What you need to know about the new weight loss drug Zepbound
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In a recent poll, KFF found that nearly half of U.S. adults were interested in taking a weight management drug like the increasingly popular Ozempic, Wegovy, and Mounjaro.
“I can understand why there would be widespread interest in these medications,” says Dr. Alyssa Lampe Dominguez, an endocrinologist and clinical assistant professor at the University of Southern California. “Obesity is a chronic disease that is very difficult to treat. And a lot of the medications that we previously used weren’t as effective.”
Now, there’s a new option available: In November 2023, the FDA approved Zepbound, another weight management medication, developed by the pharmaceutical company Eli Lilly. Zepbound is different from other drugs in many ways, including the fact that it’s proven to be the most effective option so far.
Keep reading to find out more about Zepbound, including who can take it, its side effects, and more.
What is Zepbound?
Zepbound, one of the brand names for tirzepatide, is an injectable drug with a maximum dosage of 15 mg per week. It’s based on incretin, a hormone that’s naturally released in the gut after a meal. (Mounjaro is another brand name for tirzepatide.)
Tirzepatide is considered a dual agonist because it activates the two primary incretin hormones: the glucagon-like peptide-1 (GLP-1) and gastric inhibitory peptide (GIP) hormones.
According to Dr. Katherine H. Saunders, an obesity medicine physician at Weill Cornell Medicine and co-founder of Intellihealth, tirzepatide is involved with several processes that regulate blood sugar, slow the removal of food from the stomach, and affect brain areas involved in appetite.
This means that people taking the medication feel less hungry and get fuller faster, leading to less food intake and, ultimately, weight loss.
How is Zepbound different from Ozempic?
The medications are different in many ways. Ozempic and Wegovy, which are both brand names for semaglutide, only target the GLP-1 hormone. Studies have shown that Zepbound can lead to a higher percentage of total body weight loss than semaglutide medications. In addition to being more effective, there is some evidence that Zepbound is overall more tolerable than Ozempic or Wegovy.
“I have seen overall lower rates in severity of side effects with the tirzepatide medications. Mounjaro [tirzepatide] in particular is the one that I’ve used up until this point, but there’s a thought that the GIP component of the medication actually decreases nausea,” adds Lampe Dominguez. “Anecdotally, patients that I have switched from semaglutide or Ozempic to Mounjaro say that they have less side effects with Mounjaro.”
How is Zepbound different from Mounjaro?
Zepbound and Mounjaro are the same medication—tirzepatide—but they’re approved for different conditions. Zepbound is FDA-approved for weight loss, while Mounjaro is approved for type 2 diabetes. (However, Mounjaro is also at times prescribed off-label for weight loss.)
What are some of Zepbound’s side effects?
According to the FDA, side effects include nausea, vomiting, diarrhea, constipation, stomach discomfort and pain, fatigue, and burping. See a more comprehensive list of side effects here.
Who can take Zepbound?
Zepbound is FDA-approved for adults with obesity (a BMI of 30 or greater) or who have a BMI of 27 or greater with at least one weight-related condition, like high blood pressure, type 2 diabetes, or high cholesterol.
“I tend to advise patients who don’t meet those criteria to not take these medications because we really don’t know what the risks are,” says Lampe Dominguez, adding that people with lower BMI weren’t included in the medication’s studies. “We don’t know if there are specific risks to using this medication at a lower body mass index [or] if there might be some negative outcomes.”
Both doctors agree that it’s important for people who are interested in starting any weight loss medication to talk to their doctors about the potential risks and benefits. For instance, the FDA notes that Zepbound has caused thyroid tumors in rats, and while it’s unknown if this could also happen to humans, the agency said the medication shouldn’t be used in patients with a personal or family history of medullary thyroid cancer.
“Zepbound is a powerful medication that can lead to severe side effects, vitamin deficiencies, a complete lack of appetite, or too much weight loss if prescribed without the appropriate personalization, education, and close monitoring,” says Saunders.
“With all of these medications, and particularly with Zepbound, we would want to make sure that [patients] don’t have a family history of a specific type of thyroid cancer called medullary thyroid cancer,” says Lampe Dominguez.
How long should people take Zepbound for?
“Anti-obesity medications like Zepbound are not meant for short-term weight loss, but long-term treatment of obesity, which is a chronic disease,” explains Saunders. “We prepare our patients to be on the medication (or some type of medical obesity treatment) long term for their chronic disease, which is only controlled for the duration of time they’re being treated.”
For more information, talk to your health care provider.
This article first appeared on Public Good News and is republished here under a Creative Commons license.
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Relationships: When To Stick It Out & When To Call It Quits
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Like A Ship Loves An Anchor?
Today’s article may seem a little bit of a downer to start with, but don’t worry, it picks up again too. Simply put, we’ve written before about many of the good parts of relationships, e.g:
Only One Kind Of Relationship Promotes Longevity This Much!
…but what if that’s not what we have?
Note: if you have a very happy, secure, fulfilling, joyous relationship, then, great! Or if you’re single and happy, then, also great! Hopefully you will still find today’s feature of use if you find yourself advising a friend or family member one day. So without further ado, let’s get to it…
You may be familiar with the “sunk cost fallacy”; if not: it’s what happens when a person or group has already invested into a given thing, such that even though the thing is not going at all the way they hoped, they now want to continue trying to make that thing work, lest their previous investment be lost. But the truth is: if it’s not going to work, then the initial investment is already lost, and pouring out extra won’t help—it’ll just lose more.
That “investment” in a given thing could be money, time, energy, or (often the case) a combination of the above.
In the field of romance, the “sunk cost fallacy” keeps a lot of bad relationships going for longer than perhaps they should, and looking back (perhaps after a short adjustment period), the newly-single person says “why did I let that go on?” and vows to not make the same mistake again.
But that prompts the question: how can we know when it’s right to “keep working on it, because relationships do involve work”, as perfectly reasonable relationship advice often goes, and when it’s right to call it quits?
Should I stay or should I go?
Some questions for you (or perhaps a friend you might find yourself advising) to consider:
- What qualities do you consider the most important for a partner to have—and does your partner have them?
- If you described the worst of your relationship to a close friend, would that friend feel bad for you?
- Do you miss your partner when they’re away, or are you glad of the break? When they return, are they still glad to see you?
- If you weren’t already in this relationship, would you seek to enter it now? (This takes away sunk cost and allows a more neutral assessment)
- Do you feel completely safe with your partner (emotionally as well as physically), or must you tread carefully to avoid conflict?
- If your partner decided tomorrow that they didn’t want to be with you anymore and left, would that be just a heartbreak, or an exciting beginning of a new chapter in your life?
- What things would you generally consider dealbreakers in a relationship—and has your partner done any of them?
The last one can be surprising, by the way. We often see or hear of other people’s adverse relationship situations and think “I would never allow…” yet when we are in a relationship and in love, there’s a good chance that we might indeed allow—or rather, excuse, overlook, and forgive.
And, patience and forgiveness certainly aren’t inherently bad traits to have—it’s just good to deploy them consciously, and not merely be a doormat.
Either way, reflect (or advise your friend/family member to reflect, as applicable) on the “score” from the above questions.
- If the score is good, then maybe it really is just a rough patch, and the tools we link at the top and bottom of this article might help.
- If the score is bad, the relationship is bad, and no amount of historic love or miles clocked up together will change that. Sometimes it’s not even anyone’s fault; sometimes a relationship just ran its course, and now it’s time to accept that and turn to a new chapter.
“At my age…”
As we get older, it’s easy for that sunk cost fallacy to loom large. Inertia is heavy, the mutual entanglement of lives is far-reaching, and we might not feel we have the same energy for dating that we did when we were younger.
And there may sometimes be a statistical argument for “sticking it out” at least for a while, depending on where we are in the relationship, per this study (with 165,039 participants aged 20–76), which found:
❝Results on mean levels indicated that relationship satisfaction decreased from age 20 to 40, reached a low point at age 40, then increased until age 65, and plateaued in late adulthood.
As regards the metric of relationship duration, relationship satisfaction decreased during the first 10 years of the relationship, reached a low point at 10 years, increased until 20 years, and then decreased again.❞
Source: Development of Relationship Satisfaction Across the Life Span: A Systematic Review and Meta-Analysis
And yet, when it comes to prospects for a new relationship…
- If our remaining life is growing shorter, then it’s definitely too short to spend in an unhappy relationship
- Maybe we really won’t find romance again… And maybe that’s ok, if w’re comfortable making our peace with that and finding joy in the rest of life (this widowed writer (hi, it’s me) plans to remain single now by preference, and her life is very full of purpose and beauty and joy and yes, even love—for family, friends, etc, plus the memory of my wonderful late beloved)
- Nevertheless, the simple fact is: many people do find what they go on to describe as their best relationship yet, late in life ← this study is with a small sample size, but in this case, even anecdotal evidence seems sufficient to make the claim reasonable; probably you personally know someone who has done so. If they can, so can you, if you so wish.
- Adding on to that last point… Later life relationships can also offer numerous significant advantages unique to such (albeit some different challenges too—but with the right person, those challenges are just a fun thing to tackle together). See for example:
An exploratory investigation into dating among later‐life women
And about those later-life relationships that do work? They look like this:
this one looks like the title says it all, but it really doesn’t, and it’s very much worth at least reading the abstract, if not the entire paper—because it talks a lot about the characteristics that make for happy or unhappy relationships, and the effect that those things have on people. It really is very good, and quite an easy read.
See again: Healthy Relationship, Healthy Life
Take care!
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War in Ukraine affected wellbeing worldwide, but people’s speed of recovery depended on their personality
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The war in Ukraine has had impacts around the world. Supply chains have been disrupted, the cost of living has soared and we’ve seen the fastest-growing refugee crisis since World War II. All of these are in addition to the devastating humanitarian and economic impacts within Ukraine.
Our international team was conducting a global study on wellbeing in the lead up to and after the Russian invasion. This provided a unique opportunity to examine the psychological impact of the outbreak of war.
As we explain in a new study published in Nature Communications, we learned the toll on people’s wellbeing was evident across nations, not just in Ukraine. These effects appear to have been temporary – at least for the average person.
But people with certain psychological vulnerabilities struggled to recover from the shock of the war.
Tracking wellbeing during the outbreak of war
People who took part in our study completed a rigorous “experience-sampling” protocol. Specifically, we asked them to report their momentary wellbeing four times per day for a whole month.
Data collection began in October 2021 and continued throughout 2022. So we had been tracking wellbeing around the world during the weeks surrounding the outbreak of war in February 2022.
We also collected measures of personality, along with various sociodemographic variables (including age, gender, political views). This enabled us to assess whether different people responded differently to the crisis. We could also compare these effects across countries.
Our analyses focused primarily on 1,341 participants living in 17 European countries, excluding Ukraine itself (44,894 experience-sampling reports in total). We also expanded these analyses to capture the experiences of 1,735 people living in 43 countries around the world (54,851 experience-sampling reports) – including in Australia.
A global dip in wellbeing
On February 24 2022, the day Russia invaded Ukraine, there was a sharp decline in wellbeing around the world. There was no decline in the month leading up to the outbreak of war, suggesting the change in wellbeing was not already occurring for some other reason.
However, there was a gradual increase in wellbeing during the month after the Russian invasion, suggestive of a “return to baseline” effect. Such effects are commonly reported in psychological research: situations and events that impact our wellbeing often (though not always) do so temporarily.
Unsurprisingly, people in Europe experienced a sharper dip in wellbeing compared to people living elsewhere around the world. Presumably the war was much more salient for those closest to the conflict, compared to those living on an entirely different continent.
Interestingly, day-to-day fluctuations in wellbeing mirrored the salience of the war on social media as events unfolded. Specifically, wellbeing was lower on days when there were more tweets mentioning Ukraine on Twitter/X.
Our results indicate that, on average, it took around two months for people to return to their baseline levels of wellbeing after the invasion.
Different people, different recoveries
There are strong links between our wellbeing and our individual personalities.
However, the dip in wellbeing following the Russian invasion was fairly uniform across individuals. None of the individual factors assessed in our study, including personality and sociodemographic factors, predicted people’s response to the outbreak of war.
On the other hand, personality did play a role in how quickly people recovered. Individual differences in people’s recovery were linked to a personality trait called “stability”. Stability is a broad dimension of personality that combines low neuroticism with high agreeableness and conscientiousness (three traits from the Big Five personality framework).
Stability is so named because it reflects the stability of one’s overall psychological functioning. This can be illustrated by breaking stability down into its three components:
- low neuroticism describes emotional stability. People low in this trait experience less intense negative emotions such as anxiety, fear or anger, in response to negative events
- high agreeableness describes social stability. People high in this trait are generally more cooperative, kind, and motivated to maintain social harmony
- high conscientiousness describes motivational stability. People high in this trait show more effective patterns of goal-directed self-regulation.
So, our data show that people with less stable personalities fared worse in terms of recovering from the impact the war in Ukraine had on wellbeing.
In a supplementary analysis, we found the effect of stability was driven specifically by neuroticism and agreeableness. The fact that people higher in neuroticism recovered more slowly accords with a wealth of research linking this trait with coping difficulties and poor mental health.
These effects of personality on recovery were stronger than those of sociodemographic factors, such as age, gender or political views, which were not statistically significant.
Overall, our findings suggest that people with certain psychological vulnerabilities will often struggle to recover from the shock of global events such as the outbreak of war in Ukraine.
Luke Smillie, Professor in Personality Psychology, 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 Drug & Supplement Combo That Reverses Aging
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So far, its effects have been dramatic (in a good way) in mice; human trials are now underway.
How does it work?
It builds from previous work, in which a Japanese research team created an “anti-aging vaccine”, that responded to a problem more specific than aging as a whole, namely atherosclerosis.
They found that a certain* protein was upregulated (i.e., it was made at a greater rate resulting in greater quantities) in patients (mouse and human alike) with atherosclerosis. So, they immunized the mice against that protein, and long story short, everything improved for them, from their atherosclerosis to general markers of aging—including growing back fur that had been lost due to age-related balding (just like in humans). They also lived longer, as is to be expected of a mouse who is now biologically younger.
*To avoid being mysterious: it was glycoprotein nonmetastatic melanoma protein B, known to its friends as GPNMB.
You may be wondering: how can one be immunized against a protein? If so, do bear in mind, a virus is also a protein. In this case, they developed an RNA vaccine, that works in a similar way to the COVID vaccines we all know and love (albeit with a different target).
You can read about this in abundant detail here: Senolytic vaccination improves normal and pathological age-related phenotypes and increases lifespan in progeroid mice
Hot on the heels of that, new approaches were found, including…
The combination
We’ll not keep you waiting; the combination is dasatinib plus quercetin, or else fisetin alone.
It’s about killing senescent (aging) “zombie cells” while sparing healthy cells, which that drug (dasatinib) and those supplements (quercetin and fisetin) do.
The researchers noted:
❝Senescent cells are resistant to apoptosis, which is governed through the upregulation of senescent cell anti-apoptotic pathways (SCAPs). Compounds were subsequently identified that disrupted the SCAPs, inducing death of senescent cells while leaving healthy cells unaffected. Forty-six potential senolytic agents were discovered through this process. To advance translational efforts, the majority of research has focused on agents with known safety profiles and limited off-target effects (Kirkland and Tchkonia, 2020).
The best characterized senolytic agents are dasatinib, a tyrosine kinase inhibitor approved for use in humans for cancer treatment, and quercetin, a naturally occurring plant flavonoid. The agents have a synergistic effect, making their combination more potent for senescent cell clearance (Zhu et al., 2015). As senescent cells do not divide and accumulate over a period of weeks, they can be administered using an intermittent approach, which further serves to reduce the risk of side effects (Kirkland and Tchkonia, 2020).
In preclinical trials, the combination of dasatinib and quercetin (D + Q) have been found to alleviate numerous chronic medical conditions including vascular stiffness, osteoporosis, frailty, and hepatic stenosis❞
Source: A geroscience motivated approach to treat Alzheimer’s disease: Senolytics move to clinical trials
As to how they expanded on this research:
❝In our study, oral D + Q were intermittently administered to tau transgenic mice with late-stage pathology (approximated to a 70-year-old human with advanced AD) (Musi et al., 2018). The treatment effectively reduced cellular senescence and associated senescence-associated secretory phenotype incidence. The 35 % reduction in neurofibrillary tangles was accompanied by enhanced neuron density, decreased ventricular enlargement, diminished tau accumulation, and restoration of aberrant cerebral blood flow. A subsequent preclinical study validated the findings, reporting that intermittently administered D + Q cleared senescent cells in the central nervous system, reduced amyloid-β plaques, attenuated neuroinflammation, and enhanced cognition❞
Source: Ibid.
And now taking it to humans:
❝The first clinical trial of D + Q for early-stage Alzheimer’s Disease (AD) has completed enrollment (Gonzales et al., 2021). The primary aim of the open-label pilot study was to examine the central nervous system penetrance of D and Q in a small sample of older adults with early-stage AD (NCT04063124). In addition, two placebo-controlled trials of D + Q for neurodegenerative disease are underway (NCT04685590 and NCT04785300).
One of the trials in development is a multi-site, double-blind, randomized, placebo-controlled study of senolytic therapy in older adults with amnestic mild cognitive impairment (MCI) or early-stage dementia (Clinical Dementia Rating Scale (CDR) Global 0.5–1) due to AD (elevated CSF total tau/Aβ42 ratio).
The treatment regimen will consist of 12-weeks of intermittently administered oral D + Q.❞
Source: Ibid.
The study is actually completed now, but its results are not yet published (again, at time of writing). Which means: they have the data, and now they’re writing the paper.
We look forward to providing an update about that, when the paper is published!
In the meantime…
Dasatinib is a drug usually prescribed to people with certain kinds of leukemia, and suffice it to say, it’s prescription-only. And unlike drugs that are often prescribed off-label (such as metformin for weight loss), getting your doctor to prescribe you an anticancer drug is unlikely unless you have the cancer in question.
You may be wondering: how is an anticancer drug helpful against aging? And the answer is that cancer and aging are very interrelated, and both have to do with “these old cells just won’t die, and are using the resources needed for young healthy cells”. So in both cases, killing those “zombie cells” while sparing healthy ones, is what’s needed. However, your doctor will probably not buy that as a reason to prescribe you a drug that is technically chemotherapy.
Quercetin, on the other hand, is a readily-available supplement, as is fisetin, and both have glowing (in a good way) safety profiles.
Want to know more?
You can read more about each of quercetin and fisetin (including how to get them), here:
Enjoy!
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How we diagnose and define obesity is set to change – here’s why, and what it means for treatment
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Obesity is linked to many common diseases, such as type 2 diabetes, heart disease, fatty liver disease and knee osteoarthritis.
Obesity is currently defined using a person’s body mass index, or BMI. This is calculated as weight (in kilograms) divided by the square of height (in metres). In people of European descent, the BMI for obesity is 30 kg/m² and over.
But the risk to health and wellbeing is not determined by weight – and therefore BMI – alone. We’ve been part of a global collaboration that has spent the past two years discussing how this should change. Today we publish how we think obesity should be defined and why.
As we outline in The Lancet, having a larger body shouldn’t mean you’re diagnosed with “clinical obesity”. Such a diagnosis should depend on the level and location of body fat – and whether there are associated health problems.
World Obesity Federation What’s wrong with BMI?
The risk of ill health depends on the relative percentage of fat, bone and muscle making up a person’s body weight, as well as where the fat is distributed.
Athletes with a relatively high muscle mass, for example, may have a higher BMI. Even when that athlete has a BMI over 30 kg/m², their higher weight is due to excess muscle rather than excess fatty tissue.
Some athletes have a BMI in the obesity category. Tima Miroshnichenko/Pexels People who carry their excess fatty tissue around their waist are at greatest risk of the health problems associated with obesity.
Fat stored deep in the abdomen and around the internal organs can release damaging molecules into the blood. These can then cause problems in other parts of the body.
But BMI alone does not tell us whether a person has health problems related to excess body fat. People with excess body fat don’t always have a BMI over 30, meaning they are not investigated for health problems associated with excess body fat. This might occur in a very tall person or in someone who tends to store body fat in the abdomen but who is of a “healthy” weight.
On the other hand, others who aren’t athletes but have excess fat may have a high BMI but no associated health problems.
BMI is therefore an imperfect tool to help us diagnose obesity.
What is the new definition?
The goal of the Lancet Diabetes & Endocrinology Commission on the Definition and Diagnosis of Clinical Obesity was to develop an approach to this definition and diagnosis. The commission, established in 2022 and led from King’s College London, has brought together 56 experts on aspects of obesity, including people with lived experience.
The commission’s definition and new diagnostic criteria shifts the focus from BMI alone. It incorporates other measurements, such as waist circumference, to confirm an excess or unhealthy distribution of body fat.
We define two categories of obesity based on objective signs and symptoms of poor health due to excess body fat.
1. Clinical obesity
A person with clinical obesity has signs and symptoms of ongoing organ dysfunction and/or difficulty with day-to-day activities of daily living (such as bathing, going to the toilet or dressing).
There are 18 diagnostic criteria for clinical obesity in adults and 13 in children and adolescents. These include:
- breathlessness caused by the effect of obesity on the lungs
- obesity-induced heart failure
- raised blood pressure
- fatty liver disease
- abnormalities in bones and joints that limit movement in children.
2. Pre-clinical obesity
A person with pre-clinical obesity has high levels of body fat that are not causing any illness.
People with pre-clinical obesity do not have any evidence of reduced tissue or organ function due to obesity and can complete day-to-day activities unhindered.
However, people with pre-clinical obesity are generally at higher risk of developing diseases such as heart disease, some cancers and type 2 diabetes.
What does this mean for obesity treatment?
Clinical obesity is a disease requiring access to effective health care.
For those with clinical obesity, the focus of health care should be on improving the health problems caused by obesity. People should be offered evidence-based treatment options after discussion with their health-care practitioner.
Treatment will include management of obesity-associated complications and may include specific obesity treatment aiming at decreasing fat mass, such as:
- support for behaviour change around diet, physical activity, sleep and screen use
- obesity-management medications to reduce appetite, lower weight and improve health outcomes such as blood glucose (sugar) and blood pressure
- metabolic bariatric surgery to treat obesity or reduce weight-related health complications.
Treatment for clinical obesity may include support for behaviour change. Shutterstock/shurkin_son Should pre-clinical obesity be treated?
For those with pre-clinical obesity, health care should be about risk-reduction and prevention of health problems related to obesity.
This may require health counselling, including support for health behaviour change, and monitoring over time.
Depending on the person’s individual risk – such as a family history of disease, level of body fat and changes over time – they may opt for one of the obesity treatments above.
Distinguishing people who don’t have illness from those who already have ongoing illness will enable personalised approaches to obesity prevention, management and treatment with more appropriate and cost-effective allocation of resources.
What happens next?
These new criteria for the diagnosis of clinical obesity will need to be adopted into national and international clinical practice guidelines and a range of obesity strategies.
Once adopted, training health professionals and health service managers, and educating the general public, will be vital.
Reframing the narrative of obesity may help eradicate misconceptions that contribute to stigma, including making false assumptions about the health status of people in larger bodies. A better understanding of the biology and health effects of obesity should also mean people in larger bodies are not blamed for their condition.
People with obesity or who have larger bodies should expect personalised, evidence-based assessments and advice, free of stigma and blame.
Louise Baur, Professor, Discipline of Child and Adolescent Health, University of Sydney; John B. Dixon, Adjunct Professor, Iverson Health Innovation Research Institute, Swinburne University of Technology; Priya Sumithran, Head of the Obesity and Metabolic Medicine Group in the Department of Surgery, School of Translational Medicine, Monash University, and Wendy A. Brown, Professor and Chair, Monash University Department of Surgery, School of Translational Medicine, Alfred Health, Monash University
This article is republished from The Conversation under a Creative Commons license. Read the original article.
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Wise Old Fool
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How old is this dish? Well, let’s put it this way, it used to be called “𓅮𓏏𓈖” and remnants of it have been found at neolithic burial sites in Egypt. Nowadays it’s called “فول مدمس”, which gets rendered a lot of different ways in the Latin alphabet, but “fūl mudammas” is one option. For short, it’s just called “fūl”, which is pronounced like the English word “fool”, and it’s about the beans.
From chana masala with poori to frijoles refritos to beans on toast, lots of cultures have some version of this breakfast food, and all can be great (yes, even the beans on toast). But today we’re about this particular kind of morning protein, fiber, fats, and healthful spices.
You will need
- 2x 14 oz cans fava beans (other kinds of beans work as substitute; kidney beans are common substitution, but this writer prefers black beans personally if she doesn’t have fava in), drained
- 4 garlic cloves, crushed
- 1 tbsp extra virgin olive oil
- 1 teaspoon sweet cinnamon (or ½ sweet cinnamon stick)
- 1 tsp cumin seeds
- 1 tsp chili flakes
- 1 tsp paprika
- 1 tsp black pepper
- Juice of ½ lemon
- For the relish: 1 medium tomato, finely chopped; 1 tbsp extra virgin olive oil; 2 tbsp parsley, finely chopped
- To serve: 4 pitta breads, 2 eggs (omit if vegan), and a selection of pickled vegetables, drained
Method
(we suggest you read everything at least once before doing anything)
1) Add the olive oil to a saucepan over a medium heat; add the garlic, cumin seeds, and cinnamon. Keep these moving for a minute or two before moving to the next step.
2) Add the fava beans, as well as the other seasonings (chili flakes, paprika, black pepper), and mix thoroughly
3) Add 1 cup boiling water, and keep everything on a simmer for about 20 minutes, stirring often. Add the lemon juice while it’s simmering; when the beans start to break down and the mixture starts to thicken, it’s ready.
4) Mix the relish ingredients (finely chopped tomato, olive oil, parsley) thoroughly in a small bowl
5) Toast the pitta breads, and if using, soft-boil the eggs.
6) Serve! We suggest: fūl in a bowl, with one half of a soft-boiled egg per bowl, topped with the relish, and served with the pitta bread and pickled vegetables on the side.
Enjoy!
Want to learn more?
For those interested in some of the science of what we have going on today:
- Level-Up Your Fiber Intake! (Without Difficulty Or Discomfort)
- Making Friends With Your Gut (You Can Thank Us Later)
- Less Obvious Probiotic Benefits ← the pickled vegetables contain the probiotics here, while the beans are a great source of prebiotic fiber; this is why they work so well together
- Our Top 5 Spices: How Much Is Enough For Benefits?
- A Tale Of Two Cinnamons
- Eggs: All Things In Moderation?
Take care!
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Kiwi vs Passion Fruit – Which is Healthier?
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Our Verdict
When comparing kiwi to passion fruit, we picked the passion fruit.
Why?
This fruit is so passionate about delivery nutrient-dense goodness, that at time of writing, nothing has beaten it yet!
In terms of macros, passion fruit has a little more protein, as well as 50% more carbs, and/but more than 3x the fiber. That last stat is particularly impressive, and also results in passion fruit having a much lower glycemic index, too. In short, a clear win for passion fruit in the macros category.
In the category of vitamins, kiwi has more of vitamins B9, C, E, and K, while passion fruit has more of vitamins A, B2, B3, and B6, making for a tie this time.
As for minerals, kiwi has more calcium, copper, manganese, and zinc, while passion fruit has more iron, magnesium, phosphorus, potassium, and selenium, resulting in a modest, marginal win for passion fruit in this category.
Adding up the categories gives a convincing win for passion fruit, but by all means enjoy either or both; diversity is good! And kiwi has its merits too (for example, it’s particularly high in vitamin K, appropriately enough).
Want to learn more?
You might like to read:
Top 8 Fruits That Prevent & Kill Cancer
Enjoy!
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