self and certain pathogens. This recognition provides early defense and leads to a proinflammatory signal and activation of the humoural, adaptive immune system.❞
Source: Function of C-reactive protein
Translating that from sciencese: CRP acts like a first-responder version of an antibody. Like IgG antibodies, it can activate the complement* system, latch onto immune cell receptors, and tag microbes so they are easier for immune cells to destroy. When CRP binds to these receptors, it also triggers the release of inflammatory signals that dial up the immune response.
The key difference is how it recognizes threats: antibodies such as IgG are very specific—they are custom-made to recognize one precise target and nothing else. CRP, in contrast, looks for broad patterns that signal damage or danger, whether from invading microbes or the body’s own altered cells. Thus, CRP acts as an immune surveillance sensor, providing early warning and kick-starting inflammation and the wider adaptive immune response. Which, in the case of an actual infection or similar, is a good thing.
*You may be wondering what, in turn, the complement system is and what activating it means. In simple terms, it starts off as a bunch of proteins circulating in your blood in an inactive form. When CRP (or an antibody) binds to a microbe or a damaged cell, it can activate this cascade, which then joints the fight and also does the latching on and tagging that we mentioned, by:
- directly damaging microbes: in some cases, complement proteins punch holes in bacterial membranes, leading to their death.
- tagging the target for destruction: complement proteins typically coat the surface of the microbe or damaged cell, making it easier for immune cells to recognize and engulf it.
- dialling up inflammation: small complement fragments act like chemical alarms, attracting immune cells and increasing local inflammation.
Again, if there’s actually a genuine threat to respond to, these are all good things for it to be doing.
CRP as a biomarker
CRP is a very useful biomarker of low-grade inflammation, and evidence from decades of research shows it predicts heart attacks and strokes better than LDL cholesterol and lipoprotein(a), and at least as well as blood pressure: Inflammation, Cholesterol, Lipoprotein(a), and 30-Year Cardiovascular Outcomes in Women
Same goes for when we look at mortality: C-reactive protein concentration and risk of coronary heart disease, stroke, and mortality: an individual participant meta-analysis
For this reason, the American College of Cardiology recommended universal CRP screening alongside cholesterol testing to improve cardiovascular risk assessment. You can read that in full, here:
You may be wondering about numbers: CRP under 1 mg/dL indicates low inflammation and lower risk, while CRP above 3 mg/dL signals higher inflammation and higher risk.
How likely is it that you are at risk? Well, about 52% of Americans have elevated CRP, so that’s not a promising figure to start with. Now, 10almonds readers are doubtlessly healthier than the average American as a general demographic, but still, it’s worth bearing in mind and not assuming that it could only apply to other people.
And as for how to improve your numbers? Same deal as most heart health advice that we give here: enjoy a plants-forward (if not entirely plant-based) diet, especially making sure to get a lot of fiber and as many different sources of polyphenols as is reasonable. Get good sleep, do exercise often, and don’t smoke or drink.
About the dietary aspects specifically, see:
- What Matters Most For Your Heart?
- What Do The Different Kinds Of Fiber Do? 30 Foods That Rank Highest
- 21 Most Beneficial Polyphenols & What Foods Have Them
Want to learn more?
If you’d like a comprehensive guide to reducing your heart disease risk, no matter your starting point, then you might like to consider:
Dr. Dean Ornish’s Program For Reversing Heart Disease – by Dr. Dean Ornish
Take care!
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Big Think’s #1 Antidote To Aging
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Why This Video Is Important
A lot of what we talk about here at 10almonds is focused on healthy aging. We want you – our lovely readers – to not only live for a long time, but also be healthy enough to enjoy that “long time”.
We’ve talked about anything from Dr. Greger’s eight anti-aging interventions, to the specific benefits of resveratrol or metformin in combatting aging, to even reducing stress-induced aging.
So, why is this video important? It goes beyond just talking about what we know about living longer, but also focuses on how we should live longer; there’s a big difference between living a long life but never leaving your house vs. living a long life beyond your front door.
The Takeaways
The core message that Big Think wants to convey is that our lifestyle is our best bet in slowing the aging process. Our bodies are adaptive systems, responding positively to healthy lifestyle choices. They focus on exercise: regular physical activity increases healthspan, consequently extending lifespan.
A key takeaway is the difference between physical activity and exercise. While any movement counts as physical activity, exercise is a deliberate, health-focused activity. It benefits the brain by releasing growth factors that strengthen critical areas like the hippocampus and prefrontal cortex.
The video encourages embracing physical activity in any form available to you, from gardening to walking. The goal isn’t to hit a specific number of steps but to stay active in a way that suits your lifestyle.
Science may not solve death. Yet. But focusing on maintaining a healthy, functioning state for as long as possible is the real victory in the battle against aging. And, at the moment, exercise seems to be our best bet:
How did you find that video? If you’ve discovered any great videos yourself that you’d like to share with fellow 10almonds readers, then please do email them to us!
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Viruses aren’t always harmful. 6 ways they’re used in health care and pest control
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We tend to just think of viruses in terms of their damaging impacts on human health and lives. The 1918 flu pandemic killed around 50 million people. Smallpox claimed 30% of those who caught it, and survivors were often scarred and blinded. More recently, we’re all too familiar with the health and economic impacts of COVID.
But viruses can also be used to benefit human health, agriculture and the environment.
Viruses are comparatively simple in structure, consisting of a piece of genetic material (RNA or DNA) enclosed in a protein coat (the capsid). Some also have an outer envelope.
Viruses get into your cells and use your cell machinery to copy themselves.
Here are six ways we’ve harnessed this for health care and pest control.1. To correct genes
Viruses are used in some gene therapies to correct malfunctioning genes. Genes are DNA sequences that code for a particular protein required for cell function.
If we remove viral genetic material from the capsid (protein coat) we can use the space to transport a “cargo” into cells. These modified viruses are called “viral vectors”.
Viruses consist of a piece of RNA or DNA enclosed in a protein coat called the capsid.
DEXiViral vectors can deliver a functional gene into someone with a genetic disorder whose own gene is not working properly.
Some genetic diseases treated this way include haemophilia, sickle cell disease and beta thalassaemia.
2. Treat cancer
Viral vectors can be used to treat cancer.
Healthy people have p53, a tumour-suppressor gene. About half of cancers are associated with the loss of p53.
Replacing the damaged p53 gene using a viral vector stops the cancerous cell from replicating and tells it to suicide (apoptosis).
Viral vectors can also be used to deliver an inactive drug to a tumour, where it is then activated to kill the tumour cell.
This targeted therapy reduces the side effects otherwise seen with cytotoxic (cell-killing) drugs.
We can also use oncolytic (cancer cell-destroying) viruses to treat some types of cancer.
Tumour cells have often lost their antiviral defences. In the case of melanoma, a modified herpes simplex virus can kill rapidly dividing melanoma cells while largely leaving non-tumour cells alone.
3. Create immune responses
Viral vectors can create a protective immune response to a particular viral antigen.
One COVID vaccine uses a modified chimp adenovirus (adenoviruses cause the common cold in humans) to transport RNA coding for the SARS-CoV-2 spike protein into human cells.
The RNA is then used to make spike protein copies, which stimulate our immune cells to replicate and “remember” the spike protein.
Then, when you are exposed to SARS-CoV-2 for real, your immune system can churn out lots of antibodies and virus-killing cells very quickly to prevent or reduce the severity of infection.
4. Act as vaccines
Viruses can be modified to act directly as vaccines themselves in several ways.
We can weaken a virus (for an attenuated virus vaccine) so it doesn’t cause infection in a healthy host but can still replicate to stimulate the immune response. The chickenpox vaccine works like this.
The Salk vaccine for polio uses a whole virus that has been inactivated (so it can’t cause disease).
Others use a small part of the virus such as a capsid protein to stimulate an immune response (subunit vaccines).
An mRNA vaccine packages up viral RNA for a specific protein that will stimulate an immune response.
5. Kill bacteria
Viruses can – in limited situations in Australia – be used to treat antibiotic-resistant bacterial infections.
Bacteriophages are viruses that kill bacteria. Each type of phage usually infects a particular species of bacteria.
Unlike antibiotics – which often kill “good” bacteria along with the disease-causing ones – phage therapy leaves your normal flora (useful microbes) intact.
Bacteriophages (red) are viruses that kill bacteria (green).
Shutterstock6. Target plant, fungal or animal pests
Viruses can be species-specific (infecting one species only) and even cell-specific (infecting one type of cell only).
This occurs because the proteins viruses use to attach to cells have a shape that binds to a specific type of cell receptor or molecule, like a specific key fits a lock.
The virus can enter the cells of all species with this receptor/molecule. For example, rabies virus can infect all mammals because we share the right receptor, and mammals have other characteristics that allow infection to occur whereas other non-mammal species don’t.
When the receptor is only found on one cell type, then the virus will infect that cell type, which may only be found in one or a limited number of species. Hepatitis B virus successfully infects liver cells primarily in humans and chimps.
We can use that property of specificity to target invasive plant species (reducing the need for chemical herbicides) and pest insects (reducing the need for chemical insecticides). Baculoviruses, for example, are used to control caterpillars.
Similarly, bacteriophages can be used to control bacterial tomato and grapevine diseases.
Other viruses reduce plant damage from fungal pests.
Myxoma virus and calicivirus reduce rabbit populations and their environmental impacts and improve agricultural production.
Just like humans can be protected against by vaccination, plants can be “immunised” against a disease-causing virus by being exposed to a milder version.
Thea van de Mortel, Professor, Nursing, School of Nursing and Midwifery, Griffith University
This article is republished from The Conversation under a Creative Commons license. Read the original article.
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