Built to Move – by Kelly starrett & Juliet Starrett
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In our everyday lives, for most of us anyway, it’s not too important to be able to run a marathon or leg-press a car. Rather more important, however, are such things as:
- being able to get up from the floor comfortably
- reach something on a high shelf without twinging a shoulder
- being able to put our socks on without making a whole plan around this task
- get accidentally knocked by an energetic dog or child and not put our back out
- etc
Starrett and Starrett, of “becoming a supple leopard” fame, lay out for us how to make sure our mobility stays great. And, if it’s not already where it needs to be, how to get there.
The “ten essential habits” mentioned in the subtitle “ten essential habits to help you move freely and live fully”, in fact also come with ten tests. No, not in the sense of arduous trials, but rather, mobility tests.
For each test, it’s explained to us how to score it out of ten (this is an objective assessment, not subjective). It’s then explained how to “level up” whatever score we got, with different advices for different levels of mobility or immobility. And if we got a ten, then of course, we just build the appropriate recommended habit into our daily life, to keep it that way.
The writing style is casual throughout, and a strong point of the book is its very clear illustrations, too.
Bottom line: if you’d like to gain/maintain good mobility (at any age), this book gives a very reliable outline for doing so.
Click here to check out Built to Move, and take care of your body!
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If I’m diagnosed with one cancer, am I likely to get another?
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Receiving a cancer diagnosis is life-changing and can cause a range of concerns about ongoing health.
Fear of cancer returning is one of the top health concerns. And managing this fear is an important part of cancer treatment.
But how likely is it to get cancer for a second time?
Why can cancer return?
While initial cancer treatment may seem successful, sometimes a few cancer cells remain dormant. Over time, these cancer cells can grow again and may start to cause symptoms.
This is known as cancer recurrence: when a cancer returns after a period of remission. This period could be days, months or even years. The new cancer is the same type as the original cancer, but can sometimes grow in a new location through a process called metastasis.
Actor Hugh Jackman has gone public about his multiple diagnoses of basal cell carcinoma (a type of skin cancer) over the past decade.
The exact reason why cancer returns differs depending on the cancer type and the treatment received. Research is ongoing to identify genes associated with cancers returning. This may eventually allow doctors to tailor treatments for high-risk people.
What are the chances of cancer returning?
The risk of cancer returning differs between cancers, and between sub-types of the same cancer.
New screening and treatment options have seen reductions in recurrence rates for many types of cancer. For example, between 2004 and 2019, the risk of colon cancer recurring dropped by 31-68%. It is important to remember that only someone’s treatment team can assess an individual’s personal risk of cancer returning.
For most types of cancer, the highest risk of cancer returning is within the first three years after entering remission. This is because any leftover cancer cells not killed by treatment are likely to start growing again sooner rather than later. Three years after entering remission, recurrence rates for most cancers decrease, meaning that every day that passes lowers the risk of the cancer returning.
Every day that passes also increases the numbers of new discoveries, and cancer drugs being developed.
What about second, unrelated cancers?
Earlier this year, we learned Sarah Ferguson, Duchess of York, had been diagnosed with malignant melanoma (a type of skin cancer) shortly after being treated for breast cancer.
Although details have not been confirmed, this is likely a new cancer that isn’t a recurrence or metastasis of the first one.
Australian research from Queensland and Tasmania shows adults who have had cancer have around a 6-36% higher risk of developing a second primary cancer compared to the risk of cancer in the general population.
Who’s at risk of another, unrelated cancer?
With improvements in cancer diagnosis and treatment, people diagnosed with cancer are living longer than ever. This means they need to consider their long-term health, including their risk of developing another unrelated cancer.
Reasons for such cancers include different types of cancers sharing the same kind of lifestyle, environmental and genetic risk factors.
The increased risk is also likely partly due to the effects that some cancer treatments and imaging procedures have on the body. However, this increased risk is relatively small when compared with the (sometimes lifesaving) benefits of these treatment and procedures.
While a 6-36% greater chance of getting a second, unrelated cancer may seem large, only around 10-12% of participants developed a second cancer in the Australian studies we mentioned. Both had a median follow-up time of around five years.
Similarly, in a large US study only about one in 12 adult cancer patients developed a second type of cancer in the follow-up period (an average of seven years).
The kind of first cancer you had also affects your risk of a second, unrelated cancer, as well as the type of second cancer you are at risk of. For example, in the two Australian studies we mentioned, the risk of a second cancer was greater for people with an initial diagnosis of head and neck cancer, or a haematological (blood) cancer.
People diagnosed with cancer as a child, adolescent or young adult also have a greater risk of a second, unrelated cancer.
What can I do to lower my risk?
Regular follow-up examinations can give peace of mind, and ensure any subsequent cancer is caught early, when there’s the best chance of successful treatment.
Maintenance therapy may be used to reduce the risk of some types of cancer returning. However, despite ongoing research, there are no specific treatments against cancer recurrence or developing a second, unrelated cancer.
But there are things you can do to help lower your general risk of cancer – not smoking, being physically active, eating well, maintaining a healthy body weight, limiting alcohol intake and being sun safe. These all reduce the chance of cancer returning and getting a second cancer.
Sarah Diepstraten, Senior Research Officer, Blood Cells and Blood Cancer Division, Walter and Eliza Hall Institute and Terry Boyle, Senior Lecturer in Cancer Epidemiology, University of South Australia
This article is republished from The Conversation under a Creative Commons license. Read the original article.
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Is alcohol good or bad for you? Yes.
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This article originally appeared in Harvard Public Health magazine.
It’s hard to escape the message these days that every sip of wine, every swig of beer is bad for your health. The truth, however, is far more nuanced.
We have been researching the health effects of alcohol for a combined 60 years. Our work, and that of others, has shown that even modest alcohol consumption likely raises the risk for certain diseases, such as breast and esophageal cancer. And heavy drinking is unequivocally harmful to health. But after countless studies, the data do not justify sweeping statements about the effects of moderate alcohol consumption on human health.
Yet we continue to see reductive narratives, in the media and even in science journals, that alcohol in any amount is dangerous. Earlier this month, for instance, the media reported on a new study that found even small amounts of alcohol might be harmful. But the stories failed to give enough context or probe deeply enough to understand the study’s limitations—including that it cherry-picked subgroups of a larger study previously used by researchers, including one of us, who concluded that limited drinking in a recommended pattern correlated with lower mortality risk.
“We need more high-quality evidence to assess the health impacts of moderate alcohol consumption. And we need the media to treat the subject with the nuance it requires. Newer studies are not necessarily better than older research.”
Those who try to correct this simplistic view are disparaged as pawns of the industry, even when no financial conflicts of interest exist. Meanwhile, some authors of studies suggesting alcohol is unhealthy have received money from anti-alcohol organizations.
We believe it’s worth trying, again, to set the record straight. We need more high-quality evidence to assess the health impacts of moderate alcohol consumption. And we need the media to treat the subject with the nuance it requires. Newer studies are not necessarily better than older research.
It’s important to keep in mind that alcohol affects many body systems—not just the liver and the brain, as many people imagine. That means how alcohol affects health is not a single question but the sum of many individual questions: How does it affect the heart? The immune system? The gut? The bones?
As an example, a highly cited study of one million women in the United Kingdom found that moderate alcohol consumption—calculated as no more than one drink a day for a woman—increased overall cancer rates. That was an important finding. But the increase was driven nearly entirely by breast cancer. The same study showed that greater alcohol consumption was associated with lower rates of thyroid cancer, non-Hodgkin lymphoma, and renal cell carcinoma. That doesn’t mean drinking a lot of alcohol is good for you—but it does suggest that the science around alcohol and health is complex.
One major challenge in this field is the lack of large, long-term, high-quality studies. Moderate alcohol consumption has been studied in dozens of randomized controlled trials, but those trials have never tracked more than about 200 people for more than two years. Longer and larger experimental trials have been used to test full diets, like the Mediterranean diet, and are routinely conducted to test new pharmaceuticals (or new uses for existing medications), but they’ve never been done to analyze alcohol consumption.
Instead, much alcohol research is observational, meaning it follows large groups of drinkers and abstainers over time. But observational studies cannot prove cause-and-effect because moderate drinkers differ in many ways from non-drinkers and heavy drinkers—in diet, exercise, and smoking habits, for instance. Observational studies can still yield useful information, but they also require researchers to gather data about when and how the alcohol is consumed, since alcohol’s effect on health depends heavily on drinking patterns.
For example, in an analysis of over 300,000 drinkers in the U.K., one of us found that the same total amount of alcohol appeared to increase the chances of dying prematurely if consumed on fewer occasions during the week and outside of meals, but to decrease mortality if spaced out across the week and consumed with meals. Such nuance is rarely captured in broader conversations about alcohol research—or even in observational studies, as researchers don’t always ask about drinking patterns, focusing instead on total consumption. To get a clearer picture of the health effects of alcohol, researchers and journalists must be far more attuned to the nuances of this highly complex issue.
One way to improve our collective understanding of the issue is to look at both observational and experimental data together whenever possible. When the data from both types of studies point in the same direction, we can have more confidence in the conclusion. For example, randomized controlled trials show that alcohol consumption raises levels of sex steroid hormones in the blood. Observational trials suggest that alcohol consumption also raises the risk of specific subtypes of breast cancer that respond to these hormones. Together, that evidence is highly persuasive that alcohol increases the chances of breast cancer.
Similarly, in randomized trials, alcohol consumption lowers average blood sugar levels. In observational trials, it also appears to lower the risk of diabetes. Again, that evidence is persuasive in combination.
As these examples illustrate, drinking alcohol may raise the risk of some conditions but not others. What does that mean for individuals? Patients should work with their clinicians to understand their personal risks and make informed decisions about drinking.
Medicine and public health would benefit greatly if better data were available to offer more conclusive guidance about alcohol. But that would require a major investment. Large, long-term, gold-standard studies are expensive. To date, federal agencies like the National Institutes of Health have shown no interest in exclusively funding these studies on alcohol.
Alcohol manufacturers have previously expressed some willingness to finance the studies—similar to the way pharmaceutical companies finance most drug testing—but that has often led to criticism. This happened to us, even though external experts found our proposal scientifically sound. In 2018, the National Institutes of Health ended our trial to study the health effects of alcohol. The NIH found that officials at one of its institutes had solicited funding from alcohol manufacturers, violating federal policy.
It’s tempting to assume that because heavy alcohol consumption is very bad, lesser amounts must be at least a little bad. But the science isn’t there, in part because critics of the alcohol industry have deliberately engineered a state of ignorance. They have preemptively discredited any research, even indirectly, by the alcohol industry—even though medicine relies on industry financing to support the large, gold-standard studies that provide conclusive data about drugs and devices that hundreds of millions of Americans take or use daily.
Scientific evidence about drinking alcohol goes back nearly 100 years—and includes plenty of variability in alcohol’s health effects. In the 1980s and 1990s, for instance, alcohol in moderation, and especially red wine, was touted as healthful. Now the pendulum has swung so far in the opposite direction that contemporary narratives suggest every ounce of alcohol is dangerous. Until gold-standard experiments are performed, we won’t truly know. In the meantime, we must acknowledge the complexity of existing evidence—and take care not to reduce it to a single, misleading conclusion.
This article first appeared on The Journalist’s Resource and is republished here under a Creative Commons license.
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Do You Know Which Supplements You Shouldn’t Take Together? (10 Pairs!)
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Dr. LeGrand Peterson wants us to get the most out of our supplements, so watch out for these…
Time to split up some pairs…
In most cases these are a matter of competing for absorption; sometimes to the detriment of both, sometimes to the detriment of one or the other, and sometimes, the problem is entirely different and they just interact in a way that could potentially cause other problems. Dr. Peterson advises as follows:
- Vitamin C and vitamin B12: taking these together can reduce the absorption of Vitamin B12, as vitamin C can overpower it.
- Vitamin C and copper: high amounts of vitamin C can decrease copper absorption, especially in those who are severely copper deficient.
- Magnesium and calcium: these two minerals compete for absorption in the intestines, potentially reducing the effectiveness of both.
- Calcium and iron: calcium can decrease iron absorption, so they should not be taken together, especially if you are iron deficient.
- Calcium and zinc: calcium also competes with zinc, reducing zinc absorption; they should be taken at different times.
- Zinc and copper: zinc and copper compete for absorption, so they should be taken at separate times.
- Iron and zinc: iron can decrease zinc absorption, and thus, they should not be taken together.
- Iron and green tea: perhaps a surprising one, but green tea can reduce iron absorption, so they should not be taken simultaneously.
- Vitamin E and vitamin K: vitamin E increases bleeding risk, while vitamin K promotes clotting, making them opposites and risky to take together.
- Fish oil and ginkgo biloba: both are anticoagulants and can increase the risk of bleeding, especially if taken with blood thinners like warfarin.
If you need to take supplements that compete (or conflict or otherwise potentially adversely interact) with each other, it’s recommended to separate them by at least 4 hours, or better yet, take one in the morning and the other at night. If in doubt, do speak with your pharmacist or doctor for personalized advice
You may be thinking: half my foods contain half of these nutrients! And yes, assuming you have a nutritionally dense diet, this is probably the case. Foods typically release nutrients more slowly than supplements, and unlike supplements, do not usually contain megadoses (although they can, such as the selenium content of Brazil nuts, or vitamin A in carrots). Basically, food is in most cases safer and gentler than supplements. If concerned, do speak with your nutritionist or doctor for personalized advice.
For more information on all of these, enjoy:
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Want to learn more?
You might also like to read:
Do We Need Supplements, And Do They Work?
Take care!
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What Grief Does To Your Body (And How To Manage It)
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What Grief Does To The Body (And How To Manage It)
In life, we will almost all lose loved ones and suffer bereavement. For most people, this starts with grandparents, eventually moves to parents, and then people our own generation; partners, siblings, close friends. And of course, sometimes and perhaps most devastatingly, we can lose people younger than ourselves.
For something that almost everyone suffers, there is often very little in the way of preparation given beforehand, and afterwards, a condolences card is nice but can’t do a lot for our mental health.
And with mental health, our physical health can go too, if we very understandably neglect it at such a time.
So, how to survive devastating loss, and come out the other side, hopefully thriving? It seems like a tall order indeed.
First, the foundations:
You’re probably familiar with the stages of grief. In their most commonly-presented form, they are:
- Denial
- Anger
- Bargaining
- Depression
- Acceptance
You’ve probably also heard/read that we won’t always go through them in order, and also that grief is deeply personal and proceeds on its own timescale.
It is generally considered healthy to go through them.
What do they look like?
Naturally this can vary a lot from person to person, but examples in the case of bereavement could be:
- Denial: “This surely has not really happened; I’ll carry on as though it hasn’t”
- Anger: “Why didn’t I do xyz differently while I had the chance?!”
- Bargaining: “I will do such-and-such in their honor, and this will be a way of expressing the love I wish I could give them in a way they could receive”
- Depression: “What is the point of me without them? The sooner I join them, the better.”
- Acceptance: “I was so lucky that we had the time together that we did, and enriched each other’s lives while we could”
We can speedrun these or we can get stuck on one for years. We can bounce back and forth. We can think we’re at acceptance, and then a previous stage will hit us like a tonne of bricks.
What if we don’t?
Assuming that our lost loved one was indeed a loved one (as opposed to someone we are merely societally expected to mourn), then failing to process that grief will tend to have a big impact on our life—and health. These health problems can include:
As you can see, three out of five of those can result in death. The other two aren’t great either. So why isn’t this taken more seriously as a matter of health?
Death is, ironically, considered something we “just have to live with”.
But how?
Coping strategies
You’ll note that most of the stages of grief are not enjoyable per se. For this reason, it’s common to try to avoid them—hence denial usually being first.
But, that is like not getting a lump checked out because you don’t want a cancer diagnosis. The emotional reasoning is understandable, but it’s ultimately self-destructive.
First, have a plan. If a death is foreseen, you can even work out this plan together.
But even if that time has now passed, it’s “better late than never” to make a plan for looking after yourself, e.g:
- How you will try to get enough sleep (tricky, but sincerely try)
- How you will remember to eat (and ideally, healthily)
- How you will still get exercise (a walk in the park is fine; see some greenery and get some sunlight)
- How you will avoid self-destructive urges (from indirect, e.g. drinking, to direct, e.g. suicidality)
- How you will keep up with the other things important in your life (work, friends, family)
- How you will actively work to process your grief (e.g. journaling, or perhaps grief counselling)
Some previous articles of ours that may help:
- How To Keep On Keeping On ← this is about looking after general health when motivation is low
- The Mental Health First-Aid You’ll Hopefully Never Need ← this is about managing depression
- How To Stay Alive (When You Really Don’t Want To) ← this is about managing suicidality
If it works, it works
If we are all unique, then any relationship between any two people is uniqueness squared. Little wonder, then, that our grief may be unique too. And it can be complicated further:
- Sometimes we had a complicated relationship with someone
- Sometimes the circumstances of their death were complicated
There is, for that matter, such a thing as “complicated grief”:
Read more: Complicated grief and prolonged grief disorder (Medical News Today)
We also previously reviewed a book on “ambiguous loss”, exploring grieving when we cannot grieve in the normal way because someone is gone and/but/maybe not gone.
For example, if someone is in a long-term coma from which they may never recover, or if they are missing-presumed-dead. Those kinds of situations are complicated too.
Unusual circumstances may call for unusual coping strategies, so how can we discern what is healthy and what isn’t?
The litmus test is: is it enabling you to continue going about your life in a way that allows you to fulfil your internal personal aspirations and external social responsibilities? If so, it’s probably healthy.
Look after yourself. And if you can, tell your loved ones you love them today.
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Ozempic’s cousin drug liraglutide is about to get cheaper. But how does it stack up?
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Fourteen years ago, the older drug cousin of semaglutide (Ozempic and Wegovy) came onto the market. The drug, liraglutide, is sold under the brand names Victoza and Saxenda.
Patents for Victoza and Saxenda have now expried. So other drug companies are working to develop “generic” versions. These are likely be a fraction of current cost, which is around A$400 a month.
So how does liraglutide compare with semaglutide?
Halfpoint/Shutterstock How do these drugs work?
Liraglutide was not originally developed as a weight-loss treatment. Like semaglutide (Ozempic), it originally treated type 2 diabetes.
The class of drugs liraglutide and semaglutide belong to are known as GLP-1 mimetics, meaning they mimic the natural hormone GLP-1. This hormone is released from your small intestines in response to food and acts in several ways to improve the way your body handles glucose (sugar).
How do they stop hunger?
Liraglutide acts in several regions of the unconscious part of your brain, specifically the hypothalamus, which controls metabolism, and parts of the brain stem responsible for communicating your body’s nutrient status to the hypothalamus.
Its actions here appear to reduce hunger in two different ways. First, it helps you to feel full earlier, making smaller meals more satisfying. Second, it alters your “motivational salience” towards food, meaning it reduces the amount of food you seek out.
Liraglutide’s original formulation, designed to treat type 2 diabetes, was marketed as Victoza. Its ability to cause weight loss was evident soon after it entered the market.
Shortly after, a stronger formulation, called Saxenda, was released, which was intended for weight loss in people with obesity.
How much weight can you lose with liraglutide?
People respond differently and will lose different amounts of weight. But here, we’ll note the average weight loss users can expect. Some will lose more (sometimes much more), others will lose less, and a small proportion won’t respond.
The first GLP-1 mimicking drug was exenatide (Bayetta). It’s still available for treating type 2 diabetes, but there are currently no generics. Exenatide does provide some weight loss, but this is quite modest, typically around 3-5% of body weight.
For liraglutide, those using the drug to treat obesity will use the stronger one (Saxenda), which typically gives about 10% weight loss.
Semaglutide, with the stronger formulation called Wegovy, typically results in 15% weight loss.
The newest GLP-1 mimicking drug on the market, tirzepatide (Mounjaro for type 2 diabetes and Zepbound for weight loss), results in weight loss of around 25% of body weight.
What happens when you stop taking them?
Despite the effectiveness of these medications in helping with weight loss, they do not appear to change people’s weight set-point.
So in many cases, when people stop taking them, they experience a rebound toward their original weight.
People often regain weight when when they stop taking the drug. Mohammed_Al_Ali/Shutterstock What is the dose and how often do you need to take it?
Liraglutide (Victoza) for type 2 diabetes is exactly the same drug as Saxenda for weight loss, but Saxenda is a higher dose.
Although the target for each formulation is the same (the GLP-1 receptor), for glucose control in type 2 diabetes, liraglutide has to (mainly) reach the pancreas.
But to achieve weight loss, it has to reach parts of the brain. This means crossing the blood-brain barrier – and not all of it makes it, meaning more has to be taken.
All the current formulations of GLP-1 mimicking drug are injectables. This won’t change when liraglutide generics hit the market.
However, they differ in how frequently they need to be injected. Liraglutide is a once-daily injection, whereas semaglutide and tirzepatide are once-weekly. (That makes semaglutide and tirzepatide much more attractive, but we won’t see semaglutide as a generic until 2033.)
What are the side effects?
Because all these medicines have the same target in the body, they mostly have the same side effects.
The most common are a range of gastrointestinal upsets including nausea, vomiting, bloating, constipation and diarrhoea. These occur, in part, because these medications slow the movement of food out of the stomach, but are generally managed by increasing the dose slowly.
Recent clinical data suggests the slowing in emptying of the stomach can be problematic for some people, and may increase the risk of of food entering the lungs during operations, so it is important to let your doctor know if you are taking any of these drugs.
Because these are injectables, they can also lead to injection-site reactions.
Gastrointestinal side effects are most common. Halfpoint/Shutterstock During clinical trials, there were some reports of thyroid disease and pancreatitis (inflammation of the pancreas). However, it is not clear that these can be attributed to GLP-1 mimicking drugs.
In animals, GLP-1 mimicking drugs drugs have been found to negatively alter the growth of the embryo. There is currently no controlled clinical trial data on their use during pregnancy, but based on animal data, these medicines should not be used during pregnancy.
Who can use them?
The GLP-1 mimicking drugs for weight loss (Wegovy, Saxenda, Zepbound/Mounjaro) are approved for use by people with obesity and are meant to only be used in conjunction with diet and exercise.
These drugs must be prescribed by a doctor and for obesity are not covered by the Pharmaceutical Benefits Scheme, which is one of the reasons why they are expensive. But in time, generic versions of liraglutide are likely to be more affordable.
Sebastian Furness, ARC Future Fellow, School of Biomedical Sciences, The University of Queensland
This article is republished from The Conversation under a Creative Commons license. Read the original article.
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What’s the difference between vegan and vegetarian?
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What’s the difference? is a new editorial product that explains the similarities and differences between commonly confused health and medical terms, and why they matter.
Vegan and vegetarian diets are plant-based diets. Both include plant foods, such as fruits, vegetables, legumes and whole grains.
But there are important differences, and knowing what you can and can’t eat when it comes to a vegan and vegetarian diet can be confusing.
So, what’s the main difference?
Creative Cat Studio/Shutterstock What’s a vegan diet?
A vegan diet is an entirely plant-based diet. It doesn’t include any meat and animal products. So, no meat, poultry, fish, seafood, eggs, dairy or honey.
What’s a vegetarian diet?
A vegetarian diet is a plant-based diet that generally excludes meat, poultry, fish and seafood, but can include animal products. So, unlike a vegan diet, a vegetarian diet can include eggs, dairy and honey.
But you may be wondering why you’ve heard of vegetarians who eat fish, vegetarians who don’t eat eggs, vegetarians who don’t eat dairy, and even vegetarians who eat some meat. Well, it’s because there are variations on a vegetarian diet:
- a lacto-ovo vegetarian diet excludes meat, poultry, fish and seafood, but includes eggs, dairy and honey
- an ovo-vegetarian diet excludes meat, poultry, fish, seafood and dairy, but includes eggs and honey
- a lacto-vegetarian diet excludes meat, poultry, fish, seafood and eggs, but includes dairy and honey
- a pescatarian diet excludes meat and poultry, but includes eggs, dairy, honey, fish and seafood
- a flexitarian, or semi-vegetarian diet, includes eggs, dairy and honey and may include small amounts of meat, poultry, fish and seafood.
Are these diets healthy?
A 2023 review looked at the health effects of vegetarian and vegan diets from two types of study.
Observational studies followed people over the years to see how their diets were linked to their health. In these studies, eating a vegetarian diet was associated with a lower risk of developing cardiovascular disease (such as heart disease or a stroke), diabetes, hypertension (high blood pressure), dementia and cancer.
For example, in a study of 44,561 participants, the risk of heart disease was 32% lower in vegetarians than non-vegetarians after an average follow-up of nearly 12 years.
Further evidence came from randomised controlled trials. These instruct study participants to eat a specific diet for a specific period of time and monitor their health throughout. These studies showed eating a vegetarian or vegan diet led to reductions in weight, blood pressure, and levels of unhealthy cholesterol.
For example, one analysis combined data from seven randomised controlled trials. This so-called meta-analysis included data from 311 participants. It showed eating a vegetarian diet was associated with a systolic blood pressure (the first number in your blood pressure reading) an average 5 mmHg lower compared with non-vegetarian diets.
It seems vegetarian diets are more likely to be healthier, across a number of measures.
For example, a 2022 meta-analysis combined the results of several observational studies. It concluded a vegetarian diet, rather than vegan diet, was recommended to prevent heart disease.
There is also evidence vegans are more likely to have bone fractures than vegetarians. This could be partly due to a lower body-mass index and a lower intake of nutrients such as calcium, vitamin D and protein.
But it can be about more than just food
Many vegans, where possible, do not use products that directly or indirectly involve using animals.
So vegans would not wear leather, wool or silk clothing, for example. And they would not use soaps or candles made from beeswax, or use products tested on animals.
The motivation for following a vegan or vegetarian diet can vary from person to person. Common motivations include health, environmental, ethical, religious or economic reasons.
And for many people who follow a vegan or vegetarian diet, this forms a central part of their identity.
More than a diet: veganism can form part of someone’s identity. Shutterstock So, should I adopt a vegan or vegetarian diet?
If you are thinking about a vegan or vegetarian diet, here are some things to consider:
- eating more plant foods does not automatically mean you are eating a healthier diet. Hot chips, biscuits and soft drinks can all be vegan or vegetarian foods. And many plant-based alternatives, such as plant-based sausages, can be high in added salt
- meeting the nutrient intake targets for vitamin B12, iron, calcium, and iodine requires more careful planning while on a vegan or vegetarian diet. This is because meat, seafood and animal products are good sources of these vitamins and minerals
- eating a plant-based diet doesn’t necessarily mean excluding all meat and animal products. A healthy flexitarian diet prioritises eating more whole plant-foods, such as vegetables and beans, and less processed meat, such as bacon and sausages
- the Australian Dietary Guidelines recommend eating a wide variety of foods from the five food groups (fruit, vegetables, cereals, lean meat and/or their alternatives and reduced-fat dairy products and/or their alternatives). So if you are eating animal products, choose lean, reduced-fat meats and dairy products and limit processed meats.
Katherine Livingstone, NHMRC Emerging Leadership Fellow and Senior Research Fellow at the Institute for Physical Activity and Nutrition, Deakin University
This article is republished from The Conversation under a Creative Commons license. Read the original article.
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