Carrots vs Parsnips – Which is Healthier?
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Our Verdict
When comparing carrots to parsnips, we picked the parsnips.
Why?
There are arguments for both! But we say parsnips win on overall nutritional density.
In terms of macros, parsnips vary quite a lot from region to another, but broadly speaking, parsnips have more carbs and fiber, and/but the ratios are such that carrots have the lower glycemic index. We’ll call this one a win for carrots.
When it comes to vitamins, carrots have more of vitamins A, B2, B3, B6, and choline, while parsnips have more of vitamins B1, B5, B9, C, E, and K. A small win for parsnips here.
In the category of minerals, carrots are not higher in any minerals, while parsnips are higher in calcium, copper, iron, magnesium, manganese, phosphorus, potassium, selenium, and zinc. An overwhelming win for parsnips.
While the overall vitamin and mineral content puts parsnips ahead, it’s still worth noting that carrots have highly bioavailable megadoses of vitamin A.
Another thing to note is that the glycemic index recorded for both is when peeled and boiled, whereas both of these root vegetables can be enjoyed raw if you wish, which has a much lower GI.
In short, enjoy either or both, but parsnips are the more nutritionally dense overall.
Want to learn more?
You might like to read:
Glycemic Index vs Glycemic Load vs Insulin Index
Take care!
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Long-acting contraceptives seem to be as safe as the pill when it comes to cancer risk
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Many women worry hormonal contraceptives have dangerous side-effects including increased cancer risk. But this perception is often out of proportion with the actual risks.
So, what does the research actually say about cancer risk for contraceptive users?
And is your cancer risk different if, instead of the pill, you use long-acting reversible contraceptives? These include intrauterine devices or IUDs (such as Mirena), implants under the skin (such as Implanon), and injections (such as Depo Provera).
Our new study, conducted by the University of Queensland and QIMR Berghofer Medical Research Institute and published by the Journal of the National Cancer Institute, looked at this question.
We found long-acting contraceptives seem to be as safe as the pill when it comes to cancer risk (which is good news) but not necessarily any safer than the pill.
Peakstock/Shutterstock Some hormonal contraceptives take the form of implants under the skin. WiP-Studio/Shutterstock How does the contraceptive pill affect cancer risk?
The International Agency for Research on Cancer, which compiles evidence on cancer causes, has concluded that oral contraceptives have mixed effects on cancer risk.
Using the oral contraceptive pill:
- slightly increases your risk of breast and cervical cancer in the short term, but
- substantially reduces your risk of cancers of the uterus and ovaries in the longer term.
Our earlier work showed the pill was responsible for preventing far more cancers overall than it contributed to.
In previous research we estimated that in 2010, oral contraceptive pill use prevented over 1,300 cases of endometrial and ovarian cancers in Australian women.
It also prevented almost 500 deaths from these cancers in 2013. This is a reduction of around 25% in the deaths that could have occurred that year if women hadn’t taken the pill.
In contrast, we calculated the pill may have contributed to around 15 deaths from breast cancer in 2013, which is less than 0.5% of all breast cancer deaths in that year.
Previous work showed the pill was responsible for preventing far more cancers overall than it contributed to. Image Point Fr What about long-acting reversible contraceptives and cancer risk?
Long-acting reversible contraceptives – which include intrauterine devices or IUDs, implants under the skin, and injections – release progesterone-like hormones.
These are very effective contraceptives that can last from a few months (injections) up to seven years (intrauterine devices).
Notably, they don’t contain the hormone oestrogen, which may be responsible for some of the side-effects of the pill (including perhaps contributing to a higher risk of breast cancer).
Use of these long-acting contraceptives has doubled over the past decade, while the use of the pill has declined. So it’s important to know whether this change could affect cancer risk for Australian women.
Our new study of more than 1 million Australian women investigated whether long-acting, reversible contraceptives affect risk of invasive cancers. We compared the results to the oral contraceptive pill.
We used de-identified health records for Australian women aged 55 and under in 2002.
Among this group, about 176,000 were diagnosed with cancer between 2004 and 2013 when the oldest women were aged 67. We compared hormonal contraceptive use among these women who got cancer to women without cancer.
We found that long-term users of all types of hormonal contraception had around a 70% lower risk of developing endometrial cancer in the years after use. In other words, the risk of developing endometrial cancer is substantially lower among women who took hormonal contraception compared to those who didn’t.
For ovarian cancer, we saw a 50% reduced risk (compared to those who took no hormonal contraception) for women who were long-term users of the hormone-containing IUD.
The risk reduction was not as marked for the implants or injections, however few long-term users of these products developed these cancers in our study.
As the risk of endometrial and ovarian cancers increases with age, it will be important to look at cancer risk in these women as they get older.
What about breast cancer risk?
Our findings suggest that the risk of breast cancer for current users of long-acting contraceptives is similar to users of the pill.
However, the contraceptive injection was only associated with an increase in breast cancer risk after five years of use and there was no longer a higher risk once women stopped using them.
Our results suggested that the risk of breast cancer also reduces after stopping use of the contraceptive implants.
We will need to follow-up the women for longer to determine whether this is also the case for the IUD.
It is worth emphasising that the breast cancer risk associated with all hormonal contraceptives is very small.
About 30 in every 100,000 women aged 20 to 39 years develop breast cancer each year, and any hormonal contraceptive use would only increase this to around 36 cases per 100,000.
What about other cancers?
Our study did not show any consistent relationships between contraceptive use and other cancers types. However, we only at looked at invasive cancers (meaning those that start at a primary site but have the potential to spread to other parts of the body).
A recent French study found that prolonged use of the contraceptive injection increased the risk of meningioma (a type of benign brain tumour).
However, meningiomas are rare, especially in young women. There are around two cases in every 100,000 in women aged 20–39, so the extra number of cases linked to contraceptive injection use was small.
The French study found the hormonal IUD did not increase meningioma risk (and they did not investigate contraceptive implants).
Benefits and side-effects
There are benefits and side-effects for all medicines, including contraceptives, but it is important to know most very serious side-effects are rare.
A conversation with your doctor about the balance of benefits and side-effects for you is always a good place to start.
Susan Jordan, Professor of Epidemiology, The University of Queensland; Karen Tuesley, Postdoctoral Research Fellow, School of Public Health, The University of Queensland, and Penny Webb, Distinguished Scientist, Gynaecological Cancers Group, QIMR Berghofer Medical Research Institute
This article is republished from The Conversation under a Creative Commons license. Read the original article.
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Can a drug like Ozempic help treat addictions to alcohol, opioids or other substances?
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Semaglutide (sold as Ozempic, Wegovy and Rybelsus) was initially developed to treat diabetes. It works by stimulating the production of insulin to keep blood sugar levels in check.
This type of drug is increasingly being prescribed for weight loss, despite the fact it was initially approved for another purpose. Recently, there has been growing interest in another possible use: to treat addiction.
Anecdotal reports from patients taking semaglutide for weight loss suggest it reduces their appetite and craving for food, but surprisingly, it also may reduce their desire to drink alcohol, smoke cigarettes or take other drugs.
But does the research evidence back this up?
Animal studies show positive results
Semaglutide works on glucagon-like peptide-1 receptors and is known as a “GLP-1 agonist”.
Animal studies in rodents and monkeys have been overwhelmingly positive. Studies suggest GLP-1 agonists can reduce drug consumption and the rewarding value of drugs, including alcohol, nicotine, cocaine and opioids.
Out team has reviewed the evidence and found more than 30 different pre-clinical studies have been conducted. The majority show positive results in reducing drug and alcohol consumption or cravings. More than half of these studies focus specifically on alcohol use.
However, translating research evidence from animal models to people living with addiction is challenging. Although these results are promising, it’s still too early to tell if it will be safe and effective in humans with alcohol use disorder, nicotine addiction or another drug dependence.
What about research in humans?
Research findings are mixed in human studies.
Only one large randomised controlled trial has been conducted so far on alcohol. This study of 127 people found no difference between exenatide (a GLP-1 agonist) and placebo (a sham treatment) in reducing alcohol use or heavy drinking over 26 weeks.
In fact, everyone in the study reduced their drinking, both people on active medication and in the placebo group.
However, the authors conducted further analyses to examine changes in drinking in relation to weight. They found there was a reduction in drinking for people who had both alcohol use problems and obesity.
For people who started at a normal weight (BMI less than 30), despite initial reductions in drinking, they observed a rebound increase in levels of heavy drinking after four weeks of medication, with an overall increase in heavy drinking days relative to those who took the placebo.
There were no differences between groups for other measures of drinking, such as cravings.
Some studies show a rebound increase in levels of heavy drinking. Deman/Shutterstock In another 12-week trial, researchers found the GLP-1 agonist dulaglutide did not help to reduce smoking.
However, people receiving GLP-1 agonist dulaglutide drank 29% less alcohol than those on the placebo. Over 90% of people in this study also had obesity.
Smaller studies have looked at GLP-1 agonists short-term for cocaine and opioids, with mixed results.
There are currently many other clinical studies of GLP-1 agonists and alcohol and other addictive disorders underway.
While we await findings from bigger studies, it’s difficult to interpret the conflicting results. These differences in treatment response may come from individual differences that affect addiction, including physical and mental health problems.
Larger studies in broader populations of people will tell us more about whether GLP-1 agonists will work for addiction, and if so, for whom.
How might these drugs work for addiction?
The exact way GLP-1 agonists act are not yet well understood, however in addition to reducing consumption (of food or drugs), they also may reduce cravings.
Animal studies show GLP-1 agonists reduce craving for cocaine and opioids.
This may involve a key are of the brain reward circuit, the ventral striatum, with experimenters showing if they directly administer GLP-1 agonists into this region, rats show reduced “craving” for oxycodone or cocaine, possibly through reducing drug-induced dopamine release.
Using human brain imaging, experimenters can elicit craving by showing images (cues) associated with alcohol. The GLP-1 agonist exenatide reduced brain activity in response to an alcohol cue. Researchers saw reduced brain activity in the ventral striatum and septal areas of the brain, which connect to regions that regulate emotion, like the amygdala.
In studies in humans, it remains unclear whether GLP-1 agonists act directly to reduce cravings for alcohol or other drugs. This needs to be directly assessed in future research, alongside any reductions in use.
Are these drugs safe to use for addiction?
Overall, GLP-1 agonists have been shown to be relatively safe in healthy adults, and in people with diabetes or obesity. However side effects do include nausea, digestive troubles and headaches.
And while some people are OK with losing weight as a side effect, others aren’t. If someone is already underweight, for example, this drug might not be suitable for them.
In addition, very few studies have been conducted in people with addictive disorders. Yet some side effects may be more of an issue in people with addiction. Recent research, for instance, points to a rare risk of pancreatitis associated with GLP-1 agonists, and people with alcohol use problems already have a higher risk of this disorder.
Other drugs treatments are currently available
Although emerging research on GLP-1 agonists for addiction is an exciting development, much more research needs to be done to know the risks and benefits of these GLP-1 agonists for people living with addiction.
In the meantime, existing effective medications for addiction remain under-prescribed. Only about 3% of Australians with alcohol dependence, for example, are prescribed medication treatments such as like naltrexone, acamprosate or disulfiram. We need to ensure current medication treatments are accessible and health providers know how to prescribe them.
Continued innovation in addiction treatment is also essential. Our team is leading research towards other individualised and effective medications for alcohol dependence, while others are investigating treatments for nicotine addiction and other drug dependence.
Read the other articles in The Conversation’s Ozempic series here.
Shalini Arunogiri, Addiction Psychiatrist, Associate Professor, Monash University; Leigh Walker, , Florey Institute of Neuroscience and Mental Health, and Roberta Anversa, , The University of Melbourne
This article is republished from The Conversation under a Creative Commons license. Read the original article.
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The Brain As A Work-In-Progress
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And The Brain Goes Marching On!
In Tuesday’s newsletter, we asked you “when does the human brain stop developing?” and got the above-depicted, below-described, set of responses:
- About 64% of people said “Never”
- About 16% of people said “25 years”
- About 9% of people said “65 years”
- About 5% of people said “13 years”
- About 3% of people said “18 years”
- About 3% of people said “45 years”
Some thoughts, before we get into the science:
An alternative wording for the original question was “when does the human brain finish developing”; the meaning is the same but the feeling is slightly different:
- “When does the human brain stop developing?” focuses attention on the idea of cessation, and will skew responses to later ages
- When does the human brain finish developing?” focuses on attention on a kind of “is it done yet?” and will skew responses to earlier ages
Ultimately, since we had to chose one word or another, we picked the shortest one, but it would have been interesting if we could have done an A/B test, and asked half one way, and half the other way!
Why we picked those ages
We picked those ages as poll options for reasons people might be drawn to them:
- 13 years: in English-speaking cultures, an important milestone of entering adolescence (note that the concept of a “teenager” is not precisely universal as most languages do not have “-teen” numbers in the same way; the concept of “adolescent” may thus be tied to other milestones)
- 18 years: age of legal majority in N. America and many other places
- 25 years: age popularly believed to be when the brain is finished developing, due to a study that we’ll talk about shortly (we guess that’s why there’s a spike in our results for this, too!)
- 45 years: age where many midlife hormonal changes occur, and many professionals are considered to have peaked in competence and start looking towards retirement
- 65 years: age considered “senior” in much of N. America and many other places, as well as the cut-off and/or starting point for a lot of medical research
Notice, therefore, how a lot of things are coming from places they really shouldn’t. For example, because there are many studies saying “n% of people over 65 get Alzheimer’s” or “n% of people over 65 get age-related cognitive decline”, etc, 65 becomes the age where we start expecting this—because of an arbitrary human choice of where to draw the cut-off for the study enrollment!
Similarly, we may look at common ages of legal majority, or retirement pensions, and assume “well it must be for a good reason”, and dear reader, those reasons are more often economically motivated than they are biologically reasoned.
So, what does the science say?
Our brains are never finished developing: True or False?
True! If we define “finished developing” as “we cease doing neurogenesis and neuroplasticity is no longer in effect”.
Glossary:
- Neurogenesis: the process of creating new brain cells
- Neuroplasticity: the process of the brain adapting to changes by essentially rebuilding itself to suit our perceived current needs
We say “perceived” because sometimes neuroplasticity can do very unhelpful things to us (e.g: psychological trauma, or even just bad habits), but on a biological level, it is always doing its best to serve our overall success as an organism.
For a long time it was thought that we don’t do neurogenesis at all as adults, but this was found to be untrue:
How To Grow New Brain Cells (At Any Age)
Summary of conclusions of the above: we’re all growing new brain cells at every age, even if we be in our 80s and with Alzheimer’s disease, but there are things we can do to enhance our neurogenic potential along the way.
Neuroplasticity will always be somewhat enhanced by neurogenesis (after all, new neurons get given jobs to do), and we reviewed a great book about the marvels of neuroplasticity including in older age:
Our brains are still developing up to the age of 25: True or False?
True! And then it keeps on developing after that, too. Now this is abundantly obvious considering what we just talked about, but see what a difference the phrasing makes? Now it makes it sound like it stops at 25, which this statement doesn’t claim at all—it only speaks for the time up to that age.
A lot of the popular press about “the brain isn’t fully mature until the age of 25” stems from a 2006 study that found:
❝For instance, frontal gray matter volume peaks at about age 11.0 years in girls and 12.1 years in boys, whereas temporal gray matter volume peaks at about age at 16.7 years in girls and 16.2 years in boys. The dorsal lateral prefrontal cortex, important for controlling impulses, is among the latest brain regions to mature without reaching adult dimensions until the early 20s.❞
Source: Structural Magnetic Resonance Imaging of the Adolescent Brain
There are several things to note here:
- The above statement is talking about the physical size of the brain growing
- Nowhere does he say “and stops developing at 25”
However… The study only looked at brains up to the age of 25. After that, they stopped looking, because the study was about “the adolescent brain” so there has to be a cut-off somewhere, and that was the cut-off they chose.
This is the equivalent of saying “it didn’t stop raining until four o’clock” when the reality is that four o’clock is simply when you gave up on checking.
The study didn’t misrepresent this, by the way, but the popular press did!
Another 2012 study looked at various metrics of brain development, and found:
- Synapse overproduction into the teens
- Cortex pruning into the late 20s
- Prefrontal pruning into middle age at least (they stopped looking)
- Myelination beyond middle age (they stopped looking)
Source: Experience and the developing prefrontal cortex ← check out figure 1, and make sure you’re looking at the human data not the rat data
So how’s the most recent research looking?
Here’s a 2022 study that looked at 123,984 brain scans spanning the age range from mid-gestation to 100 postnatal years, and as you can see from its own figure 1… Most (if not all) brain-things keep growing for life, even though most slow down at some point, they don’t stop:
Brain charts for the human lifespan ← check out figure 1; don’t get too excited about the ventricular volume column as that is basically “brain that isn’t being a brain”. Do get excited about the rest, though!
Want to know how not to get caught out by science being misrepresented by the popular press? Check out:
How Science News Outlets Can Lie To You (Yes, Even If They Cite Studies!)
Take care!
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Eating Disorders: More Varied (And Prevalent) Than People Think
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Disordered Eating Beyond The Stereotypes
Around 10% of Americans* have (or have had) an eating disorder. That might not seem like a high percentage, but that’s one in ten; do you know 10 people? If so, it might be a topic that’s near to you.
*Source: Social and economic cost of eating disorders in the United States of Americ
Our hope is that even if you yourself have never had such a problem in your life, today’s article will help arm you with knowledge. You never know who in your life might need your support.
Very misunderstood
Eating disorders are so widely misunderstood in so many ways that we nearly made this a Friday Mythbusting edition—but we preface those with a poll that we hope to be at least somewhat polarizing or provide a spectrum of belief. In this case, meanwhile, there’s a whole cluster of myths that cannot be summed up in one question. So, here we are doing a Psychology Sunday edition instead.
“Eating disorders aren’t that important”
Eating disorders are the second most deadly category of mental illness, second only to opioid addiction.
Anorexia specifically has the highest case mortality rate of any mental illness:
Source: National Association of Anorexia Nervosa & Associated Disorders: Eating Disorder Statistics
So please, if someone needs help with an eating disorder (including if it’s you), help them.
“Eating disorders are for angsty rebellious teens”
While there’s often an element of “this is the one thing I can control” to some eating disorders (including anorexia and bulimia), eating disorders very often present in early middle-age, very often amongst busy career-driven individuals using it as a coping mechanism to have a feeling of control in their hectic lives.
13% of women over 50 report current core eating disorder symptoms, and that is probably underreported.
Source: as above; scroll to near the bottom!
“Eating disorders are a female thing”
Nope. Officially, men represent around 25% of people diagnosed with eating disorders, but women are 5x more likely to get diagnosed, so you can do the math there. Women are also 1.5% more likely to receive treatment for it.
By the time men do get diagnosed, they’ve often done a lot more damage to their bodies because they, as well as other people, have overlooked the possibility of their eating being disordered, due to the stereotype of it being a female thing.
Source: as above again!
“Eating disorders are about body image”
They can be, but that’s far from the only kind!
Some can be about control of diet, not just for the sake of controlling one’s body, but purely for the sake of controlling the diet itself.
Still yet others can be not about body image or control, like “Avoidant/Restrictive Food Intake Disorder”, which in lay terms sometimes gets dismissed as “being a picky eater” or simply “losing one’s appetite”, but can be serious.
For example, a common presentation of the latter might be a person who is racked with guilt and/or anxiety, and simply stops eating, because either they don’t feel they deserve it, or “how can I eat at a time like this, when…?” but the time is an ongoing thing so their impromptu fast is too.
Still yet even more others might be about trying to regulate emotions by (in essence) self-medicating with food—not in the healthy “so eat some fruit and veg and nuts etc” sense, but in the “Binge-Eating Disorder” sense.
And that latter accounts for a lot of adults.
You can read more about these things here:
Psychology Today | Types of Eating Disorder ← it’s pop-science, but it’s a good overview
Take care! And if you have, or think you might have, an eating disorder, know that there are organizations that can and will offer help/support in a non-judgmental fashion. Here’s the ANAD’s eating disorder help resource page, for example.
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Red Light, Go!
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Casting Yourself In A Healthier Light
In Tuesday’s newsletter, we asked you for your opinion of red light therapy (henceforth: RLT), and got the above-depicted, below-described, set of responses:
- About 51% said “I have no idea whether light therapy works or not”
- About 24% said “Red light therapy is a valuable skin rejuvenation therapy”
- About 23% said “I have not previously heard of red light therapy”
- One (1) person said: “Red light therapy is a scam to sell shiny gadgets”
A number of subscribers wrote with personal anecdotes of using red light therapy to beneficial effect, for example:
❝My husband used red light therapy after surgery on his hand. It did seem to speed healing of the incision and there is very minimal scarring. I would like to know if the red light really helped or if he was just lucky❞
~ 10almonds subscriber
And one wrote to report having observed mixed results amongst friends, per:
❝Some people it works, others I’ve seen it breaks them out❞
~ 10almonds subscriber
So, what does the science say?
RLT rejuvenates skin, insofar as it reduces wrinkles and fine lines: True or False?
True! This one’s pretty clear-cut, so we’ll just give one example study of many, which found:
❝The treated subjects experienced significantly improved skin complexion and skin feeling, profilometrically assessed skin roughness, and ultrasonographically measured collagen density.
The blinded clinical evaluation of photographs confirmed significant improvement in the intervention groups compared with the control❞
~ Dr. Alexander Wunsch & Dr. Karsten Matuschka
RLT helps speed up healing of wounds: True or False?
True! There is less science for this than the above claim, but the studies that have been done are quite compelling, for example this NASA technology study found that…
❝LED produced improvement of greater than 40% in musculoskeletal training injuries in Navy SEAL team members, and decreased wound healing time in crew members aboard a U.S. Naval submarine.❞
Read more: Effect of NASA light-emitting diode irradiation on wound healing
RLT’s benefits are only skin-deep: True or False?
False, probably, but we’d love to see more science for this, to be sure.
However, it does look like wavelengths in the near-infrared spectrum reduce the abnormal tau protein and neurofibrillary tangles associated with Alzheimer’s disease, resulting in increased blood flow to the brain, and a decrease in neuroinflammation:
Therapeutic Potential of Photobiomodulation In Alzheimer’s Disease: A Systematic Review
Would you like to try RLT for yourself?
There are some contraindications, for example:
- if you have photosensitivity (for obvious reasons)
- if you have Lupus (mostly because of the above)
- if you have hyperthyroidism (because if you use RLT to your neck as well as face, it may help stimulate thyroid function, which in your case is not what you want)
As ever, please check with your own doctor if you’re not completely sure; we can’t cover all bases here, and cannot speak for your individual circumstances.
For most people though, it’s very safe, and if you’d like to try it, here’s an example product on Amazon, and by all means do read reviews and shop around for the ideal device for you
Take care! 😎
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28-Day FAST Start Day-by-Day – by Gin Stephens
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We have previously reviewed Gin Stephens’ other book, “Fast. Feast. Repeat.”, so what’s so special about this one that it deserves reviewing too?
This one is all about troubleshooting the pitfalls that many people find when taking up intermittent fasting.
To be clear: the goal here is not a “28 days and yay you did it, put that behind you now”, but rather “28 days and you are now intermittently fasting easily each day and can keep it up without difficulty”. As for the difficulties that may arise early in the 28 days…
Not just issues of willpower, but also the accidental breaks. For example, some artificial sweeteners, while zero-calorie, trigger an insulin response, which breaks the fast on the metabolic level (avoiding that is the whole point of IF). Lots of little tips like that peppered through the book help the reader to stop accidentally self-sabotaging their progress.
The author does talk about psychological issues too, and also how it will feel different at first while the liver is adapting, than later when it has already depleted its glycogen reserves and the body must burn body fat instead. Information like that makes it easier to understand that some initial problems (hunger, getting “hangry”, feeling twitchy, or feeling light-headed) will last only a few weeks and then disappear.
So, understanding things like that makes a big difference too.
The style of the book is simple and clear pop-science, with lots of charts and bullet points and callout-boxes and the like; it makes for very easy reading, and very quick learning of all the salient points, of which there are many.
Bottom line: if you’ve tried intermittent fasting but struggled to make it stick, this book can help you get to where you want to be.
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Learn to Age Gracefully
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