The Metabolism Reset Diet – by Alan Christianson
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The liver is an incredible organ that does a very important job, but what’s not generally talked about is how we can help it… Beyond the obvious “try to not poison it too much with alcohol, tobacco, etc”. But what can we do that’s actually positive for it?
That’s what Alan Christianson offers in this book.
Now, usually when someone speaks of a “four week cleanse” as this book advertises on its front cover, it’s a lot of bunk. The liver cleanses itself, and the liver and kidneys between them (along with some other organs and processes) detoxify your body for you. No amount of celery juice will do that. However, this book does better than that:
What it’s about, is not really about trying to do a “detox” at all, so much as supporting your liver function by:
- Giving your liver what it needs to regenerate (mostly: protein)
- Not over-taxing your liver while it does so
The liver is a self-regenerating organ (the mythological story of Prometheus aside, here in real life it can regenerate up to 80% of itself, given the opportunity), so whatever the current state of your liver, it’s probably not too late to fix it.
Maybe you’ve been drinking a little too much, or maybe you’ve been taking some meds that have hobbled it a bit (some medications strain the liver rather), or maybe your diet hasn’t been great. Christianson invites you to draw a line under that, and move forwards:
The book gives an overview of the science involved, and explains about the liver’s role in metabolism (hence the promised weight loss benefits) and our dietary habits’ impact on liver function. This is about what we eat, and also about when we eat it, and how and when our body metabolizes that.
Christianson also provides meal ideas and recipes. If we’re honest (and we always are), the science/principles part of the book are worth a lot more than the meal-plan part of the book, though.
In short: a great book for understanding how the liver works and how we can help it do its job effectively.
Click here to check out “The Metabolism Reset Diet” on Amazon today!
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Oral retinoids can harm unborn babies. But many women taking them for acne may not be using contraception
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Oral retinoids are a type of medicine used to treat severe acne. They’re sold under the brand name Roaccutane, among others.
While oral retinoids are very effective, they can have harmful effects if taken during pregnancy. These medicines can cause miscarriages and major congenital abnormalities (harm to unborn babies) including in the brain, heart and face. At least 30% of children exposed to oral retinoids in pregnancy have severe congenital abnormalities.
Neurodevelopmental problems (in learning, reading, social skills, memory and attention) are also common.
Because of these risks, the Australasian College of Dermatologists advises oral retinoids should not be prescribed a month before or during pregnancy under any circumstances. Dermatologists are instructed to make sure a woman isn’t pregnant before starting this treatment, and discuss the risks with women of childbearing age.
But despite this, and warnings on the medicines’ packaging, pregnancies exposed to oral retinoids continue to be reported in Australia and around the world.
In a study published this month, we wanted to find out what proportion of Australian women of reproductive age were taking oral retinoids, and how many of these women were using contraception.
Our results suggest a high proportion of women are not using effective contraception while on these drugs, indicating Australia needs a strategy to reduce the risk oral retinoids pose to unborn babies.
Contraception options
Using birth control to avoid pregnancy during oral retinoid treatment is essential for women who are sexually active. Some contraception methods, however, are more reliable than others.
Long-acting-reversible contraceptives include intrauterine devices (IUDs) inserted into the womb (such as Mirena, Kyleena, or copper devices) and implants under the skin (such as Implanon). These “set and forget” methods are more than 99% effective.
The effectiveness of oral contraceptive pills among “perfect” users (following the directions, with no missed or late pills) is similarly more than 99%. But in typical users, this can fall as low as 91%.
Condoms, when used as the sole method of contraception, have higher failure rates. Their effectiveness can be as low as 82% in typical users.
Oral retinoid use over time
For our study, we analysed medicine dispensing data among women aged 15–44 from Australia’s Pharmaceutical Benefit Scheme (PBS) between 2013 and 2021.
We found the dispensing rate for oral retinoids doubled from one in every 71 women in 2013, to one in every 36 in 2021. The increase occurred across all ages but was most notable in young women.
Most women were not dispensed contraception at the same time they were using the oral retinoids. To be sure we weren’t missing any contraception that was supplied before the oral retinoids, we looked back in the data. For example, for an IUD that lasts five years, we looked back five years before the oral retinoid prescription.
Our analysis showed only one in four women provided oral retinoids were dispensed contraception simultaneously. This was even lower for 15- to 19-year-olds, where only about one in eight women who filled a prescription for oral retinoids were dispensed contraception.
A recent study found 43% of Australian year 10 and 69% of year 12 students are sexually active, so we can’t assume this younger age group largely had no need for contraception.
One limitation of our study is that it may underestimate contraception coverage, because not all contraceptive options are listed on the PBS. Those options not listed include male and female sterilisation, contraceptive rings, condoms, copper IUDs, and certain oral contraceptive pills.
But even if we presume some of the women in our study were using forms of contraception not listed on the PBS, we’re still left with a significant portion without evidence of contraception.
What are the solutions?
Other countries such as the United States and countries in Europe have pregnancy prevention programs for women taking oral retinoids. These programs include contraception requirements, risk acknowledgement forms and regular pregnancy tests. Despite these programs, unintended pregnancies among women using oral retinoids still occur in these countries.
But Australia has no official strategy for preventing pregnancies exposed to oral retinoids. Currently oral retinoids are prescribed by dermatologists, and most contraception is prescribed by GPs. Women therefore need to see two different doctors, which adds costs and burden.
Rather than a single fix, there are likely to be multiple solutions to this problem. Some dermatologists may not feel confident discussing sex or contraception with patients, so educating dermatologists about contraception is important. Education for women is equally important.
A clinical pathway is needed for reproductive-aged women to obtain both oral retinoids and effective contraception. Options may include GPs prescribing both medications, or dermatologists only prescribing oral retinoids when there’s a contraception plan already in place.
Some women may initially not be sexually active, but change their sexual behaviour while taking oral retinoids, so constant reminders and education are likely to be required.
Further, contraception access needs to be improved in Australia. Teenagers and young women in particular face barriers to accessing contraception, including costs, stigma and lack of knowledge.
Many doctors and women are doing the right thing. But every woman should have an effective contraception plan in place well before starting oral retinoids. Only if this happens can we reduce unintended pregnancies among women taking these medicines, and thereby reduce the risk of harm to unborn babies.
Dr Laura Gerhardy from NSW Health contributed to this article.
Antonia Shand, Research Fellow, Obstetrician, University of Sydney and Natasha Nassar, Professor of Paediatric and Perinatal Epidemiology and Chair in Translational Childhood Medicine, University of Sydney
This article is republished from The Conversation under a Creative Commons license. Read the original article.
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Quit Drinking – by Rebecca Dolton
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Many “quit drinking” books focus on tips you’ve heard already—cut down like this, rearrange your habits like that, make yourself accountable like so, add a reward element this way, etc.
Dolton takes a different approach.
She focuses instead on the underlying processes of addiction, so as to not merely understand them to fight them, but also to use them against the addiction itself.
This is not just a social or behavioral analysis, by the way, and goes into some detail into the physiological factors of the addiction—including such things as the little-talked about relationship between addiction and gut flora. Candida albans, found in most if not all humans to some extent, gets really out of control when given certain kinds of sugars (including those from alcohol); it grows, eventually puts roots through the intestinal walls (ouch!) and the more it grows, the more it demands the sugars it craves, so the more you feed it.
Quite a motivator to not listen to such cravings! It’s not even you that wants it, it’s the Candida!
Anyway, that’s just one example; there are many. The point here is that this is a well-researched, well-written book that sets itself apart from many of its genre.
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From straight to curly, thick to thin: here’s how hormones and chemotherapy can change your hair
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Head hair comes in many colours, shapes and sizes, and hairstyles are often an expression of personal style or cultural identity.
Many different genes determine our hair texture, thickness and colour. But some people’s hair changes around the time of puberty, pregnancy or after chemotherapy.
So, what can cause hair to become curlier, thicker, thinner or grey?
Curly or straight? How hair follicle shape plays a role
Hair is made of keratin, a strong and insoluble protein. Each hair strand grows from its own hair follicle that extends deep into the skin.
Curly hair forms due to asymmetry of both the hair follicle and the keratin in the hair.
Follicles that produce curly hair are asymmetrical and curved and lie at an angle to the surface of the skin. This kinks the hair as it first grows.
The asymmetry of the hair follicle also causes the keratin to bunch up on one side of the hair strand. This pulls parts of the hair strand closer together into a curl, which maintains the curl as the hair continues to grow.
Follicles that are symmetrical, round and perpendicular to the skin surface produce straight hair.
Life changes, hair changes
Our hair undergoes repeated cycles throughout life, with different stages of growth and loss.
Each hair follicle contains stem cells, which multiply and grow into a hair strand.
Head hairs spend most of their time in the growth phase, which can last for several years. This is why head hair can grow so long.
Let’s look at the life of a single hair strand. After the growth phase is a transitional phase of about two weeks, where the hair strand stops growing. This is followed by a resting phase where the hair remains in the follicle for a few months before it naturally falls out.
The hair follicle remains in the skin and the stems cells grow a new hair to repeat the cycle.
Each hair on the scalp is replaced every three to five years.
Hormone changes during and after pregnancy alter the usual hair cycle
Many women notice their hair is thicker during pregnancy.
During pregnancy, high levels of oestrogen, progesterone and prolactin prolong the resting phase of the hair cycle. This means the hair stays in the hair follicle for longer, with less hair loss.
A drop in hormones a few months after delivery causes increased hair loss. This is due to all the hairs that remained in the resting phase during pregnancy falling out in a fairly synchronised way.
Hair can change around puberty, pregnancy or after chemotherapy
This is related to the genetics of hair shape, which is an example of incomplete dominance.
Incomplete dominance is when there is a middle version of a trait. For hair, we have curly hair and straight hair genes. But when someone has one curly hair gene and one straight hair gene, they can have wavy hair.
Hormonal changes that occur around puberty and pregnancy can affect the function of genes. This can cause the curly hair gene of someone with wavy hair to become more active. This can change their hair from wavy to curly.
Researchers have identified that activating specific genes can change hair in pigs from straight to curly.
Chemotherapy has very visible effects on hair. Chemotherapy kills rapidly dividing cells, including hair follicles, which causes hair loss. Chemotherapy can also have genetic effects that influence hair follicle shape. This can cause hair to regrow with a different shape for the first few cycles of hair regrowth.
Hormonal changes as we age also affect our hair
Throughout life, thyroid hormones are essential for production of keratin. Low levels of thyroid hormones can cause dry and brittle hair.
Oestrogen and androgens also regulate hair growth and loss, particularly as we age.
Balding in males is due to higher levels of androgens. In particular, high dihydrotestosterone (sometimes shortened to DHT), which is produced in the body from testosterone, has a role in male pattern baldness.
Some women experience female pattern hair loss. This is caused by a combination of genetic factors plus lower levels of oestrogen and higher androgens after menopause. The hair follicles become smaller and smaller until they no longer produce hairs.
Reduced function of the cells that produce melanin (the pigment that gives our hair colour) is what causes greying.
Theresa Larkin, Associate professor of Medical Sciences, University of Wollongong
This article is republished from The Conversation under a Creative Commons license. Read the original article.
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Avocado vs Blueberries – Which is Healthier?
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Our Verdict
When comparing avocado to blueberries, we picked the avocado.
Why?
These two fruits aren’t as similar as some of the comparisons we’ve made—we often go for “can be used in the same way culinarily” comparisons. But! They are both popularly in the “superfood” category, so it’s interesting to consider:
In terms of macros, avocado has more protein, (healthy!) fat, and fiber, while blueberries have more carbs. An easy win for avocado here, unless you’re on a calorie-controlled diet perhaps, since avocado is also higher in those. About that fat; it’s mostly monounsaturated, with some polyunsaturated and saturated, and is famously a good source of omega-3 in the form of ALA.
In the category of vitamins, avocado has more of vitamins A, B1, B2, B3, B5, B6, B7, B9, C, E, K, and choline, while blueberries are not higher in any vitamins. So, not a tricky decision here.
When it comes to minerals, avocado has more calcium, copper, iron, magnesium, phosphorus, potassium, selenium, and zinc, while blueberries are higher in manganese. Another win for avocados.
There is one other category that’s important to consider in this case, and that’s polyphenols. We’d be here all day if we listed them all, but in total, blueberries have about 1193x the polyphenol content that avocados do. Blueberries got the reputation for antioxidant properties for a reason; it is well-deserved!
So, out of the two, we declare avocado the overall more nutritious of the two, but blueberries absolutely deserve the acclaim they get also.
Want to learn more?
You might like to read:
Give Us This Day Our Daily Dozen
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Cilantro vs Parsley – Which is Healthier?
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Our Verdict
When comparing cilantro to parsley, we picked the parsley.
Why?
Notwithstanding that some of our recipes include “cilantro, or if you have the this-tastes-like-soap gene, parsley”, that choice is more for the taste profile than the nutrition profile. Both are good, though, and it is quite close!
Like many herbs, they’re both full of vitamins and minerals and assorted phytochemicals.
In the category of vitamins, they’re both very good sources of vitamins A, C, and K, but parsley has more of each (and in vitamin K’s case, 4–5 times more). Parsley also has about twice as much folate. For the other vitamins, they’re mostly quite equal except that cilantro has more vitamin E.
When it comes to minerals, again they’re both good but again parsley is better on average, with several times more iron, and about twice as much calcium, zinc, and magnesium. Cilantro only wins noticeably for selenium.
Both have an array of anti-inflammatory phytochemicals, and each boasts antioxidants with anticancer potential.
Both have mood-improving qualities and have research for their anxiolytic and antidepressant effects—sufficient that these deserve their own main feature sometime.
For now though, we’ll say: healthwise, these two wonderful herbs are equal on most things, except that parsley has the better micronutrient profile.
Enjoy!
Further reading
You might also enjoy:
Herbs For (Evidence-Based) Health & Healing
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What pathogen might spark the next pandemic? How scientists are preparing for ‘disease X’
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Before the COVID pandemic, the World Health Organization (WHO) had made a list of priority infectious diseases. These were felt to pose a threat to international public health, but where research was still needed to improve their surveillance and diagnosis. In 2018, “disease X” was included, which signified that a pathogen previously not on our radar could cause a pandemic.
While it’s one thing to acknowledge the limits to our knowledge of the microbial soup we live in, more recent attention has focused on how we might systematically approach future pandemic risks.
Former US Secretary of Defense Donald Rumsfeld famously talked about “known knowns” (things we know we know), “known unknowns” (things we know we don’t know), and “unknown unknowns” (the things we don’t know we don’t know).
Although this may have been controversial in its original context of weapons of mass destruction, it provides a way to think about how we might approach future pandemic threats.
Influenza: a ‘known known’
Influenza is largely a known entity; we essentially have a minor pandemic every winter with small changes in the virus each year. But more major changes can also occur, resulting in spread through populations with little pre-existing immunity. We saw this most recently in 2009 with the swine flu pandemic.
However, there’s a lot we don’t understand about what drives influenza mutations, how these interact with population-level immunity, and how best to make predictions about transmission, severity and impact each year.
The current H5N1 subtype of avian influenza (“bird flu”) has spread widely around the world. It has led to the deaths of many millions of birds and spread to several mammalian species including cows in the United States and marine mammals in South America.
Human cases have been reported in people who have had close contact with infected animals, but fortunately there’s currently no sustained spread between people.
While detecting influenza in animals is a huge task in a large country such as Australia, there are systems in place to detect and respond to bird flu in wildlife and production animals.
It’s inevitable there will be more influenza pandemics in the future. But it isn’t always the one we are worried about.
Attention had been focused on avian influenza since 1997, when an outbreak in birds in Hong Kong caused severe disease in humans. But the subsequent pandemic in 2009 originated in pigs in central Mexico.
Coronaviruses: an ‘unknown known’
Although Rumsfeld didn’t talk about “unknown knowns”, coronaviruses would be appropriate for this category. We knew more about coronaviruses than most people might have thought before the COVID pandemic.
We’d had experience with severe acute respiratory syndrome (SARS) and Middle Eastern respiratory syndrome (MERS) causing large outbreaks. Both are caused by viruses closely related to SARS-CoV-2, the coronavirus that causes COVID. While these might have faded from public consciousness before COVID, coronaviruses were listed in the 2015 WHO list of diseases with pandemic potential.
Previous research into the earlier coronaviruses proved vital in allowing COVID vaccines to be developed rapidly. For example, the Oxford group’s initial work on a MERS vaccine was key to the development of AstraZeneca’s COVID vaccine.
Similarly, previous research into the structure of the spike protein – a protein on the surface of coronaviruses that allows it to attach to our cells – was helpful in developing mRNA vaccines for COVID.
It would seem likely there will be further coronavirus pandemics in the future. And even if they don’t occur at the scale of COVID, the impacts can be significant. For example, when MERS spread to South Korea in 2015, it only caused 186 cases over two months, but the cost of controlling it was estimated at US$8 billion (A$11.6 billion).
The 25 viral families: an approach to ‘known unknowns’
Attention has now turned to the known unknowns. There are about 120 viruses from 25 families that are known to cause human disease. Members of each viral family share common properties and our immune systems respond to them in similar ways.
An example is the flavivirus family, of which the best-known members are yellow fever virus and dengue fever virus. This family also includes several other important viruses, such as Zika virus (which can cause birth defects when pregnant women are infected) and West Nile virus (which causes encephalitis, or inflammation of the brain).
The WHO’s blueprint for epidemics aims to consider threats from different classes of viruses and bacteria. It looks at individual pathogens as examples from each category to expand our understanding systematically.
The US National Institute of Allergy and Infectious Diseases has taken this a step further, preparing vaccines and therapies for a list of prototype pathogens from key virus families. The goal is to be able to adapt this knowledge to new vaccines and treatments if a pandemic were to arise from a closely related virus.
Pathogen X, the ‘unknown unknown’
There are also the unknown unknowns, or “disease X” – an unknown pathogen with the potential to trigger a severe global epidemic. To prepare for this, we need to adopt new forms of surveillance specifically looking at where new pathogens could emerge.
In recent years, there’s been an increasing recognition that we need to take a broader view of health beyond only thinking about human health, but also animals and the environment. This concept is known as “One Health” and considers issues such as climate change, intensive agricultural practices, trade in exotic animals, increased human encroachment into wildlife habitats, changing international travel, and urbanisation.
This has implications not only for where to look for new infectious diseases, but also how we can reduce the risk of “spillover” from animals to humans. This might include targeted testing of animals and people who work closely with animals. Currently, testing is mainly directed towards known viruses, but new technologies can look for as yet unknown viruses in patients with symptoms consistent with new infections.
We live in a vast world of potential microbiological threats. While influenza and coronaviruses have a track record of causing past pandemics, a longer list of new pathogens could still cause outbreaks with significant consequences.
Continued surveillance for new pathogens, improving our understanding of important virus families, and developing policies to reduce the risk of spillover will all be important for reducing the risk of future pandemics.
This article is part of a series on the next pandemic.
Allen Cheng, Professor of Infectious Diseases, Monash University
This article is republished from The Conversation under a Creative Commons license. Read the original article.
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