Research of the Week
Physical frailty predicts COVID-19 outcomes.
If you’re lifting, getting 1.62 grams of protein per kilogram of bodyweight is a nice target.
After new analysis, Ireland reduces its “excess deaths from coronavirus” numbers. Still 13% higher than normal, but lower than previous estimations.
Evidence for coronavirus presence in Brazil as early as November 2019.
New Primal Blueprint Podcasts
Episode 431: Gina Devee: Host Elle Russ chats with author Gina Devee.
Primal Health Coach Radio, Episode 67: Laura and Erin chat with Jen James about heart-centered entrepreneurism.
Is there another pandemic coming?
Interesting Blog Posts
Those pesky PSCK9 inhibitors: so effective on paper, so useless (and sometimes deadly) in real life.
Some awesome ideas for games to play with your kids.
Don’t let this be you.
Got arthritis? Try barefoot.
Things I’m Up to and Interested In
I’m not surprised: Humans use smell to get around.
Interesting finding: Very low LDL is not associated with lower cardiovascular mortality. It is associated with higher all cause mortality.
It’s just everywhere these days: Plastic found in vegetables and fruits.
Another reason everyone should exercise: It improves the quality of breast milk.
A nice piece on importance of megafauna in human diets: How eating (and killing) the megafauna changed humans forever.
Question I’m Asking
Did you roughhouse as a kid?
One year ago (Jun 28 – Jul 3)
- Diastasis Recti: What to Know – What to keep in mind.
- 7 Foods Keto Eaters Shouldn’t Fear – A few foods that get bad raps.
Comment of the Week
“Plastic rain sounds like our version of lead pipes for the Romans.”
– We will see, Chris.
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Who’s that person? Nope, it’s not me. Although health coaches are a great resource for helping you set goals, overcome obstacles, and get out of your own well-intentioned way. For the record, that person is also not your spouse, your roommate, your friends, or your kids.
The one person who can make you reach all your health goals is YOU.
I see you out there working hard, swapping your typical yogurt and banana breakfast for a protein-rich meal of eggs and bacon. I see you squeezing in a few sprint sessions a week and limiting blue light at night. You’re committed to doing everything right. Until, something goes wrong.
Tell me if any of these statements sound familiar.
“I’ll start over on Monday”
“I guess I’m not cut out for this”
“My husband/wife/kid keeps sabotaging me with sugary treats”
The thing is, there’s a big difference between people who think it would be really cool to reach their goals and those who unapologetically knock those goals out of the park. Trust me, I know this scenario firsthand. I’ve worked with hundreds of men and women with a desire for the latter, and a mindset for the former.
If you’re in that camp too, there is a solution. And it starts with having a deep-down belief that you have what it takes to show up for yourself each and every day and accomplish the tasks you set out to do, no matter what happens. This is what’s called self-efficacy.
What Exactly Is Self-efficacy?
According to Albert Bandura, the social psychologist responsible for this theory, self-efficacy refers to an individual’s belief in his or her capacity to execute the behaviors necessary to achieve specific results.https://pubmed.ncbi.nlm.nih.gov/14724662/‘>2
How to Improve Your Self-efficacy
So, how do you get more of it? According Bandura, your self-efficacy stems from four distinct sources, including:
- Mastery Experiences – having previously mastered a task or skill
- Vicarious Experiences – seeing others who you consider a role model succeed
- Verbal Persuasion – being told by influential people in your life that you have the right stuff
- Emotional & Physiological States – this is the idea that depression or chronic stress can lower your belief in yourself
Taking those sources into account, I created 8 strategies that allow you to improve self-efficacy by focusing on certain areas of your life that could use a boost. These are the same strategies I use with my own clients to help them believe they’re as insanely badass as they really are.
Strategies to Improve Your Self-efficacy
Even if you have a history of being told you don’t have the right stuff or you’ve struggled to master anything short of boiling water, you can start improving your self-efficacy right now by following these steps:
- Start small
- Get inspired
- Avoid comparison
- Do the work
- Watch your self-talk
- Know your triggers
- Adopt an “I never lose” mindset
- Add up your successes
Let’s unpack these steps.
1. Start small. Choose goals that are easier to achieve. Rather than attempting to not touch another piece of bread for the rest of your life, say “I’m not eating bread today.” Need it to be even smaller? Try this on for size: “I’m not eating bread at this meal.” Smaller goals give you easy wins.
2. Get inspired. Know someone who’s totally crushing their goals? Show your support, ask them questions, and remember that if they can do it, you can too. While it can be hard to celebrate other people’s wins (especially if you’re having a tough time achieving yours), allow yourself to get inspired by their success.
3. Avoid comparison. If scrolling through your Instagram feed or chatting with your neighbor who dropped 4 dress sizes causes your self-confidence to plummet, don’t do it. Comparing yourself to others who are at different parts of their journey isn’t a good plan for anyone (see strategy #2).
4. Do the work. Be consistent with your healthy habits every day — even when you don’t want to. Sit down to an epic protein-forward meal or make movement part of your routine without expecting an immediate result. Some days will feel awesome, others won’t. Your job here is to continue to show up and put in the work.
5. Watch your self-talk. Be aware of how you talk to yourself when the going gets tough. If you constantly beat yourself up for giving up on your workouts, try turning that negative talk into something more neutral, without emotion like, “right now, I get really tired during my workouts.” It’s just a neutral awareness. For more tips on overcoming negative self-talk, read this.
6. Know your triggers. The deli with the awesome hoagie rolls? The bakery case at your grocery store? Backyard BBQs at your neighbor’s house? If certain places or situations test your ability to stay on track, avoid them for now. Or better yet, have a plan that allows you to be successful, like not going grocery shopping hungry or bringing your own Primally-friendly foods to the party.
7. Adopt an “I never lose” mindset. I’ve always loved the quote by Nelson Mandela, “I never lose. I either win or I learn.” Pretty powerful, right? This kind of mindset allows you to look for the opportunity in every situation. Instead of an all-or-nothing, win-or-lose mentality, it helps you see what you can learn – and what you can do differently next time if something didn’t go the way you’d anticipated.
8. Add up your successes. This is a key factor in building up your self-efficacy. Start keeping track of your wins, no matter how small you think they are. Grab a journal and write each one down. You’d be surprised how fast they add up.
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You can’t change your genes. But you can program them.
The modern world presents a number of problems for our genes. The world we’ve constructed over the last 50 years is not the environment in which our genetic code evolved. Our genes don’t “expect” historically low magnesium levels in soil, spending all day indoors and all night staring into bright blue lights, earning your keep by sitting on your ass, getting your food delivered to your door, communicating with people primarily through strange scratchings that travel through the air. So when these novel environmental stimuli interact with our genetic code, we get disease and dysfunction.
The genes look bad viewed through a modern prism. They get “associated” with certain devastating health conditions. But really, if you were to restore the dietary, behavioral, and ambient environments under which those genes evolved, those genes wouldn’t look so bad anymore. They might even look great.
This is epigenetics: altering the programming language of your genes without altering the genes themselves.
Think of your genome as computer hardware. If you were to program your computer you wouldn’t be changing the hardware; you would be changing the software that tells the computer what to do. So just as we talk about reprogramming or programming a computer and don’t suggest that the hardware itself has changed we likewise can talk about reprogramming our genes without suggesting that the genes have changed.
Okay, so how does this play out in reality? Are there any good examples of epigenetics in humans?
One of the most striking cases of the environment altering gene expression was in an old study of a homogeneous population of Berbers from North Africa.https://www.eurekalert.org/pub_releases/2008-12/aafc-ilc122308.php‘>2 Since MTHFR is the gene that constructs the proteins we use to activate thousands of other genes, suppressing MTHFR suppresses all those genes that rely on MTHFR-related proteins for activation. This disrupts numerous physiological systems and can set the stage for things like birth defects, cancer, and heart disease. It’s an epigenetic disaster, and it’s one reason why smoking increases the risk of so many different diseases.
Tobacco also induces hypermethylation (overactivation) of the GCLC gene which controls glutathione production. This causes a suppression of glutathione levels, an increase in oxidative stress, and initiation of COPD (chronic obstructive pulmonary disease).https://www.ncbi.nlm.nih.gov/pubmed/22666405‘>4
If the idea of someone being an exercise “non-responder” sounds ridiculous and unbelievable, you’re right. It turns out that while regular cardio is neutral or even detrimental to this genetic profile, high-intensity training confers the normal benefits you’d expect from exercisehttps://pubmed.ncbi.nlm.nih.gov/18098291/‘>6
If you have some of the common MTHFR mutations, you need to eat more dietary choline (eggs, liver).https://pubmed.ncbi.nlm.nih.gov/20220206/‘>8
PUFA Metabolism Epigenetics
Your genes also affect fat metabolism. Some mutations in the FADS1 improve the ability of a person to elongate plant omega-3s into long-chained omega-3s like the fish fats EPA and DHA. In the context of a low-fish diet, they can still make the EPA and DHA they require to function as long as they eat some alpha-linolenic acid. This mutation is more common in populations with a long history of farming.
Another mutation impairs the ability of a person to elongate those plant fats into animal-type EPA and DHA; they need to eat a high-fish diet or supplement with fish oil to get the omega-3s their bodies need. That’s the boat I’m in—I fucntion best with a steady supply of long-chained omega-3s in my diet, probably because my recent ancestors ate a lot of seafood. This mutation is more common in populations with a shorter history of farming, or a longer history of reliance on seafood.
What’s the point of all this?
There are multiple future possible versions of you. It’s up to you to decide which version you will become. It’s up to you to make lifestyle choices that direct genes toward fat burning, muscle building, longevity and wellness, and away from fat storing, muscle wasting, disease and illness. The day-to-day choices we make—whether it’s what to pack for lunch, or hitting the snooze button and missing the gym, or even sneaking a cigarette break—don’t just impact us in the short-term (or even in ways that are immediately clear to us). That can make this scary, but it can also be empowering.
You can fix yourself. You can be better. Your genes can work better. Everyone, no matter how dire their circumstances or how “poor” the cards they were dealt were, can forge their own epigenetic destiny.
You can’t ignore the genes. They still matter. You have to figure out, of course, how your particular genes interact with diet, exercise, sleep, sun, nature, socializing, and every other lifestyle behavior. That’s the journey you’re on. That’s the journey we’re all on—it’s what this website and movement are about.
There’s a lot we don’t know about this topic. What if I don’t have a study I can refer to? What if I don’t sign up for a DNA analysis—am I out of luck?
Use your intuition when you don’t have a study or haven’t defined an epigenetic mechanism: Does it feel right? Does it feel wrong? Are you getting good results? How’s your energy? How’s your performance? Those subtle (or not-so-subtle) cues from our subconscious and direct feedback from our waking life are where true knowledge and wisdom lie. After all, your genes “want” you to do the right thing. If we’re cued into our subconscious and we’ve led a generally healthy way of life, we become more sensitive to those messages. Those flutters of doubt or little urges we get are the body’s way of telling us we’re headed for epigenetic ruin or success.
Listen to those, or at least consider and don’t ignore them.
This is what The Primal Blueprint, The Keto Reset Diet, The Primal Connection, and even Primal Endurance have all been about. It’s why the sub-title of my first book is “Reprogram Your Genes for Effortless Weight Loss, Vibrant Health and Boundless Energy”. And it’s what we talk about (either directly or indirectly) day-in and day-out here at Mark’s Daily Apple.
Now I’d love to hear from you. Do you have any questions about epigenetics? About how we can alter our genetic destiny through modifying our environments?
Leave them down below.
The post Epigenetics, or What I Mean by “Reprogram Your Genes” appeared first on Mark’s Daily Apple.
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Keto is unique compared to other diets because there is an objective marker that tells you if you’re on the right track. With an easy at-home test, you can confirm that you are, in fact, in a state of ketosis.
Regular readers probably know I’m not a big data tracker. My energy, sleep, workout performance, stamina, and enjoyment of life tell me almost everything I need to know about how well I’m doing. Nevertheless, I get that some people love to play the self-quantification game. In some medical situations, measuring ketones is advisable, even necessary, as well. I’m not a total curmudgeon about it. Heck, I’ve been known to check in on my blood glucose and ketones from time to time.
If you’re thinking about testing, you should become familiar with the three different methods. Each has its own pros and cons. You’ll want to pick the option that’s right for you.
Stay on track no matter where you are! Instantly download your Primal and Keto Guide to Eating Out
What Exactly Are You Measuring?
Let’s back up and do a quick refresher on ketogenic diets. These are any diets where carbohydrate intake is restricted below about 50 grams of total carbs per day. When you restrict carbs, you are really restricting how much glucose the body has to meet its energy needs. Without much glucose coming in, the body needs an alternative fuel source, especially for the brain, which doesn’t run well on fat. That fuel source is ketones.
The liver produces ketones from fatty acids when insulin levels are low and liver glycogen (stored glucose) becomes depleted. This happens when you follow a very-low-carb diet, fast, or engage in sustained exercise.
When your liver is producing measurable amounts of ketones, you are said to be in ketosis. This is not to be confused with ketoacidosis, a potentially fatal medical emergency. Keto diets don’t lead to ketoacidosis because the body has a safeguard that prevents ketone levels from becoming dangerously high: insulin. When ketones rise, the pancreas releases insulin, which in turn hinders the release of fatty acids from stored body fat. Fewer fatty acids in the bloodstream mean less substrate (material) for the liver to turn into ketones.
This feedback mechanism keeps ketone levels in safe ranges unless your body can’t produce insulin. Individuals with type 1 diabetes and very advanced type 2 diabetes are at risk for developing ketoacidosis for this reason. Diabetics often monitor their ketones to make sure they are within safe ranges.
For the rest of us, measuring ketones is just a way of checking whether or not we are actually in a state of ketosis. We might want to know that for a number of reasons, discussed later.
Meet The Ketones
In ketogenesis, fatty acids are metabolized in the liver to create ketone bodies. The primary ketone body is acetoacetate (AcAc), which can convert into beta-hydroxybutyrate (BHB). AcAc also spontaneously breaks down into a third ketone body, acetone.
The body primarily uses AcAc and BHB for energy. Although acetone can be converted into pyruvate, it’s generally considered a waste product.
How to Test Ketones at Home
There are three ways to test your ketones at home:
- Urine test strips, which measure AcAc
- Blood tests, which measure BHB
- Breath tests, which measure acetone
Urine Ketone Test Strips
How it works:
You can purchase urine ketone test strips online or in many pharmacies. They are cheap, costing only pennies per strip. Don’t confuse them with urine pH strips.
Simply collect your urine in a sample cup or pee directly on the strip. After a set time—usually 15 seconds, but some strips take longer—the end of the strip will change color. Compare the color on the strip to the key on the package to get your ketosis level. Rather than giving you an exact readout, the color tells you if your urine does not register any AcAc, or if it shows low, medium, or high levels.
It’s straightforward but not foolproof. For one, if you let the strip sit for too long before you interpret the results, the test can be inaccurate. Urine strips also tend to overestimate the amount of AcAc present and can give false positives.https://pubmed.ncbi.nlm.nih.gov/12081817/’>2 Results can be affected by how well hydrated you are, too.
Although urine tests are shown to correlate decently well with blood and breath tests in diabeticshttps://pubmed.ncbi.nlm.nih.gov/12081817/‘>4 AcAc in the urine is considered “spillover.” When you first start a keto diet, your cells aren’t great at utilizing ketones, so some get excreted. You’re measuring ketones the liver made but the body can’t use. As you become more keto-adapted, there should be less spillover.
Most keto dieters do find that their urine ketones decline over time. That’s a good thing, indicating less waste; but it also means the urine tests become less useful. It’s very common for experienced keto dieters to have low or no measurable ketones in their urine despite having plenty in their bloodstreams.
- Least expensive method of testing
- Does not require blood—no finger pricks
- Least accurate, especially after keto-adaptation period
- Affected by how well hydrated you are
- Does not tell you exact ketone levels
Blood Tests for Ketones
How it works:
Blood tests measure the level of BHB in the bloodstream. This is considered the gold standard in ketone testing. They require an initial investment in a meter, plus ongoing purchases of test strips. You also need a lancing device and sterile lancets to prick your finger and draw a droplet of blood. If you’re planning on testing several times a day, it can get expensive fast, not to mention your sore fingertips.
The two most popular meters in the U.S. are the Keto Mojo() and Precision Xtra. Both also measure blood glucose, but you need separate test strips. The Precision Xtra meter runs around $25 depending on where you purchase it. Ketone test strips cost about $1.20 each, and glucose test strips about $0.65.
You can get a Keto Mojo starter kit on the company’s website that includes the meter, lancing device, 10 lancets, 10 ketone test strips, 10 glucose test strips, and a travel case for $59.99. Additional ketone test strips cost $49.50 for a 50-pack. Glucose test strips are $14.99 for a 50-pack. They also offer a Bluetooth connector for $9.95 that allows you to upload your test results to an app.
Understanding blood test results:
Your meter will give you a reading of 0 or “Lo” if you aren’t in ketosis. On a typical keto diet, you might be anywhere from 0.3 to around 2.0 mmol (millimole). Fasting and exercise can each drive BHB up to 4.0 mmol or higher. Ketoacidosis occurs above 10 mmol.
In The Art and Science of Low Carbohydrate Living, renowned researchers Jeff Volek and Stephen Phinney proposed that ketosis begins at 0.5 mmol. The designated 1.0 to 2.5 mmol as the “optimal ketone zone.” Don’t get too hung up on these numbers, though. Some individuals produce high levels of ketones on a normal keto diet, while others barely register any unless they fast or use exogenous ketones (which contain BHB). I have friends who have been strictly keto for years and consistently hover around 0.3 or 0.4 mmol. We don’t really understand why these individual differences exist. I’ve offered some hypotheses, but it’s still a bit of a mystery.
Anyway, higher numbers don’t mean that you’re doing better than the next person. In certain medical situations, such as for seizure control, high BHB levels are desirable. For the average person doing keto for weight loss or general wellness, there’s no evidence that it makes a big difference. More recently, Phinney and Volek have started to talk about the “effective therapeutic range”—where you can expect to reap benefits from being in ketosis—as being anywhere between 0.5 and 4.0 mmol.https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4737348/‘>6
Breath acetone does reliably correlate with blood BHB. Multiple studies also show that acetone readings are correlated with weight loss when participants follow a calorie-restricted diet.https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5097355/‘>8 Blood tests were otherwise fairly steady throughout the day, with a modest decline in the afternoon. Urine tests showed higher ketones as the day progressed, also with a small mid-afternoon dip. The highest levels occurred before bed, at 10 p.m.
Do You Need to Test?
No, but there are some reasons you might want to.
As I said up top, those using a ketogenic diet therapeutically might need to track ketone levels. For certain conditions like epilepsy, patients might aim for ketone levels of 4.0 mmol or higher.https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4367849/’>10 A blood BHB measurement is required to calculate GKI.
You might want to track your ketones if you’re running an n=1 experiment. Maybe you want to see what happens when you eat more protein or carbs, or you’re gauging your reactions to certain foods.https://celiac.org/about-celiac-disease/what-is-celiac-disease/‘>1 Unfortunately, not everyone who develops Celiac disease will have recognizable symptoms before the condition has wreaked serious havoc in the intestinal system by flattening of the intestinal villi and subsequently decreasing the area for nutrient absorption. For these people, Celiac disease often isn’t diagnosed until after effects of malnutrition have set in (lack of growth in children, diarrhea, stomach pain and/or bloating, vomiting, behavioral changes, etc.). In these cases, biopsies are often taken to assess the extent of damage and to aid diagnosis. Even if biopsies are normal, there is still the chance that nutrient absorption is impaired.
Thankfully, methods for diagnosing gluten sensitivity and related Celiac disease have improved in recent years as awareness has increased and more research has been done. Blood tests for specific antibodies have allowed physicians to diagnose the disease in many cases before much if any damage has occurred. Researchers are also beginning to test for antibodies in the intestinal tract, which may promise an even earlier diagnosis in at-risk individuals.
Is Gluten Intolerance Common?
Gluten sensitivity or intolerance, once thought to be rare, is now believed to affect a third of the population. (Some believe this number is substantially higher.) Experts report that up to 100 million Americans will consume gluten-free food products over the course of a year.https://www.sciencedirect.com/science/article/abs/pii/0167569992900208‘>3 It can appear at any point throughout your lifetime, and sometimes doesn’t manifest itself until a person is in their thirties or even forties.
Given my stance on grains, I obviously suggest avoiding gluten. As mentioned, gluten intolerance is a very common condition and may be underestimated still. Given the relatively recent introduction of gluten (and all grains) into the human diet, gluten intolerance and the related Celiac disease are very unfortunate but not very surprising conditions. In addition to omitting grains from your diet (especially those listed above), you can avoid processed foods, which likely contain trace amounts in forms like hydrolyzed proteins, starch/modified starch, malt, binders, and natural flavorings. If anyone in your family has been diagnosed with Celiac disease or gluten intolerance, it’s a wise idea to talk to your doctor about testing options.
What to Do If You Suspect You Are Gluten Intolerant
If you think you are having reactions to gluten, visit your doctor to rule out celiac disease. Then, it’s simply a matter of avoiding gluten. It’s difficult at first, but soon, you won’t miss them.
Foods that Contain Gluten
Gluten is present in only grains and grain-based foods. Ingredients to look out for if you’re avoiding gluten include:
- Oats if not labeled gluten-free (If they’re grown too close to wheat crops, you may end up with rogue wheat grains in the mix.)
When you’re Primal, you avoid grains, so you may be avoiding gluten by default.
Gluten-free grains, starches and flours
If you’re avoiding gluten and buying replacement foods, you may see ingredients including:
- Almond flour
- Cassava root
- Coconut flour
- Potato starch
The post Dear Mark: Gluten Sensitivity, Intolerance, Celiac Disease, and Grains appeared first on Mark’s Daily Apple.
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Chicago is known for its deep dish pizza. In Southern California, you have tacos on every corner. Philadelphia loves their cheesesteaks. And you know you’re in Nashville when every third restaurant claims they have the best Hot Chicken in town.
If you’re looking for the crispy kick of hot chicken but you’re nowhere near Music City, we’ve got you covered. Our Nashville Hot Chicken recipe tastes just like the real thing, without the fried food hangover from oxidized frying oil and grain-based breading. Yes, it can be done.
This recipe is fairly involved, but it’ll be worth it in the end.
Not sure about the heat factor? You can adapt this recipe from slightly zingy to three-alarm fire. If you want to break a sweat, taste the coating mixture and the hot chicken sauce before you apply, and add more cayenne. If you want to scale back the spice level, simply reduce the cayenne pepper accordingly. If you want your chicken to have just a subtle zip, you can completely omit the cayenne. The chicken will still have a nice kick thanks to the Primal Kitchen® Buffalo Sauce.
The best way to make the prep for this dish run smoothly is to set up a station with three coatings. Move the chicken like an assembly line down each coating mix. Some of the almond flour coating will clump up as you start dredging the chicken in it. That’s okay! Press these clumps into the chicken as you bread. It will create great texture for the final product.
If you don’t have chicken thighs, you can use chicken breast. Follow the same directions, and bake at 400 degrees instead. You can also lightly spray the chicken with a spritz of Primal Kitchen Avocado Oil Spray prior to baking to prevent the chicken from drying out.
We used coconut sugar in the sauce since it melts with heat and helps the sauce come together. If you’d prefer to use a sugar substitute, your best bet may be a liquid sweetener, like a monk fruit extract based sweetener, but we have not tested this substitution.
Here’s how to make it.
Gluten Free Nashville Style Hot Chicken Recipe
- 1 lb. boneless chicken thighs
- 1 cup almond flour
- 7 Tbsp tapioca starch
- ? cup coconut milk (or other full-fat milk)
- ¼ cup Primal Kitchen Buffalo Sauce
- 1 Tbsp coconut flour
- 1 tsp lemon juice
- ½ tsp paprika
- ½ tsp onion powder
- ½ tsp garlic powder
- ½ tsp salt
- ½ tsp black pepper
- ?-1/4 tsp cayenne pepper
- Butter lettuce or iceberg lettuce
- 1.5 Tbsp Primal Kitchen Avocado Oil
- 3 Tbsp Primal Kitchen Buffalo Sauce
- 3 Tbsp water
- 1 tsp paprika
- 1 tsp sweetener
- ¼ tsp cayenne pepper
- ¼ tsp chili powder
- ¼ tsp garlic powder
- ¼ tsp salt
Pound the chicken between two pieces of parchment paper until they are of even thickness.
Set up three containers or shallow dishes. In the first, mix together two tablespoons of tapioca starch and one tablespoon coconut flour. In the second, mix together the coconut milk, Primal Kitchen Buffalo Sauce and lemon juice. In the third container, mix together the almond flour and remaining tapioca starch.
In a small bowl, mix together the paprika, onion powder, garlic powder, salt, pepper and cayenne pepper. Pour about ¼ of this mixture into the container with the coconut flour coating, and the remaining mixture into the container with the almond flour coating.
Lightly coat the chicken in the coconut flour coating in container 1. Dredge the chicken into the sauce mixture in container 2. Really coat the chicken, turning it multiple times so it picks up a lot of the sauce. Carefully move the chicken pieces one at a time to the container with the almond flour mixture, coating it on all sides. You can also press a little of the coating into the chicken. The mixture will get a little clumpy because of the sauce coating, but that’s a good thing!
Place the coated chicken on a parchment covered sheet pan and let it rest for 15 minutes. Preheat your oven to 425 degrees during this time.
Place the chicken in the oven for about 20 minutes, or until the chicken reaches an internal temperature of 170 degrees Fahrenheit. The breading is a little delicate, but you can carefully flip the chicken over halfway through the cooking if you are able to.
When the chicken is nearly cooked, prepare the sauce. Heat the avocado oil in a small pan over medium heat. Add the paprika, sweetener, cayenne pepper, chili powder, garlic powder and salt and whisk together. When the sauce comes together, add in the buffalo sauce and keep whisking. The sauce will begin to thicken. Add the water 1 tablespoon at a time until the sauces reaches a silky texture.
When the chicken is finished cooking, spoon the sauce all over the chicken thighs.
Serve immediately wrapped in butter lettuce and garnish with a pickle spear.
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Research of the Week
Adipose tissue is limited by the number of embryonic progenitor cells.
Relying only on antibody testing may not capture everyone with coronavirus immunity.
Birds who swallow fish eggs whole may deposit them intact and viable into isolated lakes.
New Primal Blueprint Podcasts
Episode 430: Shawn Baker MD: Host Elle Russ chats with Dr. Shawn Baker about all-things carnivory.
Primal Health Coach Radio, Episode 66: Laura and Erin chat with Tara Garrison.
What happened to schools and daycares that remained open despite the pandemic?
Interesting Blog Posts
How one man thinks we can solve the pandemic, and quickly.
What we’ve lost (but can regain).
One opinion on differences between China and America.
Macaques take over a Thai city.
Things I’m Up to and Interested In
I’m not surprised: There is a strong bias in which antidepressant trials get published.
Interesting finding: It’s not that power poses work. It’s that slumping is bad for your mental health and fortitude.
Video I liked: The power of swimming in wild open water.
Counterintuitive result that might not be so counterintuitive when you really think about it: “Enrichment” activities are probably bad, or at least neutral, for kids.
Now I’m worried: A computer describes the Mona Lisa.
Question I’m Asking
How are you playing these days?
One year ago (Jun 21 – Jun 27)
- Intermittent Fasting for Athletes: Benefits and Concerns – What to keep in mind.
- 12 Intermittent Fasting Tips for Athletes – A few tips.
Comment of the Week
“You missed the most important part…how to eat it! You have to pull the bottom of each leaf thru your teeth. I’ve seen people trying to bite and chew the ends.”
– Indeed, Cate. Sidenote: I would support a GMO artichoke whose leaves you could eat in their entirety.
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Contrary to what we’ve been told, cholesterol didn’t evolve to give us heart disease. It’s not here to kill us. The actual roles of cholesterol in the body include insulating neurons, building and maintaining cellular membranes, participating in the immune response, metabolizing fat soluble vitamins, synthesizing vitamin D, producing bile, and kick-starting the body’s synthesis of many hormones, including the sex hormones. Without cholesterol, it’s true that we wouldn’t have heart disease, but we also wouldn’t be alive.
Given all the work cholesterol has to do, the liver is careful to ensure the body always has enough, producing some 1000-1400 milligrams of it each day. Dietary cholesterol is a relative drop in the bucket. And besides, the liver has sensitive feedback mechanisms that regulate cholesterol production in response to how much you get from your diet. Eat more cholesterol, make less in the liver. Eat less, make more in liver.
Now, if cholesterol is so important, why do we worry about it at all? How has it garnered such a bad reputation for giving us heart attacks?
History of Cholesterol and Heart Disease
Heart disease took off in the early part of the twentieth century, and doctors frantically searched for the cause throughout the next several decades. Early studies in rabbits found that feeding them dietary cholesterol reliably increased blood cholesterol levels and induced atherosclerosis that very much resembled human atherosclerosis. Human tests in the fifties initially showed an association between early death by heart disease and fat deposits and lesions along artery walls. Because cholesterol was found to be present in those deposits and because researchers had previously associated familial hypercholesterolemia (hereditary high blood cholesterol) with heart disease, they concluded that cholesterol must be the culprit.
And while it’s true that cholesterol is involved in heart disease, the direct cause-and-effect relationship has not been established. The reality is far more complicated. To get closer to the reality, we must first understand what these cholesterol numbers actually mean.
Cholesterol versus Lipoproteins
Back in those early rabbit studies, researchers discovered a curious thing: even though feeding the rabbits cholesterol spiked their blood cholesterol and gave them heart disease, bypassing the first step and injecting it directly into the blood had no effect. It was completely harmless.
As it turns out, cholesterol doesn’t normally float around the blood by itself. It is contained within lipoproteins. You can think of lipoproteins as delivery vessels. They contain cholesterol, antioxidants, and fatty acids and along the surface have various proteins that direct the lipoprotein to different sites around the body. It’s not the cholesterol that is involved with atherosclerosis. It’s the lipoprotein.
Let’s play the freeway analogy game. Both LDL-cholesterol (LDL-C) and HDL-cholesterol (HDL-C), the standard, basic readings you get from the lab, do not reflect the number of LDL or HDL lipoproteins, or particles, in your serum. Instead, they reflect the total amount of cholesterol contained in your LDL and HDL particles. Hence, the “C” in LDL/HDL-C, which stands for “cholesterol.” Measuring the LDL/HDL-C and then making potentially life-changing health decisions based on the number is like counting the number of people riding in vehicles on a freeway to determine the severity of traffic. It’s data, and it might give you a rough approximation of the situation, but it’s not as useful as actually counting the number of vehicles. A reading of 100 could mean you’re dealing with a hundred compact cars, each carrying a single driver, or it could mean you’ve got four buses carrying 25 passengers each. Or it could be a couple buses and the rest cars. You simply don’t know how bad (or good) traffic is until you get a direct measurement of LDL and HDL particle number.
How does this relate to heart disease?
In my opinion, the most convincing heart disease hypothesis goes like this:
- LDL receptors normally “receive” LDL particles and remove them from circulation so that they can deliver nutrients and cholesterol to cells, and fulfill their normal roles in the body.
- If LDL receptor activity is downregulated, LDL particles clear more slowly from and spend more time in the blood. Particles accumulate.
- When LDL particles hang out in the blood for longer stretches of time, their fragile polyunsaturated fatty membranes are exposed to more oxidative forces, like inflammation, and their limited store of protective antioxidants can deplete.
- When this happens, the LDL particles oxidize.
- Once oxidized, LDL particles are taken up by the endothelium – a layer of cells that lines the inside of blood vessels – to form atherosclerotic plaque so they don’t damage the blood vessel. This sounds bad (and is), but it’s preferable to acutely damaging the blood vessels right away.
- So it’s the oxidized LDL that gets taken up into the endothelium and precipitates the formation of atherosclerotic plaque, rather than regular LDL. OxLDL, poor receptor activity, and inflammation are the problems.
If that’s the case, what exactly is the deal with traditional blood lipid numbers—the ones you get on a standard blood test?
This information is how I view cholesterol as it relates to my individual biology. If you have questions about your cholesterol numbers, discuss them with a qualified health professional.
Standard view: Get that TC below 200, or else you’ll have a heart attack or you’ll have to pay a higher health insurance premium, if the insurers take you on at all.
My take: Mostly meaningless. Even though the epidemiological evidence suggests a TC between 200 and 240 mg/dl is best for all-cause mortality,https://www.ncbi.nlm.nih.gov/pubmed/19903920‘>2
There is an advanced lipid test that’s worth getting: ApoB.
Every single LDL particle has a single ApoB, making ApoB an effective measurement of LDL particle count. By all accounts I could find, ApoB is reliable and accurate. Every LDL particle has one ApoB, and along with TC:HD ratio, ApoB count is a strong predictor of heart disease risk (again, with the caveat that these studies are on populations leading a decidedly unPrimal and highly inflammatory lifestyle).https://www.sciencedirect.com/science/article/abs/pii/S0306987718304729‘>6
But if you’re eating a healthy diet, your performance is good, your body comp is good (or trending that way), your energy and sleep are rock-solid, you don’t have any familial hypercholesterolemia genes—is it really dangerous to have elevated cholesterol numbers?
I don’t know. But I’m skeptical.
For one, “elevated” cholesterol isn’t necessarily linked to heart disease. Sometimes it’s even linked to lower mortality. For instance, in people older than 60, high LDL is associated with lower all-cause and cardiovascular mortality.http://atvb.ahajournals.org/content/20/6/1536.full‘>8https://www.sciencedirect.com/science/article/abs/pii/0891584993900745‘>10
To name a few. Could “high” LDL particles be closer to benign if they’re more resistant to oxidation? I would imagine so. Does resistance mean immunity to oxidation? Absolutely not. Don’t get cocky.
Substantially “elevated” cholesterol, low HDL or high LDL can be a real problem, but they may also just be a symptom of the larger concern rather than the main issue itself. Cholesterol profile can be impacted by other conditions such as hypothyroidism, untreated diabetes or pre-diabetes, pregnancy (surprise!), lactation, stress, liver conditions, heart disease (symptom, not cause of). Even weight loss or fasting can spike cholesterol numbers (turns out burning all that animal fat off your body can have a momentary effect on blood lipids). Talk to your doctor about what your numbers mean in the grand scheme of your health. And see if you can get a read on other markers, like C-reactive protein (an inflammatory indicator), oxidized LDL, and ApoB (or some other marker of LDL particle number).
High cholesterol shouldn’t be ignored, but it’s not the only thing that matters. You have to look at the whole picture. You have to take a step back (or several steps back) and consider everything—not just numbers on a readout.
If you have any more questions about this topic, drop them down below. Thanks for reading, everyone. Take care.
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How bad is working and eating late at night? Wondering why you’re not losing weight? And what if you don’t want to go back to the gym? In this week’s edition of Ask a Health Coach, Erin is back to answer more of your questions. Keep them coming in the comments below or over in our Mark’s Daily Apple Facebook Group.
“My nighttime habits are the worst. I stay up too late working, then I’m hungry and go looking for a snack at 1 or 2 am. I don’t think I should be working and eating that late, but how bad is it really?”
Your intuition is spot on here, Jacob. The late-night artificial light. The late-night insulin spike. The stress of a disrupted sleep cycle. It all comes down to your circadian rhythm, which as reiterated in this study, https://academic.oup.com/jcem/article/89/1/128/2840303)‘>16
Late-night snacking can make the problem worse. Not because “eating late at night causes you to store fat” (as our misinformed culture likes to tell us), but because, in a manner of speaking, your body can either produce metabolism hormones or sleep hormones — not both at the same time. The production of melatonin will slow or cease in order to metabolize your evening snack. This study from scientists at Universidade Federal de São Paulo in Brazil backs it up, finding that men and women who consumed high amounts of calories right before bed spent even less time in REM sleep.https://pubmed.ncbi.nlm.nih.gov/12566476/‘>18
I admit that the scale is the easiest way to measure your progress, but it’s not the most accurate. Most often, when the number changes, it’s due to fluctuations in things like water, glycogen, and waste. Even if the number is consistently going down, there could be a good chance you’re losing lean muscle tissue, not fat!
So, instead of focusing on an utterly pointless number that’s not moving — or moving in the wrong direction — there are better indicators that your body is losing fat. Here are some of my favorites:
- Your pants feel looser
- Your tops close more easily
- Your face looks slimmer
- You’re sleeping better
- You’re less hungry in between meals
- You have more energy
- People are asking if you’ve lost weight
If you’re really interested in knowing how well you’re doing, go ahead and get out the measuring tape. I had a client once who would measure herself consistently each Sunday, keeping an Excel spreadsheet of every single change. From week to week, she was seeing only small changes, but when she looked at the data over the course of a few months it was pretty mindblowing.
The post Ask a Health Coach: Sleep, Weight Loss Stalls, and Skipping the Gym appeared first on Mark’s Daily Apple.
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When you give up sugar, that doesn’t mean you have to give up sweet treats. You can find natural ways to satisfy your sweet tooth without spiking your blood sugar, and that doesn’t mean you have to resort to dangerous artificial sweeteners. Monk fruit is a keto community favorite ingredient to sweeten recipes, but what exactly is it, and where does it come from? Is there any research behind monk fruit? And how do we compare the various formulations next to each other in the supermarket aisle? Let’s break this down.
What Is Monk Fruit?
We’ve covered stevia, yacon syrup, allulose, and Swerve, but what about another popular choice in the growing selection of natural sweeteners — monk fruit? Known as Luo Han Guo in its native southern China, monk fruit (Siraitia grosvenorii) first found acclaim in the records of 13th century Luo Han Buddhist monks. The monks valued the natural sweetness of the fruit and made it their mission to cultivate the vines through the centuries. Today, most monk fruit cultivation still occurs in the misty mountains of China’s Guangxi provincehttps://link.springer.com/article/10.1007/s00216-012-6693-0‘>2 called mogrosides, with mogroside V having a sweetness 250 times that of table sugar.3 To put that sweetness in perspective, most people consider just 1/64 of a teaspoon of monk fruit extract to taste as sweet as a full teaspoon of table sugar.
But to get this natural “zero calorie” sweetener, much of the natural compounds in the fruit are lost. Most producers treat “pure” monk fruit sweeteners to remove off-flavors, then they dry it to remove other sulfurous volatiles. Finally, it gets homogenized and pasteurized. The resulting extract is very different from its original state, slightly undermining its purported status as a natural sweetener.
Other less processed natural monk fruit sweeteners provide a more wholesome version of the original fruit, but with the arguable downside of containing a small amount of glucose and fructose. More carbs also tend to mean fewer mogrosides, and hence a lower relative sweetness.
Pure Monk Fruit Sweetener vs. What’s On Grocery Shelves
Contrary to what people might claim, fresh, unprocessed monk fruit is not sugar-free. It varies between cultivar and growing region. Still, fresh monk fruit is typically one-third carbohydrate, composed of a mix of fructose and glucose.
After you extract the juice, much of those carbs are left behind. At this point, a minimally-processed monk fruit extract sweetener might only contain small amounts of sugars in the form of fructose or glucose. At this point, it becomes a low-calorie natural sweetener. A half teaspoon serving of monk fruit juice powder, for example, is made up of 10% sugar, and the rest of the carbs presumably come from of mogrosides and other indigestible sweet-tasting compounds.
At the other end of the scale, pure monk fruit extracts are zero-calorie sweeteners, with no carbs and no sugar. Manufacturers are sometimes hesitant to sell straight monk fruit extract, however, because it’s easy to overdo it when you mix it into recipes. To add bulk, manufacturers will mix in small amounts of other sweeteners like erythritol or xylitol. It’s not uncommon to find sucrose or dextrose lurking on the ingredients list of so-called natural monk fruit sweeteners, but the amounts would be pretty minimal. Check labels to be sure.
While monk fruit contains several different mogrosides, https://academicjournals.org/journal/AJPP/article-abstract/088D6DA28337‘>5 Another study showed that obese mice fed mogrosides from monk fruit had significantly reduced body and liver weights compared to control mice.https://onlinelibrary.wiley.com/doi/abs/10.1002/mnfr.200500252‘>7
In another study, diabetic rats were fed monk fruit extract for 13 weeks. Those rats fed the monk fruit extract showed improved insulin response, reduced blood sugar levels after glucose administration, and reduced oxidative stress caused by diabetes. What’s more, the monk fruit group also showed signs of lowered kidney damage, a common symptom of advanced diabetes.https://europepmc.org/abstract/med/21351724‘>9
You get the idea. Once again, more studies in humans are needed to make any definitive conclusions.
Here are some tested and true recipes that use monk fruit:
Possible Anti-cancer Benefits of Monk Fruit
While research is very much in its infancy regarding the link between monk fruit and cancer, there’s likely to be more on the horizon. A 2016 study https://pubs.acs.org/doi/abs/10.1021/jf0206320‘>11 showed that a range of triterpenoids (including several mogrosides) isolated from monk fruit showed “potent inhibitory effects” on Eppstein-Barr Virus-induced tumor growth.
It makes plenty of sense, as multiple studies have highlighted the antioxidant 12 powers of mogrosides found in monk fruit sweeteners.
Anti-Inflammatory Properties of Monk Fruit
A 2011 study indicated that mogrosides administered to mice significantly reduced inflammation by quieting genes that trigger inflammation and up-regulating anti-inflammatory genes.https://www.tandfonline.com/doi/abs/10.3109/13880209.2013.867451‘>14 Researchers have shown that monk fruit extracts reduce physical fatigue in mice (allowing them to swim for longer).http://en.cnki.com.cn/Article_en/CJFDTOTAL-YYXX200603010.htm‘>16 At the end of the trial, both mogroside groups (but particularly the low-dose group) showed significant protection against diabetes-induced immune dysfunction. Interestingly, this immune-bolstering effect was only apparent in immune-suppressed diabetic mice, suggesting it plays a vital role in restoring homeostasis in the body.
Specific monk fruit isolates’ anti-bacterial properties http://en.cnki.com.cn/Article_en/CJFDTotal-AHNY201403050.htm‘>18 That said, the use of highly concentrated monk fruit sweeteners is very much in its infancy. Moderation is a safe bet.
Tips For Buying and Using Monk Fruit Sweeteners
Which product you choose will depend on your preference. Those who prefer an entirely non-caloric formulation will want to go with pure monk fruit extract. Or you may prioritize less-processed versions, which might contain a small amount of simple sugars and a little less mogroside.
At the other end of the spectrum, those who have a hard time measuring pure monk fruit, or want to cut down on the aftertaste might opt for a blended product that includes erythritol, xylitol, and stevia.
While most people enjoy the taste of monk fruit, it’s not necessarily for everyone. Taste descriptors vary markedly from person to person, with some noting it tastes like caramel or molasses, others more like sweet licorice. Keep in mind that the more refined the monk fruit sweetener, the more it loses its butterscotch character, and the sweeter it will taste.
And speaking of sweetness, remember that mogroside V, the key ingredient in most monk fruit sweeteners, is up to 250 times sweeter than sugar, so a little goes a long way. Most labels provide a sugar substitution guide for recipes.
How to Use Monk Fruit Sweetener
How you use monk fruit sweeteners will also depend on your taste preferences. Some common uses include:
- Baked goods
- Sauces and salad dressings
- Fruit/vegetable-based drinks
- Asian dishes that call for a dash of sweetness
That’s just the beginning. Experiment, and see how it might work for you and your family.
Thanks for stopping by, folks. Have you used monk fruit as a sweetener, or would you consider trying it? Be sure to share your thoughts below.
- and free radical-scavenging [ref]https://www.sciencedirect.com/science/article/pii/S0271531708000365
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