We looked at genetic clues to depression in more than 14,000 people. What we found may surprise you
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The core experiences of depression – changes in energy, activity, thinking and mood – have been described for more than 10,000 years. The word “depression” has been used for about 350 years.
Given this long history, it may surprise you that experts don’t agree about what depression is, how to define it or what causes it.
But many experts do agree that depression is not one thing. It’s a large family of illnesses with different causes and mechanisms. This makes choosing the best treatment for each person challenging.
Reactive vs endogenous depression
One strategy is to search for sub-types of depression and see whether they might do better with different kinds of treatments. One example is contrasting “reactive” depression with “endogenous” depression.
Reactive depression (also thought of as social or psychological depression) is presented as being triggered by exposure to stressful life events. These might be being assaulted or losing a loved one – an understandable reaction to an outside trigger.
Endogenous depression (also thought of as biological or genetic depression) is proposed to be caused by something inside, such as genes or brain chemistry.
Many people working clinically in mental health accept this sub-typing. You might have read about this online.
But we think this approach is way too simple.
While stressful life events and genes may, individually, contribute to causing depression, they also interact to increase the risk of someone developing depression. And evidence shows that there is a genetic component to being exposed to stressors. Some genes affect things such as personality. Some affect how we interact with our environments.
What we did and what we found
Our team set out to look at the role of genes and stressors to see if classifying depression as reactive or endogenous was valid.
In the Australian Genetics of Depression Study, people with depression answered surveys about exposure to stressful life events. We analysed DNA from their saliva samples to calculate their genetic risk for mental disorders.
Our question was simple. Does genetic risk for depression, bipolar disorder, schizophrenia, ADHD, anxiety and neuroticism (a personality trait) influence people’s reported exposure to stressful life events?
You may be wondering why we bothered calculating the genetic risk for mental disorders in people who already have depression. Every person has genetic variants linked to mental disorders. Some people have more, some less. Even people who already have depression might have a low genetic risk for it. These people may have developed their particular depression from some other constellation of causes.
We looked at the genetic risk of conditions other than depression for a couple of reasons. First, genetic variants linked to depression overlap with those linked to other mental disorders. Second, two people with depression may have completely different genetic variants. So we wanted to cast a wide net to look at a wider spectrum of genetic variants linked to mental disorders.
If reactive and endogenous depression sub-types are valid, we’d expect people with a lower genetic component to their depression (the reactive group) would report more stressful life events. And we’d expect those with a higher genetic component (the endogenous group) would report fewer stressful life events.
But after studying more than 14,000 people with depression we found the opposite.
We found people at higher genetic risk for depression, anxiety, ADHD or schizophrenia say they’ve been exposed to more stressors.
Assault with a weapon, sexual assault, accidents, legal and financial troubles, and childhood abuse and neglect, were all more common in people with a higher genetic risk of depression, anxiety, ADHD or schizophrenia.
These associations were not strongly influenced by people’s age, sex or relationships with family. We didn’t look at other factors that may influence these associations, such as socioeconomic status. We also relied on people’s memory of past events, which may not be accurate.
How do genes play a role?
Genetic risk for mental disorders changes people’s sensitivity to the environment.
Imagine two people, one with a high genetic risk for depression, one with a low risk. They both lose their jobs. The genetically vulnerable person experiences the job loss as a threat to their self-worth and social status. There is a sense of shame and despair. They can’t bring themselves to look for another job for fear of losing it too. For the other, the job loss feels less about them and more about the company. These two people internalise the event differently and remember it differently.
Genetic risk for mental disorders also might make it more likely people find themselves in environments where bad things happen. For example, a higher genetic risk for depression might affect self-worth, making people more likely to get into dysfunctional relationships which then go badly.
What does our study mean for depression?
First, it confirms genes and environments are not independent. Genes influence the environments we end up in, and what then happens. Genes also influence how we react to those events.
Second, our study doesn’t support a distinction between reactive and endogenous depression. Genes and environments have a complex interplay. Most cases of depression are a mix of genetics, biology and stressors.
Third, people with depression who appear to have a stronger genetic component to their depression report their lives are punctuated by more serious stressors.
So clinically, people with higher genetic vulnerability might benefit from learning specific techniques to manage their stress. This might help some people reduce their chance of developing depression in the first place. It might also help some people with depression reduce their ongoing exposure to stressors.
If this article has raised issues for you, or if you’re concerned about someone you know, call Lifeline on 13 11 14.
Jacob Crouse, Research Fellow in Youth Mental Health, Brain and Mind Centre, University of Sydney and Ian Hickie, Co-Director, Health and Policy, Brain and Mind Centre, University of Sydney
This article is republished from The Conversation under a Creative Commons license. Read the original article.
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Fast Burn – by Dr. Ian K. Smith
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Intermittent fasting seems simple enough: how complicated can “stop eating for a bit” be? Well, there are nuances and tweaks and hacks and “if you do this bit wrong it will sabotage your benefits” things to know about, too.
Dr. Smith takes us through the basic essentials first, and covers each of the main kinds of intermittent fasting, for example:
- Time-restricted eating; 12:12, 16:8, etc, with those being hours fasting vs hours eating
- Caloric restriction models; for example 5:2, where one eats “normally” for 5 days a week, and on two non-consecutive days, eats only 500 calories
- Day off models and more; for example, “no eating on Sundays” that can, depending on your schedule, be anything from a 24-hour fast to 36 hours or more.
…and, most notably, what they each do metabolically.
Then, the real meat of the book is his program. Taking into account the benefits of each form of fasting, he weaves together a 9-week program to first ease us gently into intermittent fasting, and then enjoy the maximum benefits with minimum self-sabotage.
Which is the biggest stumbling-block for many trying intermittent fasting for the first time, so it’s a huge help that he takes care of this here.
He also includes meal plans and recipes; readers can use those or not; the fasting plan stands on its own two feet without them too.
Bottom line: if you’ve been thinking of trying intermittent fasting but have been put off by all the kinds or have had trouble sticking to it, this book may be just what you need.
Click here to check out Fast Burn on Amazon and see what you can achieve!
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Stop Using The Wrong Hairbrush For Your Hair Type
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When you brush your hair, you’re either making it healthier or damaging it, depending on what you’re using and how. To avoid pulling your hair out, and to enjoy healthy hair of whatever kind you have and whatever length suits you, it pays to know a little about different brushes, and the different techniques involved.
Head-to-head
Brush shapes and sizes are designed to achieve different effects in hair, not just for decoration. For example:
- Rat tail combs are excellent for parting and sectioning hair with clean lines. The rat tail part is actually more important than the comb part.
- Regular combs are multipurpose but best for use with flat irons, ensuring straighter hair for a longer time.
- Wide-tooth combs should not be used for detangling as they can cause breakage; instead, use a proper detangling brush. Speaking of detangling…
- Detangling brushes are essential for daily use. Whichever you use, start brushing from the bottom to prevent tangles from stacking and worsening. As for kinds of detangling brush:
- The “Tangle Teaser” is a good beginner option, but it may not detangle well for thicker hair.
- Wet Brush (this is a brand name, and is not about any inherent wetness) is the recommended detangling brush for most people. It can be used on wet or dry hair.
- Mason Pearson brush is a luxury detangling brush (see it here on Amazon) that works slightly more quickly and efficiently, but is expensive and not necessary for most people.
- Teasing brushes are for adding volume by backcombing—but require skill to prevent visible tangles. Best avoided for most people.
- Ceramic round brushes are the best for blow-drying, because they hold tension and help hair dry smoother and shinier.
- Blow-dryer brushes are great for easy blow-drying but should not be used on dry hair, to avoid damage.
- Denman brushes are for people with natural curls, enhancing curls without straightening them like a Wet brush would.
For more on all of these brushes, 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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Neurotransmitter Cheatsheet
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Which Neurotransmitter?
There are a lot of neurotransmitters that are important for good mental health (and, by way of knock-on effects, physical health).
However, when pop-science headlines refer to them as “feel-good chemicals” (yes but which one?!) or “the love molecule” (yes but which one?!) or other such vague names when referring to a specific neurotransmitter, it’s easy to get them mixed up.
So today we’re going to do a little disambiguation of some of the main mood-related neurotransmitters (there are many more, but we only have so much room), and what things we can do to help manage them.
Dopamine
This one predominantly regulates reward responses, though it’s also necessary for critical path analysis (e.g. planning), language faculties, and motor functions. It makes us feel happy, motivated, and awake.
To have more:
- eat foods that are rich in dopamine or its precursors such as tyrosine (bananas and almonds are great)
- do things that you find rewarding
Downsides: is instrumental in most addictions, and also too much can result in psychosis. For most people, that level of “too much” isn’t obtainable due to the homeostatic system, however.
See also: Rebalancing Dopamine (Without “Dopamine Fasting”)
Serotonin
This one predominantly helps regulate our circadian rhythm. It also makes us feel happy, calm, and awake.
To have more:
- get more sunlight, or if the light must be artificial, then (ideally) full-spectrum light, or (if it’s what’s available) blue light
- spend time in nature; we are hardwired to feel happy in the environments in which we evolved, which for most of human history was large open grassy expanses with occasional trees (however, for modern purposes, a park or appropriate garden will suffice).
Downsides: this is what keeps us awake at night if we had too much light before bed, and also too much serotonin can result in (potentially fatal) serotonin syndrome. Most people can’t get that much serotonin due to our homeostatic system, but some drugs can force it upon us.
See also: Seasonal Affective Disorder Strategies
Oxytocin
This one predominantly helps us connect to others on an emotional level. It also makes us feel happy, calm, and relaxed.
To have more:
- hug a loved one (or even just think about doing so, if they’re not available)
- look at pictures/videos of cute puppies, kittens, and the like—this triggers a similar response
Downsides: negligible. Socially speaking, it can cause us to drop our guard, most for most people most of the time, this is not a problem. It can also reduce sexual desire—it’s in large part responsible for the peaceful lulled state post-orgasm. It’s not responsible for the sleepiness in men though; that’s mostly prolactin.
See also: Only One Kind Of Relationship Promotes Longevity This Much!
Adrenaline
This one predominantly affects our sympathetic nervous system; it elevates heart rate, blood pressure, and other similar functions. It makes us feel alert, ready for action, and energized.
To have more:
- listen to a “power anthem” piece of music. What it is can depend on your musical tastes; whatever gets you riled up in an empowering way.
- engage in something competitive that you feel strongly about while doing it—or by the same mechanism, a solitary activity where the stakes feel high even if it’s actually quite safe (e.g. watching a thriller or a horror movie, if that’s your thing).
Downsides: its effects are not sustainable, and (in cases of chronic stress) the body will try to sustain them anyway, which has a deleterious effect. Because adrenaline and cortisol are closely linked, chronically high adrenal action will tend to mean chronically high cortisol also.
See also: Lower Your Cortisol! (Here’s Why & How)
Some final words
You’ll notice that in none of the “how to have more” did we mention drugs. That’s because:
- a drug-free approach is generally the best thing to try first, at the very least
- there are simply a lot of drugs to affect each one (or more), and talking about them would require talking about each drug in some detail.
However, the following may be of interest for some readers:
Antidepressants: Personalization Is Key!
Take care!
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10 Ways To Delay Aging
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This is Dr. Colin Rose; he is a Senior Associate of the Royal Society of Medicine. He’s also a main contributor to EduScience, a programme funded by the E.U. which is designed to enhance the teaching and learning of science in schools in Europe.
His most recent work has been about aging—and how to delay it. We also reviewed his latest book, here:
Delay Ageing – by Dr. Colin Rose
So, what does he want us to know? The key lies in his compilation of ten ways in which we age on a cellular level, and what we can to do slow each one of those:
Damage to DNA accumulates
While DNA can get damaged without any external stimulus to cause that, there are a lot of modifiable factors that we can do to reduce DNA damage. The list is easy: if it causes cancer, it causes aging.
Thus, check out: Stop Cancer 20 Years Ago
Cells become senescent
Our cells are replaced all the time; some sooner than others, but all of them at some point. The problem occurs when cells are outliving their usefulness. If a cell becomes completely immortal, that is cancer, but happily most don’t. Nevertheless, having senescent (aging) cells in the body means that those senescent cells are what get copied forwards by mitosis, and our DNA becomes like a photocopy of a tattered old photocopy of a tattered old photocopy. Which, needless to say, is not good for our health. So, the best thing to do is to kill them earlier:
Yes, really: Fisetin: The Anti-Aging Assassin
Mitochondria become dysfunctional
Without properly functional mitochondria, no living human cell can do its job properly.
Options: 7 Ways To Boost Mitochondrial Health To Fight Disease
Beneficial genes are switched off, harmful genes are on
It’s easy to think of our genes as being immutable, but epigenetics means that our environment (amongst other factors) can mean that our gene expression changes.
Imagine it this way: your genes are a set of instructions for your body. However, your body will act or not on those instructions, depending on other factors. Hormones often play a big part in this; for example sex hormones tell the body which set of genetic instructions to read (and thus what kind of body to build/rebuild), and cortisol or oxytocin can tell the body which set of contingency plans to activate or suppress (respectively). A milder example is gray hair; genes have the program for it, but many other factors inform the body when, if, and how to do it.
Of more concern when it comes to aging is what goes on with more critical systems, such as the brain, in which the aforementioned DNA damage can cause unhelpful instructions to get interpreted, resulting in epigenetic changes that in turn facilitate age-related degeneration.
As to what can be done, see : Klotho: Unzipping The Genes Of Aging?
Stem cells become exhausted
Stem cells can become different kinds of cells, and thus they’re very useful for maintaining a healthy body. However, they get depleted with age. We can slow down the rate of loss, though; for example, intermittent fasting can help:
Per Dr. Li’s 5 Ways To Beat Cancer (And Other Diseases)
And for more detail, see:
Doctor’s Tip: Regeneration (stem cells) — one of your body’s five defense systems
(complete with lists of foods to eat or avoid for stem cell health)
Cells fail to communicate properly
Cells need to talk to each other constantly, to continue doing their jobs. We are one big organism, after all, and not a haphazard colony of the countless cells that constitute such. However, cell signalling gets worse with age, which in turn precipitates others age-related problems. Fortunately, there are nutrients that can improve cellular communication.
For example: PS, We Love You ← this is about phosphatidylserine, also called “PS”
Telomeres become shorter
These protective caps on our DNA suffer the wear-and-tear so that our DNA doesn’t have to. However, as they get shorter, the DNA can start suffering damage. For this reason, telomere length is considered one of the most “Gold Standard” markers of cellular aging.
Here’s what can be done for that: The Stress Prescription (Against Aging!)
The body fails to sense nutritional intake properly
This is mostly about insulin signalling (though problems can occur in other systems too, but we only have so much room here), so it’s important to take care of that.
See: Turn Back The Clock On Insulin Resistance
Proteins accumulate errors
This is due to DNA damage, of course, but there are specific things that can reduce protein error accumulation; see for example:
A quick fix – preventing protein errors extends lifespan
See also: Rapamycin Can Slow Aging By 20% (But Watch Out)
The microbiome becomes unbalanced
We at 10almonds often mention that gut health affects pretty much every other kind of health, and it’s true for aging as well. So, take care of that microbiome!
Here’s a primer: Gut Health 101
Want to know more about delaying aging beyond the cellular level?
Check out: Age & Aging: What Can (And Can’t) We Do About It?
Take care!
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Semaglutide for Weight Loss?
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Semaglutide for weight loss?
Semaglutide is the new kid on the weight-loss block, but it’s looking promising (with some caveats!).
Most popularly by brand names Ozempic and Wegovy, it was first trialled to help diabetics*, and is now sought-after by the rest of the population too. So far, only Wegovy is FDA-approved for weight loss. It contains more semaglutide than Ozempic, and was developed specifically for weight loss, rather than for diabetes.
*Specifically: diabetics with type 2 diabetes. Because it works by helping the pancreas to make insulin, it’s of no help whatsoever to T1D folks, sadly. If you’re T1D and reading this though, today’s book of the day is for you!
First things first: does it work as marketed for diabetes?
It does! At a cost: a very common side effect is gastrointestinal problems—same as for tirzepatide, which (like semaglutide) is a GLP-1 agonist, meaning it works the same way. Here’s how they measure up:
- Head-to-head study: Effects of subcutaneous tirzepatide versus placebo or semaglutide on pancreatic islet function and insulin sensitivity in adults with type 2 diabetes
- Head-to-head systematic review: Semaglutide for the treatment of type 2 Diabetes Mellitus: A systematic review and network meta-analysis of safety and efficacy outcomes
As you can see, both of them work wonders for pancreatic function and insulin sensitivity!
And, both of them were quite unpleasant for around 20% of participants:
❝Tirzepatide, oral and SC semaglutide has a favourable efficacy in treating T2DM. Gastrointestinal adverse events were highly recorded in tirzepatide, oral and SC semaglutide groups.❞
What about for weight loss, if not diabetic?
It works just the same! With just the same likelihood of gastro-intestinal unpleasantries, though. There’s a very good study that was done with 1,961 overweight adults; here it is:
Once-Weekly Semaglutide in Adults with Overweight or Obesity
The most interesting things here are the positive results and the side effects:
❝The mean change in body weight from baseline to week 68 was −14.9% in the semaglutide group as compared with −2.4% with placebo, for an estimated treatment difference of −12.4 percentage points (95% confidence interval [CI], −13.4 to −11.5; P<0.001).❞
In other words: if you take this, you’re almost certainly going to get something like 6x better weight loss results than doing the same thing without it.
❝Nausea and diarrhea were the most common adverse events with semaglutide; they were typically transient and mild-to-moderate in severity and subsided with time. More participants in the semaglutide group than in the placebo group discontinued treatment owing to gastrointestinal events (59 [4.5%] vs. 5 [0.8%])❞
~ ibid.
In other words: you have about a 3% chance of having unpleasant enough side effects that you don’t want to continue treatment (contrast this with the 20%ish chance of unpleasant side effects of any extent)!
Any other downsides we should know about?
If you stop taking it, weight regain is likely. For example, a participant in one of the above-mentioned studies who lost 22% of her body weight with the drug’s help, says:
❝Now that I am no longer taking the drug, unfortunately, my weight is returning to what it used to be. It felt effortless losing weight while on the trial, but now it has gone back to feeling like a constant battle with food. I hope that, if the drug can be approved for people like me, my [doctor] will be able to prescribe the drug for me in the future.❞
~ Jan, a trial participant at UCLH
Is it injection-only, or is there an oral option?
An oral option exists, but (so far) is on the market only in the form of Rybelsus, another (slightly older) drug containing semaglutide, and it’s (so far) only FDA-approved for diabetes, not for weight loss. See:
A new era for oral peptides: SNAC and the development of oral semaglutide for the treatment of type 2 diabetes ← for the science
FDA approves first oral GLP-1 treatment for type 2 diabetes ← For the FDA statement
Where can I get these?
Availability and prescribing regulations vary by country (because the FDA’s authority stops at the US borders), but here is the website for each of them if you’d like to learn more / consider if they might help you:
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The Kitchen Prescription – by Saliha Mahmood Ahmed
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One of the biggest challenges facing anyone learning to cook more healthily, is keeping it tasty. What to cook when your biggest comfort foods all contain things you “should” avoid?
Happily for us, Dr. Ahmed is here with a focus on comfort food that’s good for your gut health. It’s incidentally equally good for the heart and good against diabetes… but Dr. Ahmed is a gastroenterologist, so that’s where she’s coming from with these.
There’s a wide range of 101 recipes here, including many tagged vegetarian, vegan, and/or gluten-free, as appropriate.
While this is not a vegetarian cookbook, Dr. Ahmed does consider the key components of a good diet to be, in order of quantity that should be consumed:
- Fruits and vegetables
- Whole grains
- Legumes
- Pulses
- Nuts and seeds
…and as such, the recipes are mostly plant-based.
The recipes are from all around the world, and/but the ingredients are mostly things that are almost universal. In the event that something might be hard-to-get, she suggests an appropriate substitution.
The recipes are straightforward and clear, as well as being beautifully illustrated.
All in all, a fine addition to anyone’s kitchen!
Get your copy of The Kitchen Prescription from Amazon today!
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