Energize! – by Dr. Michael Breus & Stacey Griffith

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We previously reviewed another book book by Dr. Breus, The Power Of When. So what’s different in this one?

While the chronotypes featured in The Power Of When also feature here (and sufficient explanation is given to make this a fine stand-alone book), this book has a lot to do with metabolism also. By considering a person’s genetically predisposed metabolic rate to be fast, medium, or slow (per being an ectomorph, mesomorph, or endomorph), and then putting that next to one’s sleep chronotype, we get 12 sub-categories that in this book each get an optimized protocol of sleep, exercise (further divided into: what kind of exercise when), and eating/fasting.

Which, in effect, amounts to a personalized coaching program for optimized energy!

The guidance is based on a combination of actual science plus “if this then that” observation-based principles—of the kind that could be described as science if they had been studied clinically instead of informally. Dr. Breus is a sleep scientist, by the way, and his co-author Stacey Griffith is a fitness coach. So between the two of them, they have sleep and exercise covered, and the fasting content is very reasonable and entirely consistent with current consensus of good practice.

The style is very pop-psychology, and very readable, and has a much more upbeat feel than The Power Of When, which seems to be because of Griffith’s presence as a co-author (most of the book is written from a neutral perspective, and some parts have first-person sections by each of the authors, so the style becomes distinct accordingly).

Bottom line: if you’d like to be more energized but [personal reason why not here] then this book may not fix all your problems, but it’ll almost certainly make a big difference and help you to stop sabotaging things and work with your body rather than against it.

Click here to check out Energize!, and do just that!

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  • New research suggests intermittent fasting increases the risk of dying from heart disease. But the evidence is mixed

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    Kaitlin Day, RMIT University and Sharayah Carter, RMIT University

    Intermittent fasting has gained popularity in recent years as a dietary approach with potential health benefits. So you might have been surprised to see headlines last week suggesting the practice could increase a person’s risk of death from heart disease.

    The news stories were based on recent research which found a link between time-restricted eating, a form of intermittent fasting, and an increased risk of death from cardiovascular disease, or heart disease.

    So what can we make of these findings? And how do they measure up with what else we know about intermittent fasting and heart disease?

    The study in question

    The research was presented as a scientific poster at an American Heart Association conference last week. The full study hasn’t yet been published in a peer-reviewed journal.

    The researchers used data from the National Health and Nutrition Examination Survey (NHANES), a long-running survey that collects information from a large number of people in the United States.

    This type of research, known as observational research, involves analysing large groups of people to identify relationships between lifestyle factors and disease. The study covered a 15-year period.

    It showed people who ate their meals within an eight-hour window faced a 91% increased risk of dying from heart disease compared to those spreading their meals over 12 to 16 hours. When we look more closely at the data, it suggests 7.5% of those who ate within eight hours died from heart disease during the study, compared to 3.6% of those who ate across 12 to 16 hours.

    We don’t know if the authors controlled for other factors that can influence health, such as body weight, medication use or diet quality. It’s likely some of these questions will be answered once the full details of the study are published.

    It’s also worth noting that participants may have eaten during a shorter window for a range of reasons – not necessarily because they were intentionally following a time-restricted diet. For example, they may have had a poor appetite due to illness, which could have also influenced the results.

    Other research

    Although this research may have a number of limitations, its findings aren’t entirely unique. They align with several other published studies using the NHANES data set.

    For example, one study showed eating over a longer period of time reduced the risk of death from heart disease by 64% in people with heart failure.

    Another study in people with diabetes showed those who ate more frequently had a lower risk of death from heart disease.

    A recent study found an overnight fast shorter than ten hours and longer than 14 hours increased the risk dying from of heart disease. This suggests too short a fast could also be a problem.

    But I thought intermittent fasting was healthy?

    There are conflicting results about intermittent fasting in the scientific literature, partly due to the different types of intermittent fasting.

    There’s time restricted eating, which limits eating to a period of time each day, and which the current study looks at. There are also different patterns of fast and feed days, such as the well-known 5:2 diet, where on fast days people generally consume about 25% of their energy needs, while on feed days there is no restriction on food intake.

    Despite these different fasting patterns, systematic reviews of randomised controlled trials (RCTs) consistently demonstrate benefits for intermittent fasting in terms of weight loss and heart disease risk factors (for example, blood pressure and cholesterol levels).

    RCTs indicate intermittent fasting yields comparable improvements in these areas to other dietary interventions, such as daily moderate energy restriction.

    A group of people eating around a table.
    There are a variety of intermittent fasting diets. Fauxels/Pexels

    So why do we see such different results?

    RCTs directly compare two conditions, such as intermittent fasting versus daily energy restriction, and control for a range of factors that could affect outcomes. So they offer insights into causal relationships we can’t get through observational studies alone.

    However, they often focus on specific groups and short-term outcomes. On average, these studies follow participants for around 12 months, leaving long-term effects unknown.

    While observational research provides valuable insights into population-level trends over longer periods, it relies on self-reporting and cannot demonstrate cause and effect.

    Relying on people to accurately report their own eating habits is tricky, as they may have difficulty remembering what and when they ate. This is a long-standing issue in observational studies and makes relying only on these types of studies to help us understand the relationship between diet and disease challenging.

    It’s likely the relationship between eating timing and health is more complex than simply eating more or less regularly. Our bodies are controlled by a group of internal clocks (our circadian rhythm), and when our behaviour doesn’t align with these clocks, such as when we eat at unusual times, our bodies can have trouble managing this.

    So, is intermittent fasting safe?

    There’s no simple answer to this question. RCTs have shown it appears a safe option for weight loss in the short term.

    However, people in the NHANES dataset who eat within a limited period of the day appear to be at higher risk of dying from heart disease. Of course, many other factors could be causing them to eat in this way, and influence the results.

    When faced with conflicting data, it’s generally agreed among scientists that RCTs provide a higher level of evidence. There are too many unknowns to accept the conclusions of an epidemiological study like this one without asking questions. Unsurprisingly, it has been subject to criticism.

    That said, to gain a better understanding of the long-term safety of intermittent fasting, we need to be able follow up individuals in these RCTs over five or ten years.

    In the meantime, if you’re interested in trying intermittent fasting, you should speak to a health professional first.

    Kaitlin Day, Lecturer in Human Nutrition, RMIT University and Sharayah Carter, Lecturer Nutrition and Dietetics, RMIT University

    This article is republished from The Conversation under a Creative Commons license. Read the original article.

    The Conversation

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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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  • Supergreen Superfood Salad Slaw

    10almonds is reader-supported. We may, at no cost to you, receive a portion of sales if you purchase a product through a link in this article.

    When it comes to “eating the rainbow”, in principle green should be the easiest color to get in, unless we live in a serious food desert (or serious food poverty). In practice, however, a lot of meals could do with a dash more green. This “supergreen superfood salad slaw” is remarkably versatile, and can be enjoyed as a very worthy accompaniment to almost any main.

    You will need

    For the bits:

    • ½ small green cabbage, finely diced
    • 7 oz tenderstem broccoli, finely chopped
    • 2 stalks celery, finely chopped (if allergic, simply omit)
    • ½ cucumber, diced into small cubes
    • 2 oz kale, finely shredded
    • 4 green (spring) onions, thinly sliced

    For the dressing:

    • 1 cup cashews (if allergic, substitute 1 cup roasted chickpeas)
    • ½ cup extra virgin olive oil
    • 2 oz baby spinach
    • 1 oz basil leaves
    • 1 oz chives
    • ¼ bulb garlic
    • 2 tbsp nutritional yeast
    • 1 tbsp chia seeds
    • Juice of two limes

    Method

    (we suggest you read everything at least once before doing anything)

    1) Combine the ingredients from the “bits” category in a bowl large enough to accommodate them comfortably

    2) Blend the ingredients from the “dressing” category in a blender until very smooth (the crux here is you do not want any stringy bits of spinach remaining)

    3) Pour the dressing onto the bits, and mix well to combine. Refrigerate, ideally covered, until ready to serve.

    Enjoy!

    Want to learn more?

    For those interested in some of the science of what we have going on today:

    Take care!

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Related Posts

  • A Therapeutic Journey – by Alain de Botton
  • Type 2 Diabetic Foot Problems

    10almonds is reader-supported. We may, at no cost to you, receive a portion of sales if you purchase a product through a link in this article.

    It’s Q&A Day!

    Have a question or a request? You can always hit “reply” to any of our emails, or use the feedback widget at the bottom!

    This newsletter has been growing a lot lately, and so have the questions/requests, and we love that! In cases where we’ve already covered something, we might link to what we wrote before, but will always be happy to revisit any of our topics again in the future too—there’s always more to say!

    As ever: if the question/request can be answered briefly, we’ll do it here in our Q&A Thursday edition. If not, we’ll make a main feature of it shortly afterwards!

    So, no question/request too big or small

    Q: I’d like to know more about type 2 diabetic foot problems

    You probably know that the “foot problems” thing has less to do with the feet and more to do with blood and nerves. So, why the feet?

    The reason feet often get something like the worst of it, is because they are extremities, and in the case of blood sugars being too high for too long too often, they’re getting more damage as blood has to fight its way back up your body. Diabetic neuropathy happens when nerves are malnourished because the blood that should be keeping them healthy, is instead syrupy and sluggish.

    We’ll definitely do a main feature sometime soon on keeping blood sugars healthy, for both types of diabetes plus pre-diabetes and just general advice for all.

    In the meantime, here’s some very good advice on keeping your feet healthy in the context of diabetes. This one’s focussed on Type 1 Diabetes, but the advice goes for both:

    !

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  • Inverse Vaccines for Autoimmune Diseases

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    Inverse Vaccines for Autoimmune Diseases

    This is Dr. Jeffrey Hubbell. He’s a molecular engineer, with a focus on immunotherapy, immune response, autoimmune diseases, and growth factor variants.

    He’s held 88 patents, and was the recipient of the Society for Biomaterials’ Founders Award for his “long-term, landmark contributions to the discipline of biomaterials”, amongst other awards and honours that would make our article too long if we included them all.

    And, his latest research has been about developing…

    Inverse Vaccines

    You may be thinking: “you mean diseases; he’s engineering diseases?”

    And no, it’s not that. Here’s how it works:

    Normally in the case of vaccine, it’s something to tell the body “hey, if you see something that looks like this, you should kill it on sight” and the body goes “ok, preparing countermeasures according to these specifications; thanks for the heads-up”

    In the case of an inverse vaccine, it’s the inverse. It’s something to tell the body “hey, this thing you seem to think is a threat, it’s actually not, and you should leave it alone”.

    Why this matters for people with autoimmune diseases

    Normally, autoimmune diseases are treated in one or more of the following ways:

    • Dampen the entire immune system (bad for immunity against actual diseases, obviously, and is part of why many immunocompromised people have suffered and died disproportionately from COVID, for example)
    • Give up and find a workaround (a good example of this is Type 1 Diabetes, and just giving up on the pancreas not being constantly at war with itself, and living on exogenous insulin instead)

    Neither of those are great.

    What inverse vaccines do is offer a way to flag the attacked-in-error items as acceptable things to have in the body. Those might be things that are in our body by default, as in the case of many autoimmune diseases, or they may even be external items that should be allowed but aren’t, as in the case of gluten, in the context of Celiac disease.

    The latest research is not yet accessible for free, alas, but you can read the abstract here:

    Synthetically glycosylated antigens for the antigen-specific suppression of established immune responses

    Or if you prefer a more accessible pop-science approach, here’s a great explanatory article:

    “Inverse vaccine” shows potential to treat multiple sclerosis and other autoimmune diseases

    Where can we get such inverse vaccines?

    ❝There are no clinically approved inverse vaccines yet, but we’re incredibly excited about moving this technology forward❞

    ~ Dr. Jeffrey Hubbell

    But! Lest you be disappointed, you can get in line already, in the case of the Celiac disease inverse vaccine, if you’d like to be part of their clinical trial:

    Click here to see if you are eligible to be part of their clinical trial

    If you’re not up for that, or if your autoimmune disease is something else (most of the rest of their research is presently focusing on Multiple Sclerosis and Type 1 Diabetes), then:

    • The phase 1 MS trial is currently active, estimated completion in summer 2024.
    • They are in the process of submitting an investigational new drug (IND) application for Type 1 Diabetes
      • This is the first step to starting clinical safety and efficacy trials

    …so, watch this space!

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  • Intuitive Eating Might Not Be What You Think

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    In our recent Expert Insights main features, we’ve looked at two fairly opposing schools of thought when it comes to managing what we eat.

    First we looked at:

    What Flexible Dieting Really Means

    …and the notion of doing things imperfectly for greater sustainability, and reducing the cognitive load of dieting by measuring only the things that are necessary.

    And then in opposition to that,

    What Are The “Bright Lines” Of Bright Line Eating?

    …and the notion of doing things perfectly so as to not go astray, and reducing the cognitive load of dieting by having hard-and-fast rules that one does not second-guess or reconsider later when hungry.

    Today we’re going to look at Intuitive Eating, and what it does and doesn’t mean.

    Intuitive Eating does mean paying attention to hunger signals (each way)

    Intuitive Eating means listening to one’s body, and responding to hunger signals, whether those signals are saying “time to eat” or “time to stop”.

    A common recommendation is to “check in” with one’s body several times per meal, reflecting on such questions as:

    • Do I have hunger pangs? Would I seek food now if I weren’t already at the table?
    • If I hadn’t made more food than I’ve already eaten so far, would that have been enough, or would I have to look for something else to eat?
    • Am I craving any of the foods that are still before me? Which one(s)?
    • How much “room” do I feel I still have, really? Am I still in the comfort zone, and/or am I about to pass into having overeaten?
    • Am I eating for pleasure only at this point? (This is not inherently bad, by the way—it’s ok to have a little more just for pleasure! But it is good to note that this is the reason we’re eating, and take it as a cue to slow down and remember to eat mindfully, and enjoy every bite)
    • Have I, in fact, passed the point of pleasure, and I’m just eating because it’s in front of me, or so as to “not be wasteful”?

    See also: Interoception: Improving Our Awareness Of Body Cues

    And for that matter: Mindful Eating: How To Get More Out Of What’s On Your Plate

    Intuitive Eating is not “80:20”

    When it comes to food, the 80:20 rule is the idea of having 80% of one’s diet healthy, and the other 20% “free”, not necessarily unhealthy, but certainly not moderated either.

    Do you know what else the 80:20 food rule is?

    A food rule.

    Intuitive Eating doesn’t do those.

    The problem with food rules is that they can get us into the sorts of problems described in the studies showing how flexible dieting generally works better than rigid dieting.

    Suddenly, what should have been our free-eating 20% becomes “wait, is this still 20%, or have I now eaten so much compared to the healthy food, that I’m at 110% for my overall food consumption today?”

    Then one gets into “Well, I’ve already failed to do 80:20 today, so I’ll try again tomorrow [and binge meanwhile, since today is already written off]”

    See also: Eating Disorders: More Varied (And Prevalent) Than People Think

    It’s not “eat anything, anytime”, either

    Intuitive Eating is about listening to your body, and your brain is also part of your body.

    • If your body is saying “give me sugar”, your brain might add the information “fruit is healthier than candy”.
    • If your body is saying “give me fat”, your brain might add the information “nuts are healthier than fried food”
    • If your body is saying “give me salt”, your brain might add the information “kimchi is healthier than potato chips”

    That doesn’t mean you have to swear off candy, fried food, or potato chips.

    But it does mean that you might try satisfying your craving with the healthier option first, giving yourself permission to have the less healthy option afterwards if you still want it (you probably won’t).

    See also:

    I want to eat healthily. So why do I crave sugar, salt and carbs?

    Want to know more about Intuitive Eating?

    You might like this book that we reviewed previously:

    Intuitive Eating – by Evelyn Tribole and Elyse Resch

    Enjoy!

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