As I’ve written before, although most people’s lipid numbers improve across the board, some people get interesting cholesterol responses to Primal ketogenic diets. LDL skyrockets, even LDL particle number. The jury’s out on whether or not they indicate negative health concerns or if keto dieters are a special breed that hasn’t received enough study. (There may be a few genetic profiles, such as APOE4 carriers, that react differently to certain dietary inputs.) Either way some people just want their cholesterol numbers to look good in a conventional way. These days, whenever I run into someone in the real world with these or similar concerns, I tell them to try “Mediterranean keto.”
What is that, anyway?
The Mediterranean diet can mean a lot of different things depending on who you ask. On one side, you have the folks who make the ridiculous claim that the Mediterranean diet consisted of pasta, low-fat dairy, beans, green veggies, seed oils with a “drizzle or two” of extra virgin olive oil for good measure, a handfuls of nuts, and a single filet of sardine once every three days. They avoided salt and red meat and full-fat cheese, somehow ignoring the vast body of salt water on their shores and the large population of sheep and goats roaming the land. I guess that livestock is only there to keep the weeds down.
On the other side, you have the people claiming that the true Mediterranean diet consisted of fatty lamb, hard cheeses, fish filets dripping with oil, skins of homemade red wine, cured meats, endless olives, vegetables at will, and the occasional legume bathing in mutton juices and a tiny piece of bread crust submerged in extra virgin olive oil.
This is probably closer to the truth, but both are a bit hyperbolic.
It also depends on where you’re looking. The Mediterranean is a big sea. Spain, Italy, Portugal, Greece, Crete, Turkey, Morocco, Algeria, Israel, Lebanon, Egypt, and even France are all technically Mediterranean countries. Are their diets identical? No. Are there common threads running through their respective cuisines? Yes.
- Olive oil
- Wine (excepting Muslim dietary practices)
- Grains and legumes (Yes, they do eat beans and pasta and bread, although perhaps not in the quantities the grain-addicted would prefer)
And that’s not even mentioning all the various social, spiritual, and lifestyle components of the Mediterranean way of life. The sun, the walking, the hills, the family connections, the religious leanings. Today’s label is all about the diet.
The Mediterranean keto diet emphasizes olive oil, fish, cheese, meat, low-carb vegetables, and red wine. In other words, it takes all the keto-compliant foods readily available to denizens of the Mediterranean and constructs a nutrient-dense diet out of them.
And you know what? It seems to work really well.
In one of the most impressive studies, people with severe obesity and metabolic syndrome tried a Mediterranean keto diet for 12 weeks. That’s three months.
Here’s what the diet consisted of:
- No calorie counting
- Unlimited protein
- Lots of fish. At least (and often more than) four days a week, subjects ate over a kilogram of fish each day, mostly sardines, trout, mackerel, and salmon. On the other days, they got their protein from shellfish, meat, fowl, eggs, and cheese.
- Lots of omega-3s. Subjects were getting over 15 grams of omega-3s on their fish days and supplementing with 9 grams of salmon oil on their non-fish days.
- At least 200-400 mL of red wine a day, 100-200 mL at lunch and dinner. That’s up to over half a bottle.
- At least 30 mL (2 tablespoons) of olive oil a day, 10 mL per meal.
- Maximum two portions of salad and one portion of low-carb vegetables (cauliflower, broccoli, eggplant, etc) per day.
- A comprehensive vitamin and mineral supplement covering all the basics.
What happened to these subjects after 12 weeks on this Mediterranean keto diet regimen?
- They lost 30+ pounds.
- Their BMIs dropped from almost 37 to 31.5, from the middle of class 2 obesity to the bottom of class 1 obesity.
- They lost 16 centimeters, or 6 inches, from their waist.
- Fasting blood sugar dropped from 118 (pre-diabetic) to 91 (ideal).
- Triglycerides dropped from 224 to 109.
- HDL increased from 44 to 58.
- They went from prehypertensive to normotensive.
- Their liver enzymes and liver fat reduced and in some cases completely resolved.
- All 22 subjects started the study with metabolic syndrome and ended it without metabolic syndrome.
That last bit is pretty interesting. Note that the majority of the participants were still obese (BMI over 30) by the end of the study, yet every single one had cured their metabolic syndrome. Sure, they lost weight, and the trend was fantastic and heading down, but they weren’t there yet. Something about the diet itself was incredibly powerful.
The only limitation? It was a pilot study, not a randomized controlled trial pitting the Mediterranean keto diet against a control diet in real time. But considering that these people were coming off control diets—which clearly weren’t working for them—and onto the Mediterranean keto diet, it has more real-world power than you might think. You can bet the participants weren’t complaining about a lack of placebo control.
I’m not saying this is the best incarnation of all the potential Mediterranean keto diets out there. But if you’re having mixed metabolic results from the keto diet and looking for a ketogenic option with more monounsaturated fat and omega-3s, it’s the one that has some clinical research behind it. It’s one that doesn’t possess any glaring red flags.
This is also a form of ketogenic dieting that most people will view as “healthy.” It can be hard to get people to accept that putting real cream in their coffee and steak on their plates is good for them, even if they’re approaching death’s door eating what they’ve always eaten. It’s not so hard to get people on board with a diet of olive oil, fish, red wine, and salad. That’s no small feature.
In the end, the ketogenic Mediterranean diet appears to be an effective way to treat metabolic syndrome without scaring people away. For that reason, it might be a good option to try if you’re having issues with cardiovascular markers, blood sugar, hypertension, body fat, or any of the components that make up the metabolic syndrome.
What do you think of the Mediterranean keto diet? Think you could stick to it?
Pérez-guisado J, Muñoz-serrano A. A pilot study of the Spanish Ketogenic Mediterranean Diet: an effective therapy for the metabolic syndrome. J Med Food. 2011;14(7-8):681-7.
Pérez-guisado J, Muñoz-serrano A. The effect of the Spanish Ketogenic Mediterranean Diet on nonalcoholic fatty liver disease: a pilot study. J Med Food. 2011;14(7-8):677-80.
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Anxiety is normal. It’s something we all have experience with—to one degree or another. Most people are anxious about something that hangs over them and follows them around like a personal rain cloud. Then there’s the deeper but still familiar anxiety many of us carry. The anxiety about our self-worth. The anxiety of performance, of social situations. This type can grip us in an uncomfortable, but hopefully not chronic, way.
But not all anxiety is run-of-the-mill—or manageable. People with Generalized Anxiety Disorder, for instance, might have trouble leaving the house, ordering a coffee from Starbucks, going to work. Anxious thoughts cycling through their brains often keep them up at night. When untreated, people with this level of anxiety can end up living in a state of perpetual fear.
The conventional approach is to take anti-anxiety meds, which can be genuinely life-saving for some people. Nonetheless, these can come with downsides that vary depending on an individual’s dosage and reactions—and the nature of the particular medication itself. Some meds result in few side effects, but others’ effects can be heavy. For instance, there are the benzodiazepines, highly-addictive tranquilizers with the potential for abuse. They make driving unsafe. They lower productivity. They sedate you. When necessary for the severity of the condition, these side effects may be worth it.
In other cases, a person might have more space to experiment and want to explore a different route.
In some cases, people choose to try natural anxiety aids. These are supplements, nutrients, and herbs that have been designed across millennia by nature (and maybe some input from green-thumbed healers). They might not always be enough for something as serious as a clinical anxiety disorder (please talk to your doctor before making any adjustment or addition to your medication), but at least some may be important complements to a prescribed regimen.
For those who want or need an alternative strategy for anxiety beyond meditative practices and general good health, these natural remedies may be worth a try.
First, the NUTRIENTS….
These are basic vitamins, minerals, and amino acids that your body needs to work. They are non-negotiable. You don’t have to get them through supplements—in fact, that should be a last resort after food—and I wouldn’t expect “drug-level” effects, but you do need to get them.
1. Long Chained Omega-3 Fatty Acids
Some human evolution experts maintain that the human brain wouldn’t be the human brain without steady and early access to coastal food resources—fish and shellfish rich in long chain omega-3s. If the long-chained omega-3s found in fatty fish and other sea creatures made our brains what they are today, it’s safe to assume that our brains work better when we eat them today. And if we’re talking about anxiety, that appears to be the case:
Studies in substance abusers find that supplementing with enough fish oil (and, yes, here’s what I use regularly) to raise serum levels of the long chain omega-3 fatty acid EPA reduces anxiety, while increases in DHA (the other long chain omega-3) reduce anger. Rising EPA levels after supplementation predicted the reduction in anxiety.
In healthy young medical students, omega-3 supplementation (2 grams EPA, 350 mg DHA) lowered inflammation and anxiety. Follow-up analyses revealed that reducing the serum omega-6:omega-3 ratio also reduced anxiety scores.
And in early pregnancy, high DHA levels predict low anxiety scores.
Magnesium deficiency is a risk factor for anxiety. The evidence, considered by some to be low quality, nonetheless suggests that supplementing with magnesium can reduce subjective anxiety. The mechanistic evidence is stronger, as magnesium is one of those minerals that plays a role in hundreds of very basic and essential physiological processes—including the generation of ATP, the body’s energy currency. Without adequate energy production, nothing works well. One’s mental health is no exception.
Magnesium supplementation reduces subjective anxiety (the only kind that matters) in the “mildly anxious” and in women with premenstrual syndrome.
Magnesium L-threonate, a form particularly good at getting into the brain, is worth trying for more immediate, noticeable effects.
Zinc deficiency is common in people with anxiety, including Chinese males and Americans. And although mainlining oyster smoothies probably won’t fix serious anxiety, a follow-up in the group of Americans with low zinc levels found that zinc supplementation did reduce anxiety levels.
4. Vitamin B6
Vitamin B6, or pyridoxine, helps regulate production of serotonin and GABA—two neurotransmitters that control depression and anxiety. In mice exposed to anxiety-producing situations, pyridoxine increases GABA, reduces glutamate, and reduces anxiety. In humans, correcting a magnesium deficiency with magnesium and vitamin B6 has a stronger effect on anxiety than magnesium alone. (Good to note: women on hormonal birth control may be depleted of vitamin B6 as well as other vitamins and minerals.)
The best sources of vitamin B6 are turkey, beef, liver, pistachios, and tuna.
Now, the NATURAL INTERVENTIONS….
These aren’t essential nutrients. Rather, they’re plant compounds with pharmacological effects and, in most cases, hundreds of years of traditional usage for dampening, inhibiting, or resolving anxiety.
Kanna comes from a succulent plant native to South Africa. The story goes that an anthropologist noticed elderly San Bushmen nibbling on a particular type of succulent plant while displaying incredible cognitive ability and remaining calm, cool, and collected. The fact that they weren’t dealing with daily commutes, traffic jams, annoying bosses, and mounting bills probably had something to do with it, but it turns out that the succulent plant wasn’t hurting the cause.
Kanna has been shown to dampen the subcortical threat response, which is normally heightened in anxious states. It also increased well-being and resistance to stress in health adults who took it in a safety study.
Theanine, an amino acid found in green tea and available as a supplement, isn’t going to obliterate your nerves before a big performance. One study showed that it (along with the benzodiazepine Xanax) reduced resting state anxiety but not experimentally-induced anxiety. Then again, neither did Xanax.
Theanine is instead a mild anxiolytic. If you get anxiety from caffeine, take 200 mg of theanine with your coffee. It will smooth out the experience, reduce/remove the anxiety, and leave the stimulation.
Kava is a plant native to the South Pacific. Traditionally, its roots were chewed fresh with the resultant liquid often spit into communal bowls for consumption, pounded to release the moisture, or sun-dried, ground, and steeped in water to make an intoxicating, relaxing mild sedative. Nowadays, the active kavalactones are also extracted and pressed into capsules.
I don’t use kava, but I have tried it a couple times in the past. For what it’s worth, I don’t have anxiety issues but it did seem to pair well with caffeine (similar to theanine).
8. Rhodiola Rosea
Rhodiola rosea is a longtime favorite adaptogen of mine. It hails from the barren wastes of Siberia, where for millennia people from all over the ancient world coveted it. There’s something about the harsh environment of the northern tundra that made rhodiola rosea incredibly resilient—and bestows upon those who consume it a similar type of mental resilience.
A 2015 study sought to determine the impact of rhodiola on self-reported anxiety, stress, cognition, and a host of other mental parameters. Eighty subjects were divided into either a twice-daily commercial formula (containing 200 mg rhodiola) group or a control group. Compared to the controls, the rhodiola group showed notable improvements in mood and significant reductions in anxiety, stress, anger, confusion and depression after 14 days.
There’s a great lavender farm on the island of Maui. One of the favorite memories from that trip is strolling through the fields of lavender, brushing against the leaves and flowers, just basking in the relaxing scent that permeated the entire property. A very low-stress environment, to be sure.
One study gave lavender oil capsules to major depressive disorder patients suffering from anxiety who were already taking antidepressants. Not only did adding the lavender reduce anxiety, it also improved sleep.
Perhaps the most impressive study is this one, where generalized anxiety disorder patients either received lavender oil or a benzodiazepine anti-anxiety drug. Patients receiving the lavender had the same beneficial effects as the benzo patients without the sedation.
Lavender oil aromatherapy also seems to reduce anxiety, at least in cancer patients. One weakness of aromatherapy research is the difficulty of giving a “placebo smell.” Essential oil scents are quite distinct.
10. CBD Oil
As I wrote a couple weeks ago, CBD is the non-psychoactive cannabinoid found in cannabis.
Most recently, a large case series (big bunch of case studies done at once) was performed giving CBD to anxiety patients who had trouble sleeping. Almost 80% had improvements in anxiety and 66% had improvements in sleep (although the sleep improvements fluctuated over time).
In a five-year-old girl with PTSD (a category of patient that just shouldn’t exist) in whom pharmaceutical anxiety medications did not work, CBD oil provided lasting relief from anxiety.
What do you folks like for anxiety? What’s worked? What hasn’t? What did I miss?
Thanks for reading, everyone. Take care.
Cunnane SC, Crawford MA. Energetic and nutritional constraints on infant brain development: implications for brain expansion during human evolution. J Hum Evol. 2014;77:88-98.
Boyle NB, Lawton CL, Dye L. The effects of magnesium supplementation on subjective anxiety. Magnes Res. 2016;29(3):120-125.
Mccarty MF. High-dose pyridoxine as an ‘anti-stress’ strategy. Med Hypotheses. 2000;54(5):803-7.
Walia V, Garg C, Garg M. Anxiolytic-like effect of pyridoxine in mice by elevated plus maze and light and dark box: Evidence for the involvement of GABAergic and NO-sGC-cGMP pathway. Pharmacol Biochem Behav. 2018;173:96-106.
De souza MC, Walker AF, Robinson PA, Bolland K. A synergistic effect of a daily supplement for 1 month of 200 mg magnesium plus 50 mg vitamin B6 for the relief of anxiety-related premenstrual symptoms: a randomized, double-blind, crossover study. J Womens Health Gend Based Med. 2000;9(2):131-9.
Lu K, Gray MA, Oliver C, et al. The acute effects of L-theanine in comparison with alprazolam on anticipatory anxiety in humans. Hum Psychopharmacol. 2004;19(7):457-65.
Terburg D, Syal S, Rosenberger LA, et al. Acute effects of Sceletium tortuosum (Zembrin), a dual 5-HT reuptake and PDE4 inhibitor, in the human amygdala and its connection to the hypothalamus. Neuropsychopharmacology. 2013;38(13):2708-16.
Nell H, Siebert M, Chellan P, Gericke N. A randomized, double-blind, parallel-group, placebo-controlled trial of Extract Sceletium tortuosum (Zembrin) in healthy adults. J Altern Complement Med. 2013;19(11):898-904.
Fißler M, Quante A. A case series on the use of lavendula oil capsules in patients suffering from major depressive disorder and symptoms of psychomotor agitation, insomnia and anxiety. Complement Ther Med. 2014;22(1):63-9.
Woelk H, Schläfke S. A multi-center, double-blind, randomised study of the Lavender oil preparation Silexan in comparison to Lorazepam for generalized anxiety disorder. Phytomedicine. 2010;17(2):94-9.
Shannon S, Opila-lehman J. Effectiveness of Cannabidiol Oil for Pediatric Anxiety and Insomnia as Part of Posttraumatic Stress Disorder: A Case Report. Perm J. 2016;20(4):16-005.
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For today’s edition of Dear Mark, I’m answering three questions. First, can LDL actually infiltrate the arteries, or is there more to the story? Malcolm Kendrick says there’s more to the story, so I dig into some literature to see if they corroborate his position. Second, is New Zealand farmed salmon good to eat? And finally, what should you do about elevated ferritin levels—and why else might they be elevated if not because of your iron?
My reading of this post by Malcolm Kendrick MD is that LDL particles cannot infiltrate the endothelial lining of our arteries:
Great read. Malcolm Kendrick is consistently fascinating, insightful, and enlightening.
He’s basically suggesting that LDL particles can’t manhandle their way into the artery wall, which are equipped with tight junctions—the same kind that regulate passage through our gut lining. Something has to “allow” them in. The something he finds most plausible is injury, trauma, or insult to the endothelial lining (artery wall, for lack of a better phrase).
A free public textbook available on PubMed since last month called The Role of Lipids and Lipoproteins in Atherosclerosis tackles the topic head on. In the abstract, they say:
Population studies have demonstrated that elevated levels of LDL cholesterol and apolipoprotein B (apoB) 100 [note: ApoB is a stand-in for LDL particle number, as each LDL-P has an ApoB attached to it], the main structural protein of LDL, are directly associated with risk for atherosclerotic cardiovascular events (ASCVE). Indeed, infiltration and retention of apoB containing lipoproteins in the artery wall is a critical initiating event that sparks an inflammatory response and promotes the development of atherosclerosis.
This seems to posit that infiltration of the LDL particle into the artery wall is a critical initiating event. But is it the critical initiating event? Does something come before it? How does the infiltration happen, exactly? Moving on:
Arterial injury causes endothelial dysfunction promoting modification of apoB containing lipoproteins and infiltration of monocytes into the subendothelial space. Internalization of the apoB containing lipoproteins by macrophages promotes foam cell formation, which is the hallmark of the fatty streak phase of atherosclerosis. Macrophage inflammation results in enhanced oxidative stress and cytokine/chemokine secretion, causing more LDL/remnant oxidation, endothelial cell activation, monocyte recruitment, and foam cell formation.
If I’m reading this correctly, they’re saying that “arterial injury” is another critical initiating event—perhaps the critical initiating event, since the injury causes “endothelial dysfunction,” which in turn modifies (or oxidizes) the LDL particles. But wait: so they’re saying the LDL particles are already there when the arterial injury occurs. They’ve already made it into the endothelial walls, and they’re just…waiting around until the arteries get injured. Okay, okay, but, just like Malcolm Kendrick points out, nowhere in the abstract have the authors actually identified how the LDL particles enter the endothelial lining. Maybe it’s “common knowledge,” but I’d like to see it explained in full.
In atherosclerosis susceptible regions, reduced expression of eNOS and SOD leads to compromised endothelial barrier integrity (Figure 1), leading to increased accumulation and retention of subendothelial atherogenic apolipoprotein B (apoB)-containing lipoproteins (low-density lipoproteins (LDL)) and remnants of very low-density lipoproteins (VLDL) and chylomicrons)
Ah ha! So, in regions of the arteries that are prone to atherosclerosis, low levels of nitric oxide synthase (eNOS)—the method our bodies use to make nitric oxide, a compound that improves endothelial function and makes our blood flow better—and superoxide dismutase—an important antioxidant our bodies make—compromise the integrity of the arterial lining. The compromised arterial lining allows more LDL particles to gain entry and stick around. So, are low levels of nitric oxide and impaired antioxidant activity the critical initiators? That’s pretty much what Malcolm Kendrick said in his blog post.
Still—high LDL particle numbers are a strong predictor of heart disease risk, at least in the studies we have. They clearly have something to do with the whole process. They’re necessary, but are they sufficient? And how necessary are they? And how might that necessariness (yes, a word) be modified by diet?
I’ll explore this more in the future.
In regards to the oily fish article (and more indirectly given the omega 6 concern- the Israeli Paradox) What do you think of NZ farmed salmon? I’m in Australia, & occasionally like a fresh piece of salmon- there are no wild caught available here sadly, but I am wondering how it measures up as an alternative?
Last year, I explored the health effects of eating farmed salmon and found that it’s actually a pretty decent alternative to wild-caught salmon, at least from a personal health standpoint—the environmental impact may be a different story.
I wasn’t able to pull up any nutrition data for New Zealand farmed salmon, called King or Chinook salmon. Next time you’re at the store, check out the nutritional facts on a NZ farmed salmon product, like smoked salmon. The producer will have actually had to run tests on their products to determine the omega-3 content, so it should be pretty accurate. Fresh is great but won’t have the nutritional facts available. I don’t see why NZ salmon would be any worse than the farmed salmon I discussed last year.
According to the NZ salmon folks, they don’t use any pesticides or antibiotics. That’s fantastic if true.
I used to eat a lot of King salmon over in California, and it’s fantastic stuff. Very fatty, full of omega-3s. If your farmed King salmon comes from similar stock, go for it.
ok can someone tell me how to reduce ferritin? Is is just by giving blood?
Giving blood is a reliable method for reducing ferritin. It’s quick, effective, simple, and you’re helping out another person in need. Multiple wins.
Someone in the comment board recommended avoiding cast iron pans in addition to giving blood. While using cast iron pans can increase iron intake and even change iron status in severe deficiency, most don’t have to go that far. Giving blood will cover you.
Ferritin is also an acute phase reactant, a marker of inflammation—it goes up in response to infections (bacterial or viral) and intense exercise (an Ironman will increase ferritin). In fact, in obese and overweight Pakistani adults, elevated ferritin seems to be a reliable indicator of inflammatory status rather than iron status.
Thanks for reading, everyone. Take care and be well!
Birgegård G, Hällgren R, Killander A, Strömberg A, Venge P, Wide L. Serum ferritin during infection. A longitudinal study. Scand J Haematol. 1978;21(4):333-40.
Comassi M, Vitolo E, Pratali L, et al. Acute effects of different degrees of ultra-endurance exercise on systemic inflammatory responses. Intern Med J. 2015;45(1):74-9.
The post Dear Mark: How Does LDL Even Penetrate the Arteries, New Zealand Farmed Salmon, Elevated Ferritin appeared first on Mark’s Daily Apple.
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For today’s edition of Dear Mark, I’m answering two questions from readers. First, is it possible to become deficient in omega-6 fats as an adult? What would that even look like, and is there anything that might make omega-6 more important?
Second is a question related to last week’s feature on prostate health. Is saw palmetto an effective supplement for prostate issues? It depends on the issue.
I have a question for “Dear Mark”
Here it is:
I am completely and totally primal for 10 years now. Can I become O6 deficient ? Since 90% of my fat intake is saturated or O3.
It’s technically possible to become deficient in omega-6 fatty acids. The early rat studies that discovered the essentiality of Omega-6s found that their complete removal made the subjects consume more food (without gaining weight), drink more water (without peeing more than rats on a normal diet), develop scaly skin, lose fur, urinate blood, go infertile, grow weird tails, and die early. All this despite eating an otherwise nutrient-dense diet with all the fat-soluble vitamins (they even removed the fat from cod liver oil and gave the vitamins), B vitamins, and other nutrients a rat could ever want. The only thing missing was a source of omega-6 fats.
Once they discovered the issue—a lack of omega-6—how’d they fix it?
Coconut oil didn’t work, for obvious reasons. It’s almost pure saturated fat.
Butter worked, but you had to use a lot. The omega-6 fraction of butter is quite low.
Cod liver oil worked, but it didn’t fully cure the deficiency disease.
Lard worked well, as did corn oil, liver, flax oil, and olive oil. All of those fat sources fully resolved the issue and eliminated the symptoms. They were all good to decent sources of omega-6 fatty acids.
They also tried pure linoleic acid (the shorter-chained omega-6 PUFA found in nuts and seeds and the animals that eat them) and arachidonic acid (the long-chain omega-6 PUFA found in animal foods). Both worked, but AA worked best.
Throughout all these trials, exactly how much omega-6 fat did the rats require in their diets to cure deficiency symptoms?
When they used lard to cure it, the rats got 0.4% of calories from omega-6 PUFA. If the numbers hold true for humans, and you’re eating 2500 calories a day, that’s just 10 calories of omega-6, or about a gram and a half of pure arachidonic acid to avoid deficiency.
When they used liver to cure it, the rats got 0.1% of calories from omega-6 PUFA. If the numbers hold true for humans, and you’re eating 2500 calories a day, that’s just 2.5 calories of omega-6, or about a third of a gram of arachidonic acid to avoid deficiency.
The truth is that omega-6 deficiency is extremely hard to produce, even when you’re trying your hardest. Way back in the 1930s, the early omega-6 researchers tried to induce deficiency in an adult by giving him a 2 grams fat/day diet for months. Nearly all fat was removed, particularly the omega-6 fats, and the rest of the diet was fat-free milk, fat-free cottage cheese, orange juice, potato starch, sugar, and a vitamin/mineral supplement. Maybe not the ideal Primal diet, but better than some.
He ended up improving his health, not hurting it. There was no sign of deficiency.
Omega-6 fats are everywhere in the food environment, even if you’re actively avoiding concentrated sources of them. No one is developing a deficiency these days. However, certain conditions might increase the tolerable or beneficial upper limits of omega-6 intake.
If you’re strength training with the intent to gain lean mass, a little extra arachidonic acid can improve your results. The dose used was 1.5 grams per day. Average intake through food runs about 250-500 mg, though Primal eaters heavy on the animal foods are probably eating more.
If you’re recovering from injury or healing a wound, a little extra arachidonic acid can speed it up. AA is an important co-factor in the inflammatory response necessary for tissue healing.
Well done, Mark. My doc just prescribed saw palmetto to reduce multiple nighttime visits to the bathroom, though the research I’m looking at says there’s no clinical evidence to support saw palmetto for prostate problems. Your take?
It depends on the problem.
Large observational trials have found no connection between saw palmetto supplementation and prostate cancer risk. It neither helps nor harms.
Saw palmetto does seem to help benign prostatic hyperplasia, a non-cancerous growth of the prostate. This won’t cause serious health issues directly, but it can impede the flow of urine and lead to multiple nighttime bathroom visits. Saw palmetto is quite effective at reducing nighttime urination. If that’s what your doc is trying to help, I’d say give it a shot.
You might ask about combining saw palmetto with astaxanthin. It’s been shown to reduce the conversion of testosterone into estradiol that can sometimes result from plain old saw palmetto supplementation.
That’s it for today, folks. Take care and be well. Chime in down below if you have any questions or comments.
Mitchell CJ, D’souza RF, Figueiredo VC, et al. Effect of dietary arachidonic acid supplementation on acute muscle adaptive responses to resistance exercise in trained men: a randomized controlled trial. J Appl Physiol. 2018;124(4):1080-1091.
Oh SY, Lee SJ, Jung YH, Lee HJ, Han HJ. Arachidonic acid promotes skin wound healing through induction of human MSC migration by MT3-MMP-mediated fibronectin degradation. Cell Death Dis. 2015;6:e1750.
Bonnar-pizzorno RM, Littman AJ, Kestin M, White E. Saw palmetto supplement use and prostate cancer risk. Nutr Cancer. 2006;55(1):21-7.
Saidi S, Stavridis S, Stankov O, Dohcev S, Panov S. Effects of Serenoa repens Alcohol Extract on Benign Prostate Hyperplasia. Pril (Makedon Akad Nauk Umet Odd Med Nauki). 2017;38(2):123-129.
Vela-navarrete R, Alcaraz A, Rodríguez-antolín A, et al. Efficacy and safety of a hexanic extract of Serenoa repens (Permixon ) for the treatment of lower urinary tract symptoms associated with benign prostatic hyperplasia (LUTS/BPH): systematic review and meta-analysis of randomised controlled trials and observational studies. BJU Int. 2018;
Angwafor F, Anderson ML. An open label, dose response study to determine the effect of a dietary supplement on dihydrotestosterone, testosterone and estradiol levels in healthy males. J Int Soc Sports Nutr. 2008;5:12.
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Back in June during the 21-Day Challenge, I asked you to share questions you had about my personal health routine, and I’m looking forward to answering those in the coming months. We talk a lot about generalities here, and for good reason. Research can and should drive principle, but oftentimes while we wait around for it (or have questions about the overall validity of what’s out there), n=1 self-experimentation can tell us a lot.
Over the years, I’ve gathered ideas for that experimentation by reading the studies and listening to others talk about the choices they make. All of it together has—and continues to—inform the routine I follow to live the life I want. Among the many questions you sent were inquiries about my supplement regimen. Today I’m sharing what I take, when I take it, and why.
As a former endurance athlete, supplements were tools of the trade. I fielded recommendations from coaches and specialists of course, but I also studied the subject intently on my own. To push my performance further, I even began developing my own formulas for training recovery back then. Though I’m not in the competitive athletic world anymore, I still feel the benefits of certain supplements in my personal health and performance, and I’ve continued to formulate those I wish to take.
Here’s a bit about my choices for supplementation and the changes I’ve made over the years in how I take them.
I’d love to hear your thoughts and any questions you have about what I take (or don’t take). And if you have other kinds of questions about my routine (or anything health-related of course), shoot me a message on the comment board. Thanks for stopping by, everyone.
Finally, for those who are curious about the supplements I’ve shared today, I have a deal on two of my favorites. Order Adaptogenic Calm today, and I’ll include a bottle of Primal Sun entirely free. Just add both Adaptogenic Calm and Primal Sun to the cart, and use the code FREESUN at checkout to redeem this offer. Valid on One-Time Purchases only. Offer expires 8/30 at midnight PDT.
The post My Supplement Routine: What I Take, When I Take It, and Why appeared first on Mark’s Daily Apple.
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It’s a short one, maybe one of the shortest reader questions ever, and it represents one of the few cut-and-dry stances in ancestral health. Humans are omnivores, seed oils are bad for you, no curls in the squat rack, and farmed salmon is toxic poison.
Right? Maybe not.
What’s with the pic of the farm raised salmon?
First of all, I’m not certain that salmon was actually farm-raised. Second, while I’m on the topic, allow me to make the case for farmed salmon. That may surprise you. For years, I’ve been a huge proponent of wild-caught salmon. It’s the only one I ever buy or consciously seek out at restaurants. I’ll eat farmed salmon if it’s the best option available, or if I’m a guest and that’s what’s for dinner—and do so happily, by the way—but I’ve always been a wild salmon guy.
However, not everyone has the means to buy fresh or frozen wild-caught salmon on a regular basis, and not everyone wants to eat canned salmon. Sometimes you just want a big slab of tender salmon with a swathe of crispy, salty skin. Sometimes all five members of your family want their own big slab of tender salmon with the crispy skin. Is farmed salmon a good, safe, effective option?
Let’s look at the evidence. First, what are the benefits of salmon, and how does farmed salmon compare?
The main reason people eat salmon is to get the long chained omega-3 fatty acids—the ones we use to quell inflammation, balance our omega-6 intake, and shift the membrane composition of our cells and structures.
Farmed salmon is a great source. A 6-ounce portion of farmed Atlantic salmon has 4.4 grams of omega-3 fatty acids, which is actually more than wild. A 6-ounce portion of wild sockeye salmon has 2 grams of omega-3s.
But what about the omega-6 fats? Isn’t farmed salmon “loaded” with them? Well, that same portion of farmed salmon has 3.3 grams of omega-6 fats to the wild salmon’s 0.3 grams. The ratio is “worse” than the wild salmon’s. But even then, it’s great. While the wild salmon’s omega-3:omega-6 ratio of 1:0.15 is about as perfect as you can get, the farmed salmon’s ratio of 1:0.75 is fantastic. Besides, it’s also the absolute amount of omega-6s that matter. Admittedly, 3.3 grams is nothing compared to what most people are getting from seed oils, junk food, or even random handfuls of almonds and pecans throughout the day.
There’s more to fish fats than the omega-3s. For instance, many fish fats have subfractional layers with specific health effects. Fats derived from organic Irish farmed salmon possess anti-thrombotic qualities—they reduce the formation of blood clots.
Astaxanthin is a carotenoid that gives salmon its pink hue and may provide neuroprotective effects, especially combined with omega-3s. Wild salmon obtain astaxanthin from the krill and other pink sea creatures they consume. Farmed salmon obtain it from the feed they eat, which has it added. Both farmed and wild salmon provide astaxanthin to those who eat it, but a recent study found that the astaxanthin in wild salmon has higher bioavailability.
What about the drawbacks of farmed salmon, like contaminants?
Even this issue isn’t so clear cut. For example, a 2017 study found higher levels of persistent organic pollutants, metals, and DHA in wild Atlantic salmon compared to farmed Atlantic salmon. Farmed salmon had more overall fat, mostly from saturated, monounsaturated, and omega-6 fats, but farmed was still loaded with omega-3s.
A recent study actually tracked the changes in blood markers of contaminants in response to a high intake of farmed salmon. Eating almost a pound of farmed salmon each week had no effect on blood levels of persistent organic pollutants or mercury.
Surprisingly, European farmed salmon seems to have the biggest contamination issue. Good news, though: a 13-year study of contaminant levels in Norwegian farmed salmon found that toxins are dropping as the years go on.
What about when the rubber hits the road, when actual living and breathing humans eat farmed salmon? Does it help or harm? Let’s see what’s out there:
In one 2016 study, overweight men and women who ate farmed salmon twice a week for 4 weeks had higher HDL, larger LDL particles, lower triglycerides, and an overall improved cardiovascular risk profile. Their large LDL particle number also increased, but I’m not sure what happened to their overall LDL particle number. Another study found farmed salmon reduced triglycerides and increased HDL compared to lean chicken.
Eating farmed salmon twice a week modified the plasma phospholipid composition in a favorable way, increasing DHA and EPA and decreasing omega-6 fats.
Chinese men with a high risk for heart disease improved cardiovascular biomarkers after adding farmed salmon to their diets.
This was an interesting one. A group of otherwise healthy overweight adults were told to eat add a large dose of either fatty fish or lean fish to their normal diets for 8 weeks. The fatty fish was farmed salmon. The lean fish was wild cod. What happened?
- Cod increased DHA in white blood cell membranes. Farmed salmon increased overall omega-3s and reduced omega-6s in white blood cell membranes.
- Farmed salmon improved postprandial blood glucose control. Cod did not.
- Farmed salmon resulted in a smaller increase in postprandial insulin than cod.
I’m not suggesting farmed salmon is better than wild, or even equivalent, but I want to impress upon everyone who reads this blog that you don’t have to drop $15 a pound for wild caught salmon if your budget doesn’t allow it. Those $6 a pound Atlantic salmon fillets might not be as vibrantly red, might have a couple more grams of omega-6, and might have more or less pollutants depending on where they were farmed, but they’ll still have way more omega-3 than omega-6, they’ll still have astaxanthin, and they can still be part of an overall healthy diet.
Thanks for reading, everyone. I’d love to get your thoughts on this down below.
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It’s been a long time since I published the Definitive Guide to Fish Oils.
Oh sure, here and there I’ve cited some research supporting the beneficial effects of fish fat, but it almost goes without saying that omega-3s are important. Everyone knows it. Even the most curmudgeonly, conventional wisdom-spouting, statin script-writing, lifestyle modification-ignoring doc will tell you to take fish oil. And research in the last few years has not only continually confirmed the health advantages but illuminated new applications—and new physiological explanations—for their essential function in the body.
But what are those benefits, exactly? Why should we be eating fatty fish or, barring access to high quality edible marine life, taking fish oil supplements?
A major reason is that fish oil can help us reclaim our ancestral omega-3:omega-6 ratio and thus restore the inflammatory backdrop of the human body.
Polyunsaturated fats convert to eicosanoids in the body. Both omega-6 and omega-3-derived eicosanoids are important signaling molecules, but each has different effects, both figuring prominently in the body’s response to inflammation. Omega-6 eicosanoids are generally pro-inflammatory, while omega-3 eicosanoids are anti-inflammatory. Omega-3-derived eicosanoids (the type we get from taking fish oil or eating fatty fish) actually reduce inflammation; in an unbalanced diet heavy in vegetable oils, the omega-6 eicosanoids far outnumber the omega-3s and contribute to a lot more inflammation.
The best available evidence points to ancient humans having an omega-3:omega-6 ratio of around 1 to 1. A typical ratio these days is 1 to 16!
As most diseases and health conditions have an inflammatory component, such lopsided ratios can predispose us to any number of health problems. Conversely, correcting those ratios with smart supplementation of fish oil has the potential to correct or prevent those health problems.
Let’s look at some of them and what the most recent research tells us.
How Omega-3s Benefit Health
Arthritis is an inflammatory disease, whether we’re talking autoimmune arthritis or wear-and-tear arthritis.
The potential mechanisms are there. In vitro studies using isolated joint tissue show that both DHA and EPA increase joint lubrication. Studies in people show that fish oil reduces inflammatory markers and may even stop the progression of inflammation into inflammatory arthritis.
In a recent study out of Thailand, knee arthritis patients who took fish oil improved their walking speed. “Everyone felt good and happy with the fish oil.” In psoriatic arthritis, fish oil reduced inflammatory markers and lowered patients’ reliance on pain meds.
Fish oil also helps reduce the symptoms of autoimmune rheumatoid arthritis (RA). In one paper, fish oil supplements had additive effects on top of RA drugs. 3-6 grams appears to be an effective dose range. If that sounds high, it is—but you need that much to quell the exaggerated inflammatory responses of RA.
Depression is another one of those conditions that we don’t often think of as an inflammatory disease, but it is. The evidence is considerable. Vets with the most severe depression also have the highest levels of inflammatory markers. Among Type 2 diabetes, depression and inflammation go hand in hand, with the latter appearing to play a causative role in the former.
There’s considerable evidence that the causation goes both ways: depression can increase inflammation, and inflammation can increase depression. Thus, treating one may treat the other. Since omega-3s are potent and broad-reaching anti-inflammatories, could fish oil treat depression?
Fish oil has proven effective with EPA having a greater effect than DHA. It’s even effective in patients with and without an official diagnosis of major depressive disorder. It’s effective in type 2 diabetics with depression.
The stress response is an inflammatory one. A healthy omega-3:omega-6 ratio—the foundation of our inflammatory response system—should produce a healthy stress response. Does it?
In response to mental stress, fish oil promotes a healthy, less reactive neurovascular response. It lowers resting heart rate, a good indicator of general stress resilience. When taken post-trauma, it even reduces psychophysiological symptoms (like pounding heart) in car accident survivors. And in alcoholics, fish oil reduces both perceived (subjective) stress and basal cortisol (objective).
General Inflammatory and Immune Responses
Name a disease and “elevated inflammation” or “exaggerated immune response” is probably part of the pathology. What effect does fish oil have on some of these inflammatory pathologies?
- Reduced inflammatory markers (HS-CRP) in Type 2 diabetes patients.
- Improved inflammatory markers in colorectal cancer, including HS-CRP.
- Reduced airway inflammation in asthma patients.
- Pre-op fish oil improved post-op inflammatory and immune markers in cancer surgery patients.
- Reduced inflammatory marker IL-10 in chronic Chagas cardiomyopathy, a serious heart condition.
- Reduced inflammatory gene expression in humans.
I could go on and on. And these are just studies done in the last year or two.
Fish Oil and Cardiovascular Disease
Not everything is so cut and dry. When it comes to certain conditions, like cardiovascular disease, the fish oil literature is confusing. Sometimes it helps, sometimes it doesn’t. What are we to make of it?
One thing that is unequivocal is that a high omega-3 index—the proportion of omega-3 fatty acids in the red blood cell membrane—is protective against cardiovascular disease (see the chart; as omega-6 content goes up, so does cardiovascular mortality). So the question isn’t if long chain fatty acids from fish oil are helpful. It’s: Are those fatty acids reaching your red blood cell membranes and being incorporated?
How To Improve Bioavailability
Several factors affect whether fish oil will increase omega-3 index and thus have the effects we’re looking for:
Omega-6 fats and omega-3 fats compete for space in the red blood cell membranes. If omega-6 intake is too high, fewer omega-3s will make it into the membranes, thereby inhibiting or even abolishing the positive effects of fish oil.
If omega-3 index is low, we’ll see effects. If it’s high enough, further fish oil has no additive effect. We see this in studies such as this one, where only older adults with a low omega-3 index experienced cognitive benefits from omega-3 supplementation. In another study of older adults and cognition that didn’t control for omega-3 index, they found no benefit.
Or in this study, where fish oil had benefits in congestive heart failure patients because they had low baseline levels of omega-3.
Or this study, where autistic patients—who tend to have lower omega-3 statuses than the general population—improved some behavioral measures after taking fish oil.
To take advantage of the full effects of fish oil, however, one must also limit the amount of omega-6 fats they eat. In one study, taking fish oil with saturated fat increased incorporation of omega-3s into red blood cell membranes, while taking it with omega-6 prevented omega-3 incorporation. The best way to do it is to eliminate seed oils—the most concentrated source of omega-6 fatty acids in the modern diet. If you don’t limit seed oils and other dense sources of omega-6s, you’ll have to consume extremely high doses of fish oil to make a dent in your inflammatory status.
Making It Easier To Get Your Omega-3s…
Thanks for reading today, folks. I take this information very personally in my life and business. To that end, this week I just released a new formula of Primal Omega-3s that enhances bioavailability and adheres to stricter environmental sustainability standards—all in a smaller capsule. The idea was to optimize benefits and maximize ease. And right now I’m also offering a deal to make this level of quality more affordable….
I’m kicking off the new formula with a BOGO deal. Buy one new Primal Omegas, get the second bottle free now through 8/10/18 at midnight PDT. Just add two Primal Omegas to your cart and use code NEWOMEGAS at checkout. Limit 1 per customer. One-time purchase only.
Thanks again, everybody. Have a great end to the week.
The post Omega-3 for Health: What the Latest Research Shows appeared first on Mark’s Daily Apple.
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People go keto for many different reasons. Some want to get better at burning fat so they have a clean, reliable source of steady energy at all times. Some people are treating a neurodegenerative disease, or trying to prevent one from occurring in the first place. Others just want to lose body fat, take advantage of the cognitive effects of ketosis, or stop seizures. Those are all common reasons to go keto. Another reason people go keto is for the benefits to physical performance.
Keto increases energy efficiency. You can do more in the aerobic (fat-burning) zone than a sugar-burner.
Keto spares glycogen. The more fat you’re able to utilize, the more glycogen you preserve for truly intense efforts.
Keto builds new mitochondria. Mitochondria are the power plants of our cells. More mitochondria means a larger engine.
That said, the performance benefits take a few weeks to manifest. During this time, a common side effect of the keto transition is reduced performance in the gym. People report feeling sluggish, slow, weak, and flabby in the days and weeks leading up to their adaptation. It’s understandable (and somewhat expected) why this can happen:
Fat provides tons of energy at a slow rate—but you’re not great at accessing it yet.
Glucose is more scarce but provides energy rapidly—and you just took it out of your diet.
Is there anything you can do to improve your performance in the gym during the transition?
Preserving Performance During the Keto Transition
Increase Fat Content
This goes without saying. Of course you’ll be eating more fat on a ketogenic diet. Right? What I mean is you should increase fat even more than you think for the first week. This has the effect of increasing AMPK activity, which hastens the creation of fat-burning mitochondria, upregulates fat metabolism, and speeds up your ability to utilize ketone bodies.
Increase Intake of Specific Fats
Certain fatty acids seem to increase AMPK more than others. The most potent ones I’ve found are:
- Long-chain omega 3 fatty acids, found in fish oil, fatty fish (salmon, mackerel, sardines), and shellfish.
- Extra virgin olive oil rich in polyphenols. The more peppery the oil, the more polyphenols.
- Palmitoleic acid, an omega-7 monounsaturated fat. The best source is mac nuts, unless you’re the type to eat whale blubber.
Include some mac nuts, EVOO, and wild fatty fish (or quality fish oil) on a regular basis.
Take Your Electrolytes
Electrolytes are already essential when transitioning toward a ketogenic diet. Since they regulate muscle contractions, heart function, intracellular fluid balance, and nerve impulses, they’re even more important when you’re exercising, Try 4.5 grams sodium (about 2 teaspoons of fine salt or a little under 3 teaspoons of kosher salt), 300-400 mg magnesium, and 1-2 grams of potassium each day on top of your normal food. Going keto really flushes out water weight, and tons of electrolytes leave with it.
Stick To Weights and Walking
The big problem with physical performance during the keto transition is that you’re not great at burning fat, you’re still reliant on glucose to fuel your training, and you don’t have much glucose coming in. For the transition window, this makes high intensity, high volume training a bad idea.
Running a race-pace 10k is going to be hard. Participating in the CrossFit Games is a bad idea. You haven’t yet built the machinery necessary to make those work, nor do you have the glucose necessary to tide you over. You know what will work? Weights and walking.
Walking is totally aerobic, using almost no glycogen of note. Weight training can be glycogen-dependent, but doesn’t have to be if you keep weights high and volume low. Think low (2-6 reps) volume weight training. Whatever you do, the key is to make sure your training is low-stress.
Stick to weights and walking and you’ll hasten keto-adaptation, not harm it. Then you can resume some of your normal activities.
Creatine boosts muscle content of phosphocreatine, which we can use to generate large amounts of ATP in a short period of time for quick bursts of speed or strength. This doesn’t dip into glycogen or fat. It’s ATP-PC, or ATP-phosphocreatine. If you’re going to sprint or lift heavy stuff, you’ll definitely want extra creatine in your muscles.
No need to “pre-load” creatine. Just take 5 grams a day and be sure to drink plenty of water and get plenty of electrolytes (which you’ll already be doing on keto).
If you’re going to sprint on keto, keep a few tips in mind.
Short sprints—3-5 seconds.
Plenty of rest—as much as you need to go as hard and fast as the last one. This gives you the chance to replenish some of your phosphocreatine.
This won’t fully replenish your ATP-PC stores. You won’t be able to go as hard, or do as many reps as you’d like in subsequent sprints. But if you absolutely must sprint, this the way to do it without relying on glucose. Look for the sensation of diminished power. That’s when you’re hitting the PC wall and will start dipping into glucose. Avoid that sensation. Stop short of it.
Don’t freak out if you “dip into glucose,” though. Yeah, dipping into glucose constantly will inhibit keto-adaptation in the early stages, but once or twice won’t make a big difference. Just don’t make glucose-intensive work a habit.
Get Primal Endurance
Brad Kearns and I wrote Primal Endurance because endurance athletes needed a better, safer, healthier way to do the thing they love-hated. I know, because that was us. We both got out of serious endurance athletics because it was harming more than helping us. But that doesn’t mean we stopped missing it. Once an endurance athlete, always an endurance athlete. You can’t shake the bug.
Primal Endurance shows you how to build a powerful, long-lasting aerobic base using primarily stored body fat. It’s the perfect complement to a keto lifestyle, especially if you want to optimize your athletic performance and make your physical activity support rather than inhibit keto-adaptation.
Understand the Purpose of Training
Lifting in the gym isn’t a competition. You’re not being paid. The whole point of lifting weights, running sprints, and doing low level aerobic activity is to get better at doing those things. It’s not about “winning” every workout. That’s what training is—accepting paltry results with the assurance that you’re getting better. Think about it.
When you add 50 pounds to the bar, it’s harder. The bar moves more slowly. You can’t do as many reps. From your brain’s perspective, you’re suddenly “weaker.” Yet, it’s the best way to get stronger in the long run.
When you try a new sport or physical activity, you’re no good. You’re a beginner. People you’re sure you could trounce in your preferred activities are destroying you. This doesn’t mean you should give up. It means you have to get better. And if you stick with it, you will get better.
When you train on your newly keto diet, think of it like you’re increasing weight, upping the intensity, or learning a new sport. You’re not weaker. You’re not getting worse. The training is getting harder. The pain is increasing. And, although it might not feel like it right now, you’re going to be better off in the long run.
Once you’re fully fat-adapted and able to utilize fats, ketones, and glycogen, you’re going to be an unstoppable force.
Okay, that’s short term. What about long term?
How To Enhance Performance Long-Term With Keto
Carb Cycle When Necessary
Once you’ve been keto for at least a month, don’t be afraid to cycle in carbs to support your intense training. If you’ve depleted muscle glycogen with an intense training session, you’ve created a glycogen debt and any carbs you eat in the hours following that workout will go to repleting that glycogen. Best of all, intense training upregulates insulin-independent glycogen uptake immediately post-workout. That means if you do it right, you don’t even need to increase insulin to shove those glucose molecules into your muscles.
Carb Cycle the Right Way
Many people do carb cycling on keto completely wrong. They spend two days binging on bear claws and gummy bears then wonder why they’ve gained weight and lost progress. A few tips:
You probably need fewer carbs than you think. A little snack of 20-40 grams of carbs right after a really intense workout can make all the difference in the world without knocking you out of ketosis, provided you’ve accumulated enough of a glycogen debt.
Choose the right carbs. A sweet potato the night before to top off glycogen stores, a cooked-and-cooled white potato (diced and quickly seared until crispy in a pan is my favorite way to eat these), or UCAN Superstarch (whose slow absorption has minimal impact on insulin and thus ketones) are all good choices.
Do it for the right reasons. Don’t carb cycle because you miss French fries. Carb cycle because you’ve depleted glycogen.
And hell, briefly exiting ketosis isn’t the end of the world. Most people doing keto aren’t doing it as a life or death intervention. They just want to look, feel, and perform better. Don’t let keto become an ideology. It is a tool for your pleasure.
Chase Results, Not Ketones
In my experience, the people who focus on results rather than ketone readings do best.
Heck, if you spend half your time stressing about your ketone levels, the resultant cortisol will probably trigger gluconeogenesis and inhibit keto-adaptation by introducing a flood of new glucose into your body.
Are you leaning out? Thinking more clearly? Skipping the afternoon nap and breakroom donuts without even thinking about it? Lifting more? Running easier? Lab tests improving?
Then you’re good. That’s what matters.
Besides, the point of keto-adaptation is fat-adaptation—the ability of your muscles to utilize free fatty acids. That’s the real power of going keto, because once the fat-burning machinery is established and your muscles can use fats directly, you have more leeway to eat protein and cycle carbs.
Those are the tips I’ve found to be most useful for people acclimating to exercise on a keto diet. What’s worked for you?
The post Exercising While Keto: 11 Tips for the Transition (and Long-Term) appeared first on Mark’s Daily Apple.
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One of the biggest mistakes I see among people who exercise is they forget this core truth: we get fitter not from training, but from recovering from training. This doesn’t just occur in beginners either. Some of the most experienced, hardest-charging athletes I know fail to heed the importance of recovery. Hell, the reason my endurance training destroyed my life and inadvertently set the stage for creation of the Primal Blueprint was that I didn’t grasp the concept of recovery. I just piled on the miles, thinking the more the merrier.
It didn’t work.
What is recovery, anyway?
There’s short-term recovery. Your heart rate slows back down, your body temperature drops, your sweat dries, your muscles and lungs stop burning.
Long-term recovery is less conspicuous, more internal. You replace lost energy stores, repair damaged muscle, clear out waste products, and begin the process of adaptation to the training.
When both short- and long-term recovery happen together, you “feel ready” to go again.
Some portion of how quickly we recover from training is out of our direct control.
Genetics is one factor we can’t control. Researchers have found genetic variants of collagen-encoding genes that increase or decrease the rate at which we recover from exercise-induced muscle damage, muscle tissue genes that increase resistance to exercise-induced muscle soreness, immune genes that affect the speed of adaptation to training. But even many genetic variants purported to affect recovery act through decisions carriers make. A carrier of a genetic variant linked to muscle power experienced more muscle damage and required more recovery after a soccer match, but only because that carrier “performed more speed and power actions during the game.”
Age is another factor out of our direct control. Sure, living, eating, and training right can stave off many of the worst effects of aging. Sure, a sedentary 70-year-old will recover from a workout far more slowly (if he or she can be cajoled into training) than a 70-year-old master athlete. But time does tick on. Following training that fatigues but doesn’t damage the muscles, like easy cycling, light weight training, or a sub-aerobic threshold jog, older athletes recover muscle function and performance at similar rates to younger athletes. After intense exercises that damage the muscles, like sprints, heavy lifting, intervals, or longer race-pace runs, however, older athletes recover more slowly than younger athletes.
Other factors, while preventable and modifiable over the long haul, inexorably inhibit workout recovery once they’re in place:
If you’re sick, you won’t recover as quickly. Illness diverts some of the resources that would otherwise be used to recover from training.
If you have heart disease, you’ll recover more slowly. In one study, having heart disease was the greatest predictor of a slower rate of heart rate recovery after exercise.
If your hormones are out of whack, you’ll likely recover more slowly. Hormones are the messengers and managers that tell our cells what to do. That includes muscle repair, hypertrophy, fuel replenishment, inflammatory signaling, and every other cellular function related to recovery.
Now I’ve got bad news and good news. Everything else that slows down workout recovery is under your direct control.
Factors We Can Control
Stress is stress. Traffic is a stressor. A job you hate is a stressor. Procrastinating until you absolutely must get working is a stressor. And yes, exercise is a stressor. Too much of the psychological, lifestyle, or mental stress we all face impairs our ability to recover from exercise-induced stress.
Recent research confirms that “mental stress” impairs workout recovery, and it doesn’t speak in generalities. Thirty-one undergrads were assessed for stress levels using a battery of psychological tests, then engaged in a heavy lower body strength workout. At an hour post-workout, students in the high stress group had regained 38 percent of their leg strength, while students in the low stress group had regained 60 percent of their strength.
I developed my anti-stress supplement Primal Calm (now, Adaptogenic Calm) back in the chronic cardio days as a way to improve my training recovery. That’s what gave the product so much momentum in the endurance community—it turns out that beating back stress of all kinds quickened recovery from a very specific type of training stress.
Some stress is unavoidable. But most of us create additional stress in our lives and fail to do enough to counter or manage it. Stop making unforced errors.
Sleep debt impairs exercise recovery primarily via two routes: by increasing cortisol, reducing testosterone production, and lowering muscle protein synthesis; and by disrupting slow wave sleep, the constructive stage of slumber in which growth hormone secretion peaks, tissues heal, and muscles rebuild. That’s probably why sleep deprivation has been linked to muscular atrophy and increased urinary excretion of nitrogen, and why the kind of cortisol excess caused by sleep deprivation reduces muscle strength.
Additionally, sleep loss can increase the risk of injuries by decreasing balance and postural control. If you trip and fall, or throw out your back due to poor technique, you won’t even have a workout to recover from.
Most people think bad sleep is unavoidable. It happens to the best of us from time to time, but a night of bad sleep here and there isn’t going to slow down recovery. The real recovery killer is chronically bad sleep, and that’s the kind most of us can avoid by sticking to a good sleep hygiene regimen.
Since every physiological function requires a micronutrient substrate—vitamin, mineral, hormone, neurotransmitter, etc.—and physiological functions increase with exercise and recovery, active people require more micronutrients in their diet. “More of everything” is a safe bet, but there are a few key nutrients that working out especially depletes:
Zinc: Exercise, especially weight training, works better with plenty of testosterone on hand to build muscle and develop strength. Zinc is a key substrate for the production of testosterone, and studies show that exercise probably increases the need for zinc. In fact, one study found that exhaustive exercise depleted testosterone (and thyroid) hormones in athletes, while supplementing with zinc restored it.
Magnesium and Other Electrolytes: Magnesium is required for a number of physiological processes related to workout recovery, including oxygen uptake by cells, energy production, and electrolyte balance. Unfortunately, as one of the main electrolytes, lots of magnesium is lost to sweat during exercise. The same could be said for other electrolytes like calcium, sodium, and potassium, but most people get plenty of those minerals from a basic Primal eating plan. Getting enough magnesium, however, is a bit tougher, making magnesium deficiency a real issue for people trying to recover from workouts.
Iron: Intense exercise depletes iron, which is instrumental in the formation of red blood cells and oxygen delivery to your tissues during training and the immune response after it. They even have a name for it—exercise-induced anemia.
Post-workout delayed onset muscle soreness, or DOMS, is no joke. While many of you folks reading this probably enjoy DOMS and take it as feedback for a job well done, it’s a hurdle that many beginners never move past. They join a gym, d0 a workout, feel great, go to bed feeling awesome, sleep like a baby, then wake up and find they have the bipedal capacity of a three-month-old. They can barely walk. Lifting their arms to brush their teeth is agony. Walking downstairs is out of the question. Some will move past the DOMS and get back into the gym. Many will not.
Low Fuel Availability
Working out expends energy. That energy must be replenished before you’re fully recovered and prepared to do another workout. Unless you’re trying to increase efficiency by training in a state of low fuel availability, like the “train low-carb, race high-carb” method, you should recover what’s been lost. What you replenish is conditional on the type of exercise you did. If you went for a long hike or easy bike ride that burned primarily body fat, you don’t need to—and probably shouldn’t—”replenish what you lost.” If you’re coming off a 30-minute full body CrossFit session that left you gasping on the ground in a puddle of sweat, you probably have some glycogen stores to refill.
This is a common issue for folks trying to lose weight through diet and exercise. Inadequate calorie intake coupled with intense exercise sends a “starvation” signal to the body, causing a down-regulation of anabolic hormones. Instead of growing lean mass and burning body fat, starvation (whether real or simulated) promotes muscle atrophy and body fat retention. Either alone can be somewhat effective, but combining the two for too long will only impair recovery.
Drinking directly impairs muscle protein synthesis, the essential step in muscle recovery and adaptation to training. Moderate or “social” drinking is probably safe (just don’t use alcohol as a post-workout recovery drink), but even just a single day per week of binge drinking is linked to 4x the risk of sarcopenia, or muscle-wasting. It’s hard to recover from your workouts if your muscles are atrophying.
Oddly, drinking directly after a training session also increases testosterone levels. One theory is that testosterone levels rise after drinking because it becomes less bioavailable; your muscle cells’ resistance to testosterone goes up, so it just circulates and gives “false” readings.
Things You Can Try
The obvious thing to try is the opposite of all the modifiable and preventable recovery-inhibitors mentioned above. Get good sleep, don’t drink too much (especially post-workout), get a handle on your stress, eat enough food, eat enough protein, get your micronutrients. What else?
L-citrulline is an amino acid found in watermelon that shows a significantly ameliorative effect on post-workout muscle pain, or delayed onset muscle soreness (DOMS). You can also supplement directly with L-citrulline, which may work, but watermelon is so good right now with a little salt, lime juice, and cayenne pepper, and it’s actually lower in carbs than you probably think (about 10 grams per cup of watermelon). I recommend fresh watermelon over pasteurized juice, as heat treatment reduces the effect.
Beets (and beet juice) aren’t only good for exercise performance. They also reduce DOMS. Nitrates have been posited as the primary constituent responsible for the effect, but beet juice works better than pure sodium nitrate.
Tart Cherry Juice
Tart cherry juice is best used to recover during competition, when your primary concern is to get back out there and perform. Its extreme effectiveness at killing muscle pain, reducing local and systemic inflammation and exercise-induced muscle damage suggests it may hamper training adaptations, however. It does also improve sleep, which should translate into better adaptations.
Massage feels great, and the evidence shows that it’s great for recovery from exercise. It alleviates DOMS. It speeds up the recovery of muscle strength and enhances proprioception. It improves central nervous system parasympathetic/sympathetic balance, even if the masseuse is one of those weird back massage machines.
These aren’t just for show. A recent meta-analysis of the available research concluded that compression garments enhance muscle recovery after strength training and improve next-day cycling performance.
Although we get creatine from red meat and fish, supplementary creatine can boost our recovery from exercise via a couple mechanisms. First, it increases muscle content of phosphocreatine. That’s the stuff we use for quick bursts of maximal effort, so carrying a little extra can do wonders for our ability to perform. Second, it enhances muscle glycogen replenishment without increasing insulin.
Fish Oil (or Fatty Fish)
A cold water plunge after training enhances the recovery of muscle function. However—and this is a big “however”—post training cold water plunges also seem to impair long term muscular adaptations to resistance training. In other words, a cold plunge might help you get back in the game for the short term at the cost of long-term adaptations.
I always say “Eat the carbs you earn.” While that often means eating fewer carbs than before, it can also mean eating more if you’ve trained hard enough to warrant them. This even applies to keto folks; depleting glycogen through exercise creates a “glycogen debt” that you can repay without inhibiting ketosis or fat-adaptation too much. The carbs—which you don’t need much of—go into muscle glycogen stores for recovery and later use without disrupting ketosis.
Don’t take this final section as a blanket recommendation, however. Before taking ice baths, dropping $500 on massages every week, taking a long list of expensive supplements, and walking around in a full body compression suit, make sure you’re sleeping, eating enough food, and giving yourself enough time between workouts. Quite often, handling the basics will be enough.
What have you found to be the best way to recover from your training? What are the biggest roadblocks? Let me know down below, and thanks for reading!
The post What Causes Slow Post-Workout Recovery—and What Can You Do About It? appeared first on Mark’s Daily Apple.
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For today’s edition of Dear Mark, I’m answering three questions. First, what are some less expensive sources of marine fat high in omega-3s? Is canned salmon a good, safe, effective option? Second, a reader is training hard, eating low-carb/keto, doing IF, and feels pretty good despite not losing or gaining any weight? What should she do? What could she be doing wrong? And third, should you go keto while nursing?
Marine fat. Good examples? I have tried to eat sardines, I really have. I don’t know why they repulse me so. Where else can I turn? Safe salmon is just so expensive unless you get canned, and even then, can you trust it? If it’s true satiety I’m going for, a supplement (cod liver oil?) is probably not going to give me that.
I hear you on the canned salmon. When I was first looking into this years ago, I worried that canned fish would be damaged by heat and perform worse than supplements. Turns out it’s very useful. In one study, researchers gave women with a high risk of breast cancer omega-3 fats via fish oil caps or canned salmon. Both “supplements” worked at increasing levels of DHA and EPA. Fish oil increased the EPA content of red blood cells and plasma four-fold; canned salmon increased it two-fold. The change in DHA was similar in both groups, as was the overall change in breast tissue fatty acids. Fish oil may be more potent, but it’s unclear if quadrupling your RBC EPA is necessarily more desirable than doubling. You also have to consider the two things the fish eaters got that the fish oil quaffers didn’t: all the micronutrients (selenium, iodine, astaxanthin, etc) and macronutrients (protein) salmon provides.
Canned salmon is a good option, and most of it is BPA-free these days (but verify). If you enjoy it (some do not), look for salmon that includes the bones and skin. Tons of benefits there—calcium, collagen, extra oil. Trader Joe’s used to carry one like that. They still might.
Fresh mackerel is good. Here’s a buying and cooking guide to mackerel I did awhile back. It’s affordable and full of omega-3s.
If you can find them, fresh sardines are a totally different animal. Just make sure the fish smells clean, has clear eyes, is firm, and resists sagging when held parallel to the floor by the tail.
#6 is me right now. I am eating low carb (maybe even Keto), and I’m IF’ing every day (allowing only coffee w/ a splash of cream in the morning). My appetite is finally feeling quite suppressed. The nice thing is that I’m not counting. I am eating intuitively; and at the end of the day, I log what I ate as best as I know how (since I didn’t measure), to just check, and everything seems to be on point with my calories and macros. I train brazilian jiu jitsu several times a week, as well as do HITT style workouts, with strength training on my off days. I usually have a couple days a week that I don’t train.
My question is, I’m not losing and I’m not gaining – so do I keep doing what I’m doing? Or do I change things up? I feel fine – plenty of energy, and I’m not hungry. If I were hungry, I’d eat. My goal is to lose another 15 lbs, and I love the keto/IF style for me because it works well with my lifestyle.
First, make sure you actually need to lose another 15 pounds. 15 pounds of what? Fat, lean? Rather than thinking in terms of bodyweight, it’s often more helpful to have concrete goals. Is there an article of clothing you want to be able to fit into?
You’re training a ton. That’s great, it can be incredibly rewarding—I know the feeling. But that, paired with “my appetite is finally feeling quite suppressed” is a bit of a warning sign. When I trained daily, my appetite was through the roof. I couldn’t get enough food. You’re hitting it really hard. BJJ, extremely demanding, glucose-intensive. HIIT, extremely demanding, glucose-intensive. Weights, extremely demanding. You should be hungrier, not less.
All in all, the message your training and restricted eating may be sending to your body is one of scarcity. It’s good that you’re neither gaining nor losing and have plenty of energy, but that could change quickly. Try giving your body a few more signals of abundance; it may be exactly what you need, and it could help you avoid problems in the future.
Try eating a few more carbs and calories on your training days, timed after your workouts. You’re burning through a lot of glycogen, and if you’re eating keto with IF you’re probably not replenishing it.
Good luck and keep us posted.
Is it safe to do a moderate keto diet while breast feeding?
If you recall from previous posts, oxaloacetate is necessary for finishing the Krebs’ cycle and producing ATP from fat and glucose. Running out of oxaloacetate means we can’t make ATP from fat and glucose and need an alternate energy source: Ketones. Lactating women also use it to produce lactose, the milk sugar that provides much of the nursing baby’s energy needs. That means that lactating women can eat more carbs and protein and still remain in ketosis. It also means that eating a strict ketogenic diet extremely low in carbs and protein is likely to impair milk production.
While many women report remaining ketogenic while nursing without issue, there are a few case studies of breastfeeding women suffering lactation ketoacidosis, a dangerous condition where chronically low insulin prevents the cells from accessing blood glucose and promotes unchecked ketone production that make the body overly acidic. This can be life threatening. Triggers of lactation ketoacidosis have included starvation (don’t starve yourself or even fast while breastfeeding), twin lactation (feeding two increases the amount of lactation substrate you need to consume), and a low-calorie/low-carb/high-fat diet (bad combo).
Had I a set of breasts from which an infant would be suckling, I’d just opt for a regular old low-carb diet, Primal style. I wouldn’t worry about ketone production so much as eating enough calories.
That’s it for today, folks. Thanks for reading, take care, and chime in down below with your own input!
The post Dear Mark: Marine Fat Sources, Not Gaining/Losing, Keto Breastfeeding appeared first on Mark’s Daily Apple.
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