Mark Sisson's Blog, page 82

Dear Mark: Mortality Risk, Fish Heads, Metformin and Exercise, and Cooking Frozen Veggies

For today’s edition of Dear Mark, I’m answering four questions from readers. First, what does an “increased risk of mortality” actually mean if everyone’s going to die in the end? Second, what makes fish heads so delicious and nutritious? Third, what is the relationship between metformin and exercise? And finally, how do you prevent frozen vegetables from getting all mushy when you cook them?

Let’s go:

Hey Mark,

In regards to the “garbage” meat study, how does relative versus absolute risk work? Does 3% increased risk of dying mean that if my chance of dying this year based on mortality tables is say, 10%, if I eat red meat my chance of dying is 10.3%?

Thanks,

Steve

Yep, you got it. It means that for the duration of the study, the subjects eating more meat had a 3% higher risk of dying. Some people lived, some died.

It’s not open-ended, though (because as everyone knows, everyone dies someday). The risk is confined to the duration of the study.

Since you mentioned eating whole organisms, I was wondering if there are any specific nutritional benefits to fish heads? I can get really cheap great fresh fish heads from my fishmonger which are fantastic steamed, and I’m curious as to their nutritional value. I can’t get much data on the heads particularly—surely the eyes and fish brain must have some unique stats and benefits? And while I’m at it… could I overdose on them? How much would be too much too consume each week in your opinion?

Grizzlies know the deal. During salmon season, they camp out on the river and snag salmon on their way to spawn. They’ll often eat the brain, eyes, roe, and belly, then toss the rest. They’ll go through dozens of them in a day, focusing only on the head and belly. Why? What’s good about the head?

Let me tell you about the beauty of the fish head.

The brain: A cow brain is incredibly rich in omega-3s, especially DHA. A salmon brain is INSANELY rich in omega-3s. Not only that, they are in phospholipid form, a structure that’s far more bioavailable than other types of fatty acids. The roe of a salmon is another excellent source of phospholipid-bound omega-3s.

The eyes: Eyes in general (like yours) are also loaded with DHA. A fish eye will have even more.

But a fish head is also delicious, not just nutritious (although the two often pair up, especially when you’re talking about whole Primal foods).

You’ve got the collar, that meaty ring of flesh and skin. Any Japanese spot worth its salt will have grilled yellowtail (hamachi kama) or salmon collar on their menu. Get it—it’s a great deal and a marriage of meat, skin, and collagen.

You’ve got the cheeks, unctuous bits of tender fish meat.

You’ve got the skin, which is incredibly fatty and collagenous.

You’ve got the brain, whose nutritious merits I’ve extolled. The brain is mild.

The eyes are pretty good, too. A bit chewy with a large deposit of collagen.

And if you’re willing to get messy, you can just dissect the head and look for the meat, fat, and skin. A good-sized wild salmon head roasted in the oven with just some salt and pepper is a solid meal that leaves you incredibly satiated because it’s so nutrient-dense.

Peter Attia has noted that in healthy people (non T2D, no metabolic issues) metformin blunts the benefits of exercise, especially the Primal type of low-intensity training. It therefore may decrease mitochondrial function. In other words, the more healthy you are, the less helpful metformin may be and can possibly make you less healthy, though that is not completely confirmed. Basically, if you’re healthy and Primal and do some intermittent fasting here and there, you may at best not benefit by taking metformin. See his podcast with Iñigo San Millán for more details.

There’s definitely something to this.

According to an interesting study in older adults without chronic disease, metformin actually inhibits mitochondrial adaptations to aerobic training. Exercising increases insulin sensitivity, unless you take metformin. Exercises improves mitochondrial respiration in the muscles, unless you take metformin.

It also appears to blunt the anabolic response to strength training in older men. In this study, those taking metformin and training saw less muscle gain than those training and taking a placebo. If true, this is a big blow against metformin supplementation for this population. The older you are, the more muscle you need to stay healthy and avoid morbidity. Every gram of muscle is crucial.

And it’s not just in “healthy” people. For instance, type 2 diabetics who take metformin and exercise regularly have worse glucose control than those who do neither. The authors of the study suggest that it may be “too much of a good thing”—that trying to stack metformin and exercise leads to a counter-signal, reversing the benefits.

Metformin might make exercise feel harder. Of course, it also increases fat-burning during exercise, and if you’re not used to burning fat during exercise, a sudden shift in that direction might  make your workout feel harder.

There’s a confusing relationship between exercise and metformin for sure.

I’m not sure what to think about metformin, to be honest. Another interesting study came out in the middle of last year comparing metformin alone to an intensive lifestyle modification program for weight loss. What happened?

Around 29% of the subjects who took metformin lost at least 5% of their weight in the first year. Almost 65% of the subjects who underwent the lifestyle program lost at least 5% of their weight.

Then, they followed up to see who’d kept the weight off from year 6 to year 15.

The metformin group won this one; 6.2% of that group maintained the weight loss while just 3.7% of the lifestyle group did.

So metformin can definitely help your average person who can’t (or won’t) maintain the lifestyle changes necessary to make a real difference. But if you can maintain the lifestyle that brings so much initial success—the diet, the training, the sleep, and everything else—it’s far superior than any pill you can take.

I would really appreciate any suggestions on how to cook frozen vegetables to make them taste delicious and crisp rather than soggy and limp… many thanks.

The trick is to use high heat. Whether you’re going to roast your veggies in the oven or cook them in a pan, you must get everything good and hot before introducing the vegetables. That means preheating the pan with fat (avocado oil works great here, obviously) before you add the vegetables. Cast iron can help here, as it really gets hot and holds that heat.

If you’re using the oven, hit 450°F or so. If you’re using the stove, go medium-high to high heat.

Also, don’t crowd the pan and cool things down by overfilling with frozen plant matter. You want room between each piece of vegetable. You want them to caramelize and crisp, not steam.

Thanks for reading, everyone. Take care, ask any followups you might have, and have a great day!

The post Dear Mark: Mortality Risk, Fish Heads, Metformin and Exercise, and Cooking Frozen Veggies appeared first on Mark's Daily Apple.

How Long Does It Take Get Rid of Sugar Cravings After Going Keto?

One of the purported benefits of a keto diet is that it will help tame unwanted sugar cravings. On the surface, it makes sense. If you want to get rid of sugar cravings, stop including a bunch of sugar in your diet. Out of sight, out of mind.

Or does it make sense? Maybe following a ketogenic diet where even nutrient-dense carbs are limited turns sweet foods into forbidden fruit (no pun intended). Sugar could theoretically become even more tempting because you can’t have it.

So which is it?



It’s clear that for a lot of people, keto does kick sugar cravings to the curb. There is abundant (anecdotal) evidence from the Keto Reset community and indeed across the keto-sphere that keto works to quash cravings and hunger. Empirical studies back this up. Compared to other diets, people find it easier to stick to their goals on keto. It’s one of the big reasons keto is so popular right now.

Of course, the next question people always ask is: How long does it take?

When Can I Expect My Sugar Cravings to Vanish?

It takes two to three days of very-low-carb eating for the liver to start pumping out ketones, and research shows that cravings are significantly reduced almost immediately as people get into ketosis. The “expert” consensus seems to be that cravings will decrease noticeably within three to ten days.

Don’t expect cravings to vanish into thin air, though. While many folks do feel significant relief from cravings almost right away, not everyone is so lucky. There is a lot of individual variability, and some people do find that their cravings are as strong as ever—or stronger—on keto. Although there’s not much research that speaks to why some people get relief where others do not, my hunch is that it depends on the root cause of your sugar cravings.

One reason you might crave sugar is simply that you’ve trained your body to rely on sugar for energy—you’re carb-dependent. Perhaps it’s not the sugar you crave specifically, so much as the energy it provides. In that case, you should notice your desire for sugar is significantly reduced as soon as your body starts to produce ketones. Moreover, I’d expect it to get easier and easier to avoid sugary treats as you become more keto-adapted.

Sugar cravings can also be conditioned (learned) responses. Decades of experience have taught you that eating sugary treats is comforting and enjoyable. You’ve come to have a strong positive association with sugar. In some ways, you might think of eating sugar as a very entrenched, reinforced habit you need to break. Habits can be broken, but it takes weeks or months, not days.

The complicating factor here is that sugar is not just pleasant or fun to eat, it’s also physiologically rewarding. Sugar activates neurological reward pathways, creating a physiological drive for more sugar.

For some people, sugar is so rewarding that it feels like an addiction. These are the folks who struggle the most. The question of whether sugar is a true addiction, on par with other addictive substances like nicotine, alcohol, and certain drugs, is hotly contested. Academic debates aside, many people experience sugar, and quitting sugar, as an addiction. They struggle mightily even when motivation and intention are high. One “relapse” can send them spiraling. There is no doubt that there are physiological drivers at play that keep the desire for sugar burning so hot in these individuals.

All this is to say: It’s different for everyone.

What If You’ve Been Keto For a While, Yet You’re Still Struggling with Sugar Cravings?

What does “a while” mean? As I mentioned, it takes only a matter of days for your liver to start producing ketones once you drop your carbs low enough. The full process of keto-adaptation can take months, though. A recent review concluded that while fat-oxidation rates and ketone production increase significantly in the first week or two of keto, it can take months for the whole body to become efficient at using ketones for energy.

You don’t want to wait that long, though. There are other things you can do to fight back against sugar cravings. First, make sure you are properly fueled. Caloric restriction increases the reward value of food. That means you’re more drawn to food, especially palatable foods, when you’re eating in a caloric deficit, at least at first. That’s one of the reasons I suggest eating plenty of fat and sufficient calories when transitioning to keto.

If you’re also restricting calories, chances are your cravings will diminish according to this meta-analysis, but it will happen slowly over the course of months. (The analysis also showed that it gets easier and easier over time. Good news if you can stick with it.)

It’s Not Always About the Food

Next, ensure you have your lifestyle ducks in a row. Sleep deprivation and chronic stress have been shown time and time again to cause sugar cravings as the body scrambles for quick energy. Even dehydration and boredom can trigger hunger and cravings. If you want to get rid of sugar cravings, you need to practice good self-care.

You crave sugar due to the hormonal response to those stressors, but don’t underestimate the comfort factor here, too. It doesn’t feel good to be sleep deprived, stressed, and bored. There’s a good chance you’ve used sugar in the past to lift your spirits. If you’re using sugar to self-soothe, you also need to develop better coping mechanisms.

Dig deep and look at what really underlies these sugar cravings. I suggest you start journaling about your cravings. Each time a sugar craving hits, make a note of the following:

How you’re feeling (bored, anxious, nervous, angry, etc.)
Time of day
Hunger: what time you last ate, and what you ate
Where you are
Who’s around
Any other clues to possible triggers.

After a week or two, you might be able to spot some patterns. If it’s obvious that there are specific trigger(s) like time of day, workplace stress, or fatigue that precede your cravings, work at developing other coping methods that aren’t food-related. Solve the root problem. Meditate, exercise, drink a glass of water, eat an actual meal or snack with some protein and healthy fat.

Finally, try a period of cold turkey if you haven’t yet. Eliminate all sweeteners, even keto-friendly ones like stevia. Look at your fruit and beverage habits. See if you’re still using “sweet” even if you’ve eliminated the major sources of refined sugar from your diet. On the flip side, if you’ve been cold turkey, consider allowing yourself some low-glycemic fruit, for example. Maybe being too restrictive doesn’t work for you. Try to find your personal sweet spot.

Check out this Mark’s Daily Apple post for more concrete ideas for managing cravings.

If you have tried the strategies I suggested, you’ve given yourself enough time to be fully keto-adapted, and you truly feel addicted, it might be time to seek out a doctor, nutritionist, or therapist that specializes in sugar dependency. For you, there might be physiological factors at play that mean you need additional support.

Remember, though, that occasionally wanting or even craving sugar doesn’t mean you’re doing something wrong. Don’t beat yourself up. You might need to adjust your strategy, or it might just be a blip on the radar. Once you’re metabolically flexible, you can decide on a case by case basis how to respond.

Related Posts from Mark’s Daily Apple:

Dear Mark: Your Brain on Junk Food
The Definitive Guide to Sugar
Dear Mark: Sugar Cravings
Why We Eat: Cravings

 

References:

Anton SD, Moehl K, Donahoo WT, et al. Flipping the Metabolic Switch: Understanding and Applying the Health Benefits of Fasting. Obesity (Silver Spring, Md.). 2018 Feb;26(2):254-268.

Avena NM, Rada P, Hoebel BG. Evidence for sugar addiction: behavioral and neurochemical effects of intermittent, excessive sugar intake. Neurosci Biobehav Rev. 2008;32(1):20–39.

Berridge KC, Robinson TE, Aldridge JW. Dissecting components of reward: ‘liking’, ‘wanting’, and learning. Curr Opin Pharmacol. 2009;9(1):65–73.

DiNicolantonio JJ, O’Keefe JH, Wilson WL. Sugar addiction: is it real? A narrative review. British Journal of Sports Medicine 2018;52:910-913.

Phinney SD, Horton ES, Sims EA, Hanson JS, Danforth E Jr, LaGrange BM. Capacity for moderate exercise in obese subjects after adaptation to a hypocaloric, ketogenic diet. J Clin Invest 1980;66(5):1152–61.

Volek JS, Freidenreich DJ, Saenz C, Kunces LJ, Creighton BC, Bartley JM, Davitt PM, Munoz CX, Anderson JM, Maresh CM, et al. Metabolic characteristics of keto-adapted ultra-endurance runners. Metabolism 2016;65(3):100–10.

Wiss DA, Avena N, Rada P. Sugar Addiction: From Evolution to Revolution. Front Psychiatry. 2018;9:545.

The post How Long Does It Take Get Rid of Sugar Cravings After Going Keto? appeared first on Mark's Daily Apple.

Keto Bison Burger

What Primal, keto, or low-carb eater doesn’t love a burger? You can never have too many burger recipes in my opinion, and this bison burger makes a tender, flavorful patty topped with just enough gooey cheese to add a cloak of rich saltiness. We topped our keto bison burger with sautéed mushrooms, pungent thinly sliced red onion, a slice of bright and acidic tomato, and Primal Kitchen Spicy Ketchup. Wrap in butter lettuce leaves, and you have an all-in-one handheld dinner or lunch that’s easy to switch up according to your tastes or what you have on hand in the kitchen. Use your favorite ground meat in lieu of bison: grass-fed beef, chicken, or turkey would be great substitutes. These burgers would also be delicious with Primal Kitchen Spicy Mustard.

Keto Bison Burgers

Time: 20 minutes

Servings: 4

Ingredients

Burgers:

1 lb. bison, ground
½ cup parsley, chopped
4 cloves garlic, garlic
½ tsp. salt
¼ tsp. black pepper
1 Tbsp. Primal Kitchen Avocado Oil or Olive Oil

Mushrooms:

8 oz. mushrooms, sliced
1 Tbsp. salted butter
Salt and pepper, to taste

Fixings:

8 butter lettuce leaves, separated
½ tomato, sliced (about ½ cup)
½ red onion, thinly sliced (about ¼ cup)
2 oz. cheddar cheese
¼ cup Primal Kitchen Spicy Ketchup

Instructions

Preheat your oven to 375ºF. In a large bowl, combine the ground meat, chopped parsley, grated garlic, salt, and pepper. Form four patties and make a slight indent in the center of each of the patties. Set aside.

Melt the butter in an oven-safe pan on your stovetop over medium heat. Once melted, add the sliced mushrooms and sauté for 3–5 minutes, or until soft. Sprinkle with salt and pepper. Once soft, set aside.

Add the avocado or olive oil to the same pan and heat over medium heat. Once hot, add the patties. Sear for 1–2 minutes on both sides. Transfer the pan to the oven and continue cooking until the patties reach your desired doneness.

Add the cheddar cheese to the tops of the burgers and increase the oven temperature to 425ºF. Place the pan back into the oven for a few minutes until the cheese is melted. Remove the pan from the oven and set aside.

Build your burgers by placing 1–2 pieces of lettuce on a plate. Place the burger on top, followed by a slice of tomato, 1–2 slices of onion, ¼ of the mushrooms and a dollop of Primal Kitchen Spicy Ketchup. Top with 1–2 more lettuce slices, and enjoy.

Nutrition Information (1 burger, ¼ of mushrooms, and fixings):

Calories: 335

Total Carbs: 7 grams

Net Carbs: 8 grams

Fat: 22 grams

Protein: 29 grams

The post Keto Bison Burger appeared first on Mark's Daily Apple.

Weekly Link Love – Edition 67

Research of the Week

Sales taxes work better than fat taxes.

More breastfeeding, more mitochondria in blood in adolescence.

Traditional architecture gives a better sense of well-being than modern architecture.

Garbage anti-meat study. I’ll address this in Sunday with Sisson. (If you don’t already subscribe to our emails, sign up here to read Sunday with Sisson.)

New Primal Blueprint Podcasts

Episode 402: Courtney Contos: Elle Russ chats with Courtney Contos, chef, wellness expert, and certified Functional Medicine Health Coach.

Primal Health Coach Radio, Episode 46: Erin and Laura chat with Robb Wolf, the man himself.

Media, Schmedia

Starbucks shifts away from dairy.

The cartels turn to avocados.

Interesting Blog Posts

A different way to think about agriculture.

Social Notes

Who needs tortilla chips?

Everything Else

This is the future I always dreamed of.

Paul’s response.

Things I’m Up to and Interested In

Chat I enjoyed having: “The Great Fiber Myth” with Shawn Baker, Paul Saladino, Brian Sanders, and yours truly.

I have to ask why: Toddler milk.

Good deal I’m passing along: 20% off Tribali food orders with discount code “Primal20.”

Interesting diet: The Everest Diet.

Someone else goes carnivore: Joe Rogan’s experience.

Question I’m Asking

Is very high LDL cholesterol always a problem?

Recipe Corner

Tex-Mex beef and rice casserole, for those higher-carb days.

Lasagna… soup?

Time Capsule

One year ago (Feb 1 – Feb 7)

10 Moves to Help Ease Joint Pain — Lube for your tissues.

Can I Eat Fruit on a Keto Diet? — Can you?

Comment of the Week

“I’ve been telling my kids that success is like a lottery and that school, work experience, travel, and your social network are the lottery tickets.”

I like that, Mike.

The post Weekly Link Love – Edition 67 appeared first on Mark's Daily Apple.

Dear Mark: How Often I Eat Organ Meat and Should You Take Metformin for Longevity?

For today’s edition of Dear Mark, I’m answering a couple questions taken from Instagram followers. Normally every Wednesday, I do a quick Q&A on Instagram. I wasn’t able to get to them last week so I’ll be answering some here on the blog. First, how often do I eat organ meat, and how do I like it? And finally, what’s the deal with using metformin for longevity?

Let’s go:

How often do you eat organ meats?

Maybe twice a month. I should probably do it more.

It’s not that I dislike them. Every time I eat heart or liver, I enjoy it. It’s not something that comes intuitively to me. Because I wasn’t raised in a household where organs were a normal part of the daily diet, I have to remind myself to do it.

If you’re counting marrow, I eat that far more frequently. I order it every time I see it on a menu. I eat lamb chops frequently, which often come with little pockets of marrow.

And personally, I include eggs and shellfish as “organs.” Reason being, you’re eating the entire organism. The whole animal. Well, the egg isn’t an animal yet, but it contains everything one needs to construct an entire animal. These tend to be far more nutrient-dense than muscle meats.

If you’re looking to eat more organs, there are some great options.

You can go the product route. US Wellness carries fantastic organ sausages. Check out the braunschweiger (60/40 blend of grass-fed beef and grass-fed beef liver) or the liverwurst (GF beef, liver, kidney, heart). I’ve crumbled these up into ground beef and mixed into spaghetti sauce.

You can usually ask any butcher to make sausages or meat grinds with different muscle/organ ratios. You could do 70% beef chuck with 15% liver and 15% heart, or whatever ratio you prefer.

Ancestral Supplements does great organs in supplement form.

There are awesome recipes out there that “hide” the organs. I wrote an entire post on slipping organs into normal meals that you don’t even notice.

Or you could just figure out a way to cook organs that you’ll consistently enjoy and consume. Here are some of my favorite ways:

Ginger garlic chicken liver: Chop chicken liver into small pieces. In a pan, sauté ginger and garlic in butter or avocado oil. When it’s all softened, add a generous cup of gelatinous bone broth and reduce, reduce, reduce. When it’s getting syrupy, drop in the liver and stir over medium high heat for 2 minutes. The liver will cook quickly without overcooking.
Beef liver sashimi: Get the best, freshest organic grass-fed beef liver you can find. Slice thin and marinate in fish sauce, sesame oil, and lemon juice for an hour. Eat raw, or briefly sear in a pan. If eating raw, might be advisable to freeze for two weeks first.
Chicken heart skewers: Marinate chicken hearts in lemon juice, soy sauce, and a little bit of honey. Place on skewers and grill over coals or flame.
Lamb/beef heart steaks: Slice a heart into steaks. Season with salt and pepper, and place on roasting rack in a 275°F oven for 15 minutes. Remove and sear briefly over high heat on both sides. Do not overcook. It will get tough and inedible.

What’s your take on supplementing Metformin for longevity?

There are certainly reasons to suspect it could help.

Metformin activates AMPK, the same autophagy pathway activated by exercise, fasting, polyphenol consumption, and reduced calorie intake.

Metformin also seems to protect against many of the conditions that kill people, like cancer. It lowers hyperinsulinemia and may protect against insulin-related cancers (breast, colon, etc.). Early treatment during adolescence, for example, protects rats against later tumor growth.

Type 2 diabetics (a population with lower overall mortality) who take metformin live longer than age-matched controls who don’t have diabetes. That’s huge. Type 2 diabetes isn’t enough to offset the longevity gains.

Metformin appears to work on lifespan via hormesis. Diabetics who need it just to keep their blood sugar in check are taking (and should take) it regularly, but if you’re just an experimenter interested in potential life extension, treating it like a hormetic input like fasting or intense exercise is probably a better, safer approach. Instead of daily, maybe intermittently. Cycle it.

It appears that metformin may also act via modulation of the gut bacteria (surprise, surprise). It increases mucus production in the gut, which the resident bacteria are able to feed upon and increase in strength and number. It’s been shown to boost Akkermensia count, the strain commonly linked to leanness and anti-diabetic effects. Some studies have even shown that Akkermensia can improve gut barrier function in obese subjects, so metformin may be especially helpful for this population. Additional effects include reduced carb absorption by the host (that’s you), leaving more to be consumed by gut bacteria (a la resistant starch).

If you don’t want to (or can’t) find real metformin, berberine might be a “natural alternative” to metformin. Like metformin, berberine can activate AMPK, lower blood sugar and improve blood sugar control, and enhance short chain fatty acid production by gut bacteria. Being a whole plant extract, berberine isn’t identical to metformin, so I wouldn’t suggest diabetics switch without consulting their doctors, but it is a promising alternative that doesn’t require a prescription. It might be a viable alternative for someone looking to improve their longevity.

Overall, metformin looks promising. I’m not sure it’s an essential part of a longevity-promoting regimen if you’re already fasting, training, and eating colorful polyphenol-rich fruits, vegetables, spices, and dark chocolate. Many of the populations it seems to help in studies aren’t doing these things and metformin is likely acting as a “healthy living mimetic”—but I’m certainly open to the idea, and await further research.

That’s it for today, folks. Take care and keep the questions coming! If you have anything to add or ask, go for it down below.

The post Dear Mark: How Often I Eat Organ Meat and Should You Take Metformin for Longevity? appeared first on Mark's Daily Apple.

What Might Fasting Insulin Predict About Health?

In the comment section of my recent Definitive Guide to Blood Sugar, someone asked about fasting insulin. What does it predict? Is it the preeminent health marker? Does it actually cause harm, or is it just an indicator? Great questions and a great idea, I thought. Let’s do it. Let’s dig in.

It looks like it’s all true. Elevated insulin is both a direct cause of certain unwanted health conditions and an indicator of several other unwanted health conditions.



There are difficulties inherent to insulin. It varies wildly. There is no universally-agreed-upon reference range for healthy and unhealthy insulin levels. In the studies that find connections between elevated insulin and disease, they use quantiles—breaking up the subjects into groups of low, medium, and high insulin levels. It’s all relative.

We need to figure out what normal looks like. We can’t measure the insulin levels of paleolithic hunter-gatherers (insulin degrades pretty quickly and cannot be recovered from fossils). We can look at extant hunter-gatherers, but those are slipping away with every passing year (and to my knowledge, no one has actually tested the Hadza or Tsimane). The best way do it would be to measure the fasting insulin in a healthy, non-industrialized population largely free of disease, like the Kitava of the South Pacific. Staffan Lindeberg did test their fasting insulin levels, finding them to be very low—an average range of 3-6 uIU/mL in both men and women of all ages. He then compared them to modern Swedes, whose insulin ranged from 4-11 uIU/mL and went up with age. The average American fasting insulin runs about 8.4 uIU/mL, which likely isn’t physiologically normal.

That the Kitavans’ fasting insulin was relatively low and consistent throughout their entire lives, and they were largely free of the degenerative diseases that plague industrialized societies, suggests that a fasting insulin somewhere between 3-6 uIU/mL is the physiological norm for humans. It’s what we should be walking around with.

What’s the problem, exactly, with hyperinsulinemia?

Insulin and Overweight

One primary function of insulin is to suppress lipolysis—the release of fatty acids from body fat to be burned. This makes sense. You eat carbohydrates, glucose goes up, and the glucose has to go somewhere. Insulin rises to help you dispose of the glucose and suppress the release of free fatty acids. It’s harder to burn fat when glucose is in the picture, and insulin keeps fat locked away so you can dispose of the glucose.

Studies as far back as the 80s are pretty clear that the higher your insulin level, the higher your hunger and the more you eat. These aren’t just observational, either. Researchers actually pushed subjects’ insulin higher or lower, both with and without increasing their glucose, and found that raising their insulin was the most reliable way to increase hunger, food intake, and junk food cravings.

So hyperinsulinemia hits you from two sides:

It prevents you from burning your own body fat.
It makes you hungrier than your energy stores would actually suggest you should be.

That’s probably why a recent study found that reducing insulin could reduce diet-induced weight gain.

Insulin and Cancer

Another major function of insulin is to make things grow. This is an important function that makes total sense in certain situations, like when you’re trying to gain muscle, heal a wound, or if you’re a toddler who needs to grow your skeleton and get taller. But there are times where cellular growth is unwanted. Consider cancer, a disease of unchecked cellular growth. It’s no surprise that hyperinsulinemia is a risk factor for most, if not all cancers. 

While insulin isn’t everything when it comes to cancer, the links are undeniable and myriad—and worrying.

The link between colon cancer and hyperinsulinemia likely involves the tendency of insulin to increase the availability and potency of insulin-like growth factor. Post-menopausal women with genetic variants related to insulin resistance and hyperinsulinemia have a greater risk of colorectal cancer, and colon cancer patients who eat the most insulinogenic foods have poorer outcomes.

In breast cancer, hyperglycemia increases the tumors’ resistance to chemotherapy. Fixing the hyperglycemia makes chemotherapy more effective.

People with a genetic predisposition toward hyperinsulinemia have a higher chance of developing pancreatic cancer.

Independent of bodyweight, hyperinsulinemia predicts endometrial cancer; so does a high postprandial insulin response.

Diabetics who use insulin therapy have an increased risk of liver cancer. One study of Taiwanese diabetics found that those on insulin therapy have an elevated risk of dying from cancer and from non-cancer.

Most cancer cells overexpress insulin receptors, suggesting a unique affinity of cancer for circulating insulin.

Across the board, in both obese and people of normal bodyweight, hyperinsulinemia, whether it’s genetic, simulated, or diet-driven, increases cancer incidence and mortality. 

Okay, okay. That’s all rather convincing, but there’s a chance that these are merely associations and some common factor is causing both the hyperinsulinemia/insulin resistance and the cancer. Right?

What seems to counter that hypothesis is the effect of metformin, an anti-diabetic drug, on cancer. Compared to other diabetic drugs, metformin reduces the risk of cancer in type 2 diabetics. Metformin’s mechanism of action? A reduction in insulin levels and improvement of insulin resistance.

Insulin and Heart Disease

As far as heart disease risk factors go, hyperinsulinemia might be the strongest one yet. Hyperinsulinemia predicts the risk of heart attack. And it’s an independent risk factor. That’s key. You can control for LDL cholesterol, LDL particle number, triglycerides, HDL cholesterol, and it doesn’t matter. You can control for blood pressure and family history of heart disease, and it doesn’t matter. Among middle-aged men who do not have heart disease, hyperinsulinemia remains a significant and independent predictor of their risk of having a heart attack.

What about ApoB, the lipoprotein biomarker that most of the top cardiovascular health experts are pointing to as “causative” of heart disease? It’s actually one of the better predictors of insulin resistance and hyperinsulinemia. Whichever way you approach heart disease, insulin keeps popping up. Can’t escape it.

These are association studies, but the mechanisms for causality exist. As far back as 1990, researchers had established the pro-atherogenic effects of elevated insulin levels. As a review from that year explains:

Long-term treatment with insulin results in lipid-containing lesions and thickening of the arterial wall in experimental animals. Insulin also inhibits regression of diet-induced experimental atherosclerosis, and insulin deficiency inhibits the development of arterial lesions.

Could what they call an “insulin deficiency” be physiologically-normal levels of insulin? Could we all use a little “insulin deficiency”?

Insulin and Hypertension

Elevated insulin levels lead to sodium retention and water retention, which increases blood pressure. Dropping insulin—like, say, by eating a low-carb or keto diet—will counteract this effect and reduce blood pressure.

That’s why hyperinsulinemia is a consistent and independent predictor of hypertension, especially in women. Controlling for BMI doesn’t affect this relationship.

Insulin and Arthritis

There is growing evidence that insulin has an inflammatory effect on joints, reducing collagen deposition and increasing collagen degeneration. That’s in vitro research, but it jibes with many hundreds of anecdotes from people who went keto or low-carb or carnivore, dropped their insulin, and improved their arthritis—and with the common experience of reintroducing carbs and seeing the pain return.

Insulin and Fatty Liver

Among patients with non-alcoholic fatty liver, insulin resistance is almost a law. It’s very rare to see fatty liver without elevated insulin levels. Cause or effect?

Well, one job of insulin is to shove glucose into cells. It does this quite well, so long as there are vacancies. If the cell is already loaded with glucose, the liver converts the glucose into fat in a process called de novo lipogenesis. Some of this fat is exported to other cells, but a large portion is stored in the liver, especially in hyperinsulinemia.

Insulin and Mortality

Mortality is the endpoint of all endpoints. When it comes down to it, we’re trying to avoid dying. We don’t hope to live forever, but we do hope to live long and well as late into the game as possible. One way to do it is to reduce our insulin levels.

In cancer patients, for example, those who eat the most insulin-producing foods have worse cancer and overall mortality.

In middle aged adults, hyperinsulinemia predicts cancer mortality, even when you control for diabetes, obesity, and metabolic syndrome.

In older adults with type 2 diabetes, insulin use predicts mortality.

You won’t find a dietary philosophy that promotes the “benefits of hyperinsulinemia.” At the very worst, you might find folks who think elevated insulin is merely an indicator, and not a cause of disease. But this is one of those areas where almost everyone agrees “less is better.”

Where people disagree is on how to reduce hyperinsulinemia and maintain a healthy insulin level. That’s a post for another time.

Thanks for reading, everyone. Take care and be well, and may your insulin levels approach that of a Kitavan!

References

Chakrabarti P, Kim JY, Singh M, et al. Insulin inhibits lipolysis in adipocytes via the evolutionarily conserved mTORC1-Egr1-ATGL-mediated pathway. Mol Cell Biol. 2013;33(18):3659-66.

Rodin J, Wack J, Ferrannini E, Defronzo RA. Effect of insulin and glucose on feeding behavior. Metab Clin Exp. 1985;34(9):826-31.

Kaur P, Choudhury D. Insulin Promotes Wound Healing by Inactivating NFk?P50/P65 and Activating Protein and Lipid Biosynthesis and alternating Pro/Anti-inflammatory Cytokines Dynamics. Biomol Concepts. 2019;10(1):11-24.

Jung SY, Rohan T, Strickler H, et al. Genetic variants and traits related to insulin-like growth factor-I and insulin resistance and their interaction with lifestyles on postmenopausal colorectal cancer risk. PLoS ONE. 2017;12(10):e0186296.

Yuan C, Bao Y, Sato K, et al. Influence of dietary insulin scores on survival in colorectal cancer patients. Br J Cancer. 2017;117(7):1079-1087.

Al qahtani A, Holly J, Perks C. Hypoxia negates hyperglycaemia-induced chemo-resistance in breast cancer cells: the role of insulin-like growth factor binding protein 2. Oncotarget. 2017;8(43):74635-74648.

Carreras-torres R, Johansson M, Gaborieau V, et al. The Role of Obesity, Type 2 Diabetes, and Metabolic Factors in Pancreatic Cancer: A Mendelian Randomization Study. J Natl Cancer Inst. 2017;109(9)

Nead KT, Sharp SJ, Thompson DJ, et al. Evidence of a Causal Association Between Insulinemia and Endometrial Cancer: A Mendelian Randomization Analysis. J Natl Cancer Inst. 2015;107(9)

Liu XL, Wu H, Zhao LG, Xu HL, Zhang W, Xiang YB. Association between insulin therapy and risk of liver cancer among diabetics: a meta-analysis of epidemiological studies. Eur J Gastroenterol Hepatol. 2018;30(1):1-8.

Bowker SL, Majumdar SR, Veugelers P, Johnson JA. Increased cancer-related mortality for patients with type 2 diabetes who use sulfonylureas or insulin. Diabetes Care. 2006;29(2):254-8.

Baghbani-oskouei A, Tohidi M, Hasheminia M, Azizi F, Hadaegh F. Impact of 3-year changes in fasting insulin and insulin resistance indices on incident hypertension: Tehran lipid and glucose study. Nutr Metab (Lond). 2019;16:76.

Qiao L, Li Y, Sun S. Insulin Exacerbates Inflammation in Fibroblast-Like Synoviocytes. Inflammation. 2020;

Yuan C, Bao Y, Sato K, et al. Influence of dietary insulin scores on survival in colorectal cancer patients. Br J Cancer. 2017;117(7):1079-1087.

Perseghin G, Calori G, Lattuada G, et al. Insulin resistance/hyperinsulinemia and cancer mortality: the Cremona study at the 15th year of follow-up. Acta Diabetol. 2012;49(6):421-8.

Damluji AA, Cohen ER, Moscucci M, et al. Insulin provision therapy and mortality in older adults with diabetes mellitus and stable ischemic heart disease: Insights from BARI-2D trial. Int J Cardiol. 2017;241:35-40.

 

The post What Might Fasting Insulin Predict About Health? appeared first on Mark's Daily Apple.

Fresh Versus Frozen Food: Which Is More Nutritious?

In the hierarchy of vegetables, the best choices are fresh, in-season, and local.

Realistically, though, that’s not always going to happen. For one thing, you might live in a climate where access to a variety of local and in-season vegetables just isn’t a thing. It’s also well established that lower income areas have fewer supermarkets, so fresh produce is less available.

Although home-grown is the best of the best, I know that saying, “Just grow your own!” is presumptuous on a lot of levels. Assuming that you have the space and resources to plant a garden, time is a big consideration. Plus, once they’re grown, preparing fresh vegetables takes more time than preparing frozen or canned, which are already washed and chopped for you.

All this is to say, I’m sure many of you find yourself turning to frozen and canned vegetables—as well as fruit, seafood, and meat—for reasons of availability and convenience. You might wonder if you are sacrificing any health benefits or if I’m giving you the side-eye for eating vegetables that aren’t farm-fresh.

Are Frozen and Canned Foods Inherently Less Primal?

Let me put that concern to rest immediately.

True, Grok would not have frozen or canned foods. Food preservation as a concept is nothing new, though. Just because a technology is new does not mean it’s “un-Primal.” I am not now, nor have I ever been, opposed to using modern methods of food preservation and storage that make it safer or more convenient to eat healthy foods. I like safety and convenience.

So, if you’ve been avoiding frozen or canned foods because you think you’ll have to turn in your Primal card, rest assured that isn’t the case. That said, I have historically avoided canned vegetables in the store due to concerns over BPA in the can linings. (Home-canned in jars is different, of course. I’m all for home canning.)

Since people sounded the alarm about BPA in the past decade, industry reports suggest a significant number of manufacturers have moved away from BPA-lined cans, but not all of them. I still strongly favor frozen over industrially canned vegetables. If nothing else, the taste and texture is usually superior. Nutritionally, though, the data show that frozen and canned are comparable overall.

Frozen Vegetables and Fruit: As Good As Fresh?

The frozen food industry dates back to 1925, when Clarence Birdseye began quick-freezing fish. It really took off after WWII as more homes had freezers. Since then, food scientists have worked to improve freezing, packaging, and transporting methods so that today (spoiler alert!) frozen foods are nutritionally comparable to their fresh counterparts. They also taste better and maintain a more pleasing texture and appearance compared to our grandparents’ frozen options.

Factors that affect nutrients in the produce you buy, whether fresh or frozen, include:

the particular nutrient in question,
the type of vegetable, including cultivar (what specific type of bean, apple, etc.),
growing conditions (soil, weather, and so on),
post-harvest handling and storage,
how you cook them.

Frozen vegetables are typically blanched before freezing to halt enzymatic reactions. This step cleans the vegetables and preserves flavor and texture, but the heat also reduces the levels of some nutrients, notably vitamin C.

On the other hand, fat-soluble vitamins like vitamins A and E and carotenoids are released from their cellular matrices by heat. This might make them more bioavailable in frozen foods. The jury is still out on the bioavailability question according to Dr. Diane Barrett of the UC Davis Department of Food Science and Technology. Fiber is relatively impervious to processing and so isn’t affected by freezing.

From Farm to Table

Although there is an initial loss of some nutrients in the freezing process, this seems to even out by the time the vegetables make it to your plate.

At the very top of the nutritional hierarchy are vegetables that go from dirt to plate with the fewest stops in between. The best option is picking vegetables out of your garden and eating them more or less right away. That’s not usually how it works, though.

Supermarket produce might have been in the supply chain for several weeks before you even purchase it (and it was almost certainly not allowed to fully ripen before harvesting). Even if you buy your produce at a local farmer’s market, several days to a week might pass before you consume it.

During that time between farm and plate, nutrients are oxidizing and degrading. On the other hand, frozen vegetables are usually picked at the peak of ripeness and frozen as quickly as possible to preserve the nutrients.

Show Me the Data

Li and colleagues measured vitamin C, beta-carotene, and folate in broccoli, cauliflower, corn, green beans, green peas, spinach, blueberries, and strawberries that were fresh, “fresh-stored” (refrigerated for five days to mimic what happens when we actually buy produce), or frozen. They found a high degree of nutritional similarity overall and further concluded, “In the cases of significant differences, frozen produce outperformed ‘fresh-stored’ more frequently than ‘fresh-stored’ outperformed frozen.”

These findings are typical. Compared to fresh vegetables, frozen compare favorably in study after study. For example:

Two studies from Bouzari and colleagues at UC Davis compared eight common fruits and vegetables that were either stored in a refrigerator for 3 or 10 days, or frozen up to 90 days. For vitamin C, riboflavin, alpha-tocopherol (a form of vitamin E), calcium, magnesium, zinc, copper, iron, fiber, and total phenolics, the researchers concluded that fresh and frozen were highly similar, with frozen sometimes outperforming fresh.
British researchers measured vitamin C, total polyphenols, total anthocyanins, and carotenoids (beta-carotene and lutein) in six common fruits and vegetables. Immediately after purchase from the grocery store, fresh and frozen were mostly similar. Levels of nutrients tended to decrease in the fresh vegetables over three days of storage.
Researchers from Virginia Tech and the USDA found that 5-methyltetrahydrofolate, the most bioavailable form of folate, did not decline in seven common vegetables over 12 months in frozen storage.

I could go on, but you get the picture. Note that across all the studies, results varied somewhat between different types of produce and nutrients. Dr. Barrett also points out that there is little research beyond that looking at key vitamins. More is needed to examine other nutritive compounds, as well as to explore the bioavailability question.

Don’t get caught up in the minutiae, though. Looking at the big picture, researchers consistently agree that taking everything into consideration, frozen is on par with fresh-stored. Frozen vegetables also have favorable nutrient-to-price ratios.

Go Ahead and Hit Up the Freezer Section

The fact is, you can’t stand in a grocery store with a head of fresh cauliflower in one hand and a bag of frozen florets in the other and know for sure which has more nutrients. There’s no reason to feel bad about choosing frozen over fresh, especially when fresh seasonal and local options are lacking.

Consider, too, that if convenience is key, and your choice is between a frozen meal containing vegetables, or grabbing a drive-thru meal, the frozen food is often the better choice.

Using data from the National Health and Nutrition Examination Survey (NHANES) longitudinal study, researchers compared adults who reported eating frozen meals or “restaurant fast food/pizza.” Using the standardized Healthy Eating Index, the frozen meal eaters scored higher overall and specifically for total vegetable intake and total protein food. They also had lower intake of refined grains and empty calories.

A separate analysis of NHANES data showed that people who eat frozen vegetables eat more total vegetables and get more fiber, potassium, calcium and vitamin D, than those who don’t.

In terms of covering your nutrient bases, your best option is to choose a wide variety of produce, fresh and local when possible, and frozen when needed. If you can grow some fresh herbs and a tomato plant outside your window, all the better.

What About Meat and Seafood?

The expert consensus is that frozen meat and seafood is also nutritionally on par with fresh.

For fish in particular, freezing is the only viable way besides canning for many consumers to access safe products. According to the Seafood Storage Guide from the National Fisheries Institute, most fresh fish (not shellfish) should be eaten within 36 hours of catching.

As a final note, if you opt for frozen food products, check out the USDA Freezing and Food Safety fact sheet and USDA guide to Safe Defrosting Methods to make sure you are maximizing safety and quality.

 

References

Composition of Foods Raw, Processed, Prepared. USDA National Nutrient Database for Standard Reference, Release 28 (2015) – Documentation and User Guide.

Kmiecik W, Lisiewska Z, Korus A. Retention of mineral constituents in frozen brassicas depending on the method of preliminary processing of the raw material and preparation of frozen products for consumption. Eur. Food Res. Technol. 2007; 224:573–79.

Li, M. Ho, K., Hayes, M. Ferruzzi, M. G. The Roles of Food Processing in Translation of Dietary Guidance for Whole Grains, Fruits, and Vegetables. Annual Review of Food Science and Technology. 2019; 10:569-596.

MacTavish-West, H. Vegetables: is fresh best? The Journal of the Institute of Food Science and Technology. 2014.

Miller SR, Knudson WA. 2014. Nutrition and cost comparisons of select canned, frozen, and fresh fruits and vegetables. Am. J. Lifestyle Med. 2014; 8:430–37.

Produce for Better Health Foundation. State of the Plate: 2015 Study on America’s Consumption of Fruit & Vegetables.

Rickman JC, Barrett DM, Bruhn CM. Nutritional comparison of fresh, frozen and canned fruits and vegetables. Part 1. Vitamins C and B and phenolic compounds. 2007; J. Sci. Food Agric. 87:930–44.

Rickman JC, Bruhn CM, Barrett DM. Nutritional comparison of fresh, frozen, and canned fruits and vegetables. II. Vitamin A and carotenoids, vitamin E, minerals and fiber. J. Sci. Food Agric. 2007; 87:1185–96.

Villa-Rodriguez, J.A., et al. Maintaining antioxidant potential of fresh fruits and vegetables after harvest. Crit. Rev. Food Sci. Nutr. 2015; 55: 806–822.

The post Fresh Versus Frozen Food: Which Is More Nutritious? appeared first on Mark's Daily Apple.

Cioppino

A substantial, acidic, briny, bright one-pot meal with a heady dry white wine broth, cioppino originated in San Francisco from fishermen’s daily catch and the Italian-American influences around the wharf and surrounding areas. The warm, comforting, aromatic stew chases away any chill from the thick fog that can blanket the area.

This seafood stew can work with a variety of seafood and fish. We like shrimp, scallops and clams because they’re widely available and cook quickly. Steaming the clams in the sauce gives the sauce great flavor. Halibut is a wonderful fish choice, but can be substituted for other firm, white-fleshed fish. If you notice the stew is becoming too dry, you can add additional wine or broth until it reaches the consistency of your liking.

Cioppino
Ingredients

1 cup chopped onions
8 Campari tomatoes, halved
3 Tbsp. olive oil
6 cloves garlic, whole with skin on
1 tsp. dried basil
1 tsp. dried oregano
1/4 tsp. ground fennel
1/4 tsp. black pepper
1/4 tsp. salt
1 cup white wine (we used Sauvignon Blanc)
1 cup Primal Kitchen Tomato Basil Marinara Sauce
6 clams
¼ lb. shrimp, peeled and deveined
¼ lb. scallops
10 oz. halibut, half cut into chunks, half cut in small pieces
1 Tbsp. butter
Parsley, to garnish
Red pepper flakes, to garnish

Instructions

Preheat your oven to 375ºF. Toss the tomatoes and garlic in 1 tablespoon of oil and place on a parchment covered sheet pan. Roast for about 15 minutes.

Heat the remaining olive oil in a pot over medium heat. Once hot, add the chopped onions and sauté for 5 minutes, or until they are soft. Add in the roasted tomatoes with any juices that accumulated while roasting.

Squeeze the garlic out from the skins and crush the garlic with the side of your knife. Roughly chop the soft garlic and add it to the pot. Add the basil, oregano, fennel, and black pepper to the pot, and stir.

Pour the wine and marinara sauce into the pot and stir. Reduce the heat to a simmer and cover the pot for 10 to 15 minutes.

While the sauce is simmering, cook the halibut portions by heating the butter in a pan over medium heat. Once the butter is hot, season the halibut pieces with salt and pepper and add them to the hot butter. Sear for 2 minutes on each side, then baste the halibut with the hot butter until the inside of the fish is opaque. Set the fish aside.

Uncover the pot with the stew, and season with salt. Add the clams to the pot and make sure they are covered with sauce. Cover for 5 to 7 minutes, then uncover and remove the clams as they open their shells and set them aside. If any clams do not open after 12 minutes, discard those clams.

Add in the uncooked fish pieces and shrimp and cover for 2 to 3 minutes. Add the scallops and cook for an additional 1 to 2 minutes, or until the fish begins to flake and the shrimp is opaque. Remove the pot from the heat and add the clams back to the pot.

Portion into bowls and top with the seared halibut pieces. Season with salt and pepper to taste and top with chopped parsley and red pepper flakes.

Nutrition Information per serving (1/3 of recipe):

Calories: 485

Total Carbs: 21 grams

Net Carbs: 18 grams

Fat: 22 grams

Protein: 37 grams

The post Cioppino appeared first on Mark's Daily Apple.

Weekly Link Love – Edition 66

Research of the Week

How evidence-based are the official diet guidelines?

Hyperinsulinemia induces insulin resistance.

Africans may have Neanderthal ancestry, too.

New review on low-carb diets for cardiovascular disease (it’s good).

They found Pliny the Elder’s cranium.

Eating sprouted potatoes during pregnancy may have consequences for the offspring.

New Primal Blueprint Podcasts

Episode 401: Keith and Michelle Norris: Elle Russ chats with Keith and Michelle Norris, founders of Paleo f(x).

Primal Health Coach Radio, Episode 45: Laura and Erin chat with Julie Raich Dieme about building online health programs.

Subscribe to the Primal Blueprint Podcast here so you never miss an episode.

Media, Schmedia

Santa Cruz decriminalizes plant and fungi entheogens.

The Department of Veterans Affairs is testing keto for type 2 diabetes patients. Hell yeah.

Interesting Blog Posts

How might a vegan diet affect your intelligence?

The definitive guide to microworkouts.

Social Notes

Certainly sounds preposterous.

A good thread on local food’s carbon footprint.

LinkedIn, Facebook, Instagram, Tinder.

Everything Else

Blocked arteries may not warrant stents.

Peaceful standoff.

How stress turns hair white.

Things I’m Up to and Interested In

Case study series that pleased me to see: Using ketogenic diets to curb binge-eating and food addiction—looks like “restrictive fad diets” can actually help.

Job opening I think some of you should apply for: Help out the Nutrition Coalition. Another job opening that’s close to home.

I’m coming to terms with the realization that they’ll never stop pumping out these ridiculous studies: Will a week of keto damage you?

Interesting coronavirus research: It depletes selenium and may target Asian males more aggressively (small sample sizes, though).

I love how they undermine keto even when it works: Restricting carbohydrates “tricks” your body into burning fat.

Question I’m Asking

With Google stopping development of its glucose-monitoring lens and all the other failures and dubious advancements, tech is realizing that biology’s a hard nut to crack. Do you think technology will ever figure out human biology and vault us into sci-fi territory?

Recipe Corner

Eggs in purgatory, what a great name.
Smoke your own salmon.

Time Capsule

One year ago (Jan 25– Jan 31)

Does Vegetarian Collagen Exist? – Well, does it?
13 Functional Exercises You Can Do at Work– How to make it work at work.

Comment of the Week

“For the past many years I have tried to find something nice to say to someone every day. An article of clothing, their car, the way they walk, even the smile on their face. Occasionally I will get a brush off which only means that they are suspicious and rightly so in this society. However most of the time it makes someone feel good and always it does so for me.”

– A lot of nice ideas in the comments.

The post Weekly Link Love – Edition 66 appeared first on Mark's Daily Apple.

The Definitive Guide to Saturated Fatty Acids

I’ve written guides to fat in general, animal fats in particular, and edible oils as well. I’ve written a definitive guide to saturated fat. But what are these fats, exactly? Today, I’m writing the Definitive Guide to Saturated Fatty Acids—a guide to all the individual fatty acids that make up the saturated fats we eat, store, and burn.

I won’t cover every single saturated fatty acid in existence. Some of them don’t play any significant role in human health or diet. Like cerotic acid, which appears mainly in beeswax. Or arachidic acid, which you can get by hydrogenating arachidonic acid or eating a ton of durian. There are a few more that aren’t very relevant.

I will instead cover the most important ones.

But First, a Word about Saturated Fatty Acids…

Saturated fats have all available carbon bonds paired with hydrogen atoms, making them highly stable and resistant to oxidation and rancidity—even when heated. That’s why our bodies tend to build cellular membranes with a significant portion of saturated fats. They provide stability and a strong foundation.

Caproic Acid, Caprylic Acid and Capric Acid

I included these together because their names come from the Latin word for “goat,” and all three are found most famously in goat milk—they run about 15% of goat milk fat. Capric acid is also found in coconut oil (10% of coconut fat) and palm oil (4% of palm fat).

The “goat” fats are what give goat milk its distinctive “goaty” odors. Come to think of it, I’ve had coconut oil that had a “funk” to it, and I bet the capric/caprylic acid was to blame. But if you can get past the goatiness, there are benefits to these fatty acids.

Capric acid has been used to inhibit seizures in people with epilepsy, and if you combine it with caprylic acid, the anti-seizure effect seems to increase.
As medium-chain triglycerides, the goat fatty acids increase ketone production. In fact, caprylic acid is the most ketogenic medium-chain triglyceride of all.
Capric acid has anti-fungal properties, showing particular efficacy against Candida, while all three are effective against oral bacteria.

Best sources: goat milk, coconut oil, palm oil.

Lauric Acid

Another medium-chain triglyceride, lauric acid is the primary fatty acid in coconut fat (40-50% lauric acid) and palm kernel fat. It also appears in human breast milk (about 6.2% of total fat).

Lauric acid is anti-microbial. That’s why it appears in breast milk—to help infants ward off pathogens while their immune systems are still developing. And it’s probably why people report getting rid of foot and toenail fungus by smearing their feet with coconut oil at night.
Lauric acid reduces hunger. In one study, people who had lauric acid shot directly into their guts ate less food than the people who had oleic acid shot in.
When you consume lauric acid, some of it is converted into monolaurin, a more potent compound (both coconut oil and breast milk also contain some monolaurin directly) with anti-viral, anti-microbial, and anti-fungal properties.
Lauric acid is not as directly ketogenic as the “goaty” medium-chain triglycerides.

Best sources: coconut fat, palm kernel fat, breast milk.

Myristic Acid

Myristic acid is a perplexing one. Some studies find that its presence in the blood indicates metabolic issues, whereas, as you’ll see below, in the diet it can have some good effects and play some important roles.

The odor of myristic acid draws the newborn to the breast and helps trigger the appetite for mother’s milk.
Myristic acid in milk also possesses anti-listeria activity.
Eating 1-2% of calories as myristic acid—about what you’d get from including a little coconut or moderate amounts of full-fat dairy in your daily diet—improves red blood cell membrane fluidity and lipid profile. Eating that much also improves omega-3 status.
High-fat dairy is consistently linked to better cardiovascular health despite being one of the best sources of myristic acid.
The Tokelau islanders ate a coconut-based diet that was very high in myristic acid; they had excellent cardiovascular health.

What’s happening? Why the discrepancies?

Some in the diet is way better than none. Too much more than 1-2% of calories (about 10% of calories from dairy fat), and the benefits start dropping and even reversing. However, that “1-2%” limit was in the context of a higher-carb diet. If you’re lower carb, you can probably benefit from higher intakes.
Myristic acid in the blood isn’t so much “dangerous” as it is indicative of metabolic dysfunction. For instance, the most reliable way to reduce blood levels of myristic acid is to reduce your carbohydrate intake.

Best sources: nutmeg butter (don’t eat that and go driving, though; nutmeg is downright psychoactive), coconut fat, palm kernel oil, milk fat, breast milk.

Stearic Acid

Stearic acid is enjoying a bit of a renaissance lately. People are mixing isolated stearic acid into clarified butter to create a “super-stearic butter.” Why?

Stearic acid is one of the saturated fats that even SFA-phobes admit has a neutral effect on cholesterol levels. If anything it boosts HDL.
Dietary stearic acid appears to cause “fusing” of our mitochondria—the power plants of our cells—and increase fatty acid oxidation shortly after consumption. In other words, it’s a potent boost to our ability to generate energy.
Diets based on either red meat or cheese—two foods high in stearic acid—improve metabolic and blood markers.

It’s getting really tough to deny the benefits of stearic acid.

Best sources: cocoa butter, beef fat (steer/stearic), dairy, lard.

Palmitic Acid

Palmitic acid gets a terrible rap. In study after study, we find palmitic acid doing bad things to our cells and our health markers. And when you douse cells in pure palmitic acid, they tend to suffer and even die. This looks really bad.

For instance, palmitic acid lowers expression of the LDL receptor gene. Less LDL receptor activity, more time for LDL to hang around in the bloodstream and cause trouble. That’s not good.

Or the fact that palmitic acid is toxic to skeletal muscle cells, impairing glucose uptake and increasing insulin resistance.

Or that palmitic acid induces inflammation and disrupts insulin signaling, suggestive of diabetes. We don’t want diabetes, we don’t want heart disease, and we like our muscle cells to function, so we should probably stop eating any palmitic acid, right?

Except a modicum of oleic acid stimulates LDL receptor activity. And arachidonic acid, a polyunsaturated fat found in animal products often alongside palmitic acid, prevents cell toxicity. And finally, if you throw in a little oleic acid alongside that “inflammatory” palmitic acid, you obliterate the inflammation.

Okay, but what about serum palmitic acid being a harbinger of metabolic disorder? Easy. When you overeat sugar and there’s nowhere to put it and you can’t burn it, the liver converts any extra into palmitic acid to be stored. Elevated palmitic acid is a marker of eating too many carbohydrates (and food in general).

Best sources: dairy fat, ruminant fat, palm oil.

What does it all mean?

Even though today’s post was about the individual saturated fatty acids, we very rarely eat individual fatty acids. Instead, we’re eating fats that contain a half dozen fatty acids or more, or foods that contain fats that contain a half dozen fatty acids. We aren’t cooking with lauric acid or sprinkling pure palmitic acid in the pan. We’re eating foods. And, as part of the food matrix, all the saturated fatty acids I’ve examined have important and valid roles to play.

If you want to avoid palmitic acid but welcome stearic acid, guess what? You’re gonna have to craft some Frankenstein-fat. Foods that contain stearic acid also contain palmitic acid. The best sources of lauric acid are also pretty high in stearic, palmitic, and myristic acid. And so it goes. You can’t avoid palmitic acid and only eat lauric and stearic acid while eating actual food.

If you have any questions, drop them down below.

Thanks for reading, everyone!

References

Wlaz P, Socala K, Nieoczym D, et al. Acute anticonvulsant effects of capric acid in seizure tests in mice. Prog Neuropsychopharmacol Biol Psychiatry. 2015;57:110-6.

Huang CB, Alimova Y, Myers TM, Ebersole JL. Short- and medium-chain fatty acids exhibit antimicrobial activity for oral microorganisms. Arch Oral Biol. 2011;56(7):650-4.

Feltrin KL, Little TJ, Meyer JH, et al. Comparative effects of intraduodenal infusions of lauric and oleic acids on antropyloroduodenal motility, plasma cholecystokinin and peptide YY, appetite, and energy intake in healthy men. Am J Clin Nutr. 2008;87(5):1181-7.

Intorre F, Venneria E, Finotti E, et al. Fatty acid content of serum lipid fractions and blood lipids in normolipidaemic volunteers fed two types of cheese having different fat compositions: a pilot study. Int J Food Sci Nutr. 2013;64(2):185-93.

Gutiérrez-garcía AG, Contreras CM, Díaz-marte C. Myristic acid in amniotic fluid produces appetitive responses in human newborns. Early Hum Dev. 2017;115:32-37.

Chen X, Zhao X, Deng Y, Bu X, Ye H, Guo N. Antimicrobial potential of myristic acid against Listeria monocytogenes in milk. J Antibiot. 2019;72(5):298-305.

Prior IA, Davidson F, Salmond CE, Czochanska Z. Cholesterol, coconuts, and diet on Polynesian atolls: a natural experiment: the Pukapuka and Tokelau island studies. Am J Clin Nutr. 1981;34(8):1552-61.

Hunter JE, Zhang J, Kris-etherton PM. Cardiovascular disease risk of dietary stearic acid compared with trans, other saturated, and unsaturated fatty acids: a systematic review. Am J Clin Nutr. 2010;91(1):46-63.

Thorning TK, Raziani F, Bendsen NT, Astrup A, Tholstrup T, Raben A. Diets with high-fat cheese, high-fat meat, or carbohydrate on cardiovascular risk markers in overweight postmenopausal women: a randomized crossover trial. Am J Clin Nutr. 2015;102(3):573-81.

Mustad VA, Ellsworth JL, Cooper AD, Kris-etherton PM, Etherton TD. Dietary linoleic acid increases and palmitic acid decreases hepatic LDL receptor protein and mRNA abundance in young pigs. J Lipid Res. 1996;37(11):2310-23.

Wen H, Gris D, Lei Y, et al. Fatty acid-induced NLRP3-ASC inflammasome activation interferes with insulin signaling. Nat Immunol. 2011;12(5):408-15.

The post The Definitive Guide to Saturated Fatty Acids appeared first on Mark's Daily Apple.