Collagen or whey. Which should you choose?
For years, collagen/gelatin was maligned by bodybuilding enthusiasts as an “incomplete protein” because it doesn’t contain all the essential amino acids, nor does it contribute directly to muscle protein synthesis. There’s definitely truth to this. If you ate nothing but gelatin for your protein, you’d get sick real quick. That’s exactly what happened to dozens of people who tried the infamous “liquid protein diet” fad of the 70s and 80s, which relied heavily on a gelatin-based protein drink. Man—or woman—shall not live by collagen alone.
As for whey, it’s an extremely complete protein. It’s one of the most bioavailable protein sources around, a potent stimulator of anabolic processes and muscle protein synthesis. I consider it essential for people, especially older ones in whom protein metabolism has degraded, and for anyone who wants to boost their protein intake and get the most bang for their buck.
This said, which is best for your needs today? Let’s take a look….
Collagen and whey are two completely different foods. Whether you take one or the other depends on a number of factors.
The first thing to do is explore the different benefits and applications of whey and collagen.
Whey Protein: Uses and Benefits
Whey is one of two primary dairy proteins, the other one being casein. It gained its reputation in the fitness world as a proven muscle-builder, but it actually has some interesting health effects that have little to do with hypertrophy.
In fact, whey is more than just protein. It also includes bioactive components such as lactoferrin (which improves bone health), beta-lactoglobulin (which can promote glutathione synthesis and protect against allergy), alpha-lactoalbumin (which can improve resistance to the cognition-depleting effects of stress), and immunoglobulins (which have antimicrobial effects). Whey also turns into some interesting peptide metabolites upon digestion which, according to a review, can improve blood lipids and lower blood pressure.
What Are Some Good Applications Of Whey?
Obesity: Whey tends to reduce fasting insulin levels in the obese and overweight (but not healthy prepubertal boys, who could use the growth promotion), increase satiety, reduce food intake, and improve resting energy expenditure. If you’re trying to lose weight or prevent obesity, you can’t ask for a better trifecta than increased energy burning, increased satiety, and reduced intake.
Diabetes: Eaten before a meal, whey reduces the glucose spike from the subsequent meal in non-diabetics and type 2 diabetics alike. It achieves this by “spiking” insulin, but transiently; the insulin area under the curve improves even as the immediate insulin response increases. Plus, as seen above, fasting insulin tends to lower in people consuming whey protein. Spikes are not persistent elevations.
Fatty liver: In obese women, a whey supplement reduces liver fat (and as a nice side effect increases lean mass a bit). Fatty liver patients also benefit from whey, enjoying improvements in glutathione status, liver steatosis, and antioxidant capacity. Rats who supplement with whey see reduced fat synthesis in the liver and increased fatty acid oxidation in the skeletal muscle.
Stress: In “high-stress” subjects, a whey protein shake improved cognitive function and performance by increasing serotonin levels. The same shake had no effect on “low-stress” subjects. And dietary whey also lowers oxidative brain stress, at least in mice.
Cancer: Both the lactoferrin found in whey and the glutathione synthesis whey promotes may have anti-cancer effects. Lactoferrin shows potential to prevent cancer that has yet to occur and induce cell death in existing cancer cells. In a recent human study, oral lactoferrin suppressed the formation of colonic polyps. And in animal cancer studies and human cancer case studies, whey protein has been shown to increase glutathione (“foremost among the cellular protective mechanisms”) and have anti-tumor effects.
HIV: People with HIV experience a drastic reduction in glutathione levels. As the master antioxidant, getting glutathione higher is pretty important. Whey won’t cure anything, but it does improve CD4 (a type of white blood cell) count, lower the number of co-infections, and persistently increase glutathione status.
Cardiovascular disease: Last year, a review of the effect of whey on major cardiometabolic risk factors found that whey protein improves the lipid profile, reduces hypertension, improves vascular function, and increases insulin sensitivity and glucose tolerance. Whey peptides that form during digestion actually act as ACE-inhibitors, reducing blood pressure similarly to pharmaceuticals without the side effects.
Sarcopenia: Muscle wasting, whether cancer-related or a product of age and inactivity, is a huge threat to one’s health and happiness. Studies show that whey protein is the most effective protein supplement for countering sarcopenia, especially compared to soy. An anti-sarcopenia smoothie I always have people drink on bed rest is 20-30 grams of whey isolate, a couple egg yolks, milk, cream, and ice. Tastes like ice cream and works like a charm. One time a friend even gave this to his grandmother who was on bedrest in the hospital with diarrhea, mental confusion, and a total lack of appetite. She was in a bad state. After a day or two of the smoothie, she recovered quite rapidly, regaining her appetite and alertness.
Gastrointestinal disorders: Dairy gets a bad rap in some corners for its supposed effects on the gut, but a component of dairy can actually improve gut health, even in patients with gastrointestinal disorders. In Crohn’s disease patients, a whey protein supplement reduces leaky gut. In rodent models of inflammatory bowel disease, whey protein reduce gut inflammation and restore mucin (the stuff used to build up the gut barrier) synthesis.
Oh, and whey is great for hypertrophy.
When To Choose Whey
- If you lift and want some extra protein, whey’s a great choice.
- If you’re older and worry about your ability to metabolize and utilize protein, some extra protein via whey can help.
- If you have any of the conditions listed above, whey’s a great choice. Do note that some of the benefits may stem from simply eating more protein than before. Whey itself may not be the whole cause; an extra slab of steak or a few more eggs could possibly have the same effect.
Along with foods like organ meats, egg yolks, and shellfish, I consider whey to be an important “supplemental food”—a food that acts like a high-density nutrition supplement, powerful in small doses and worth including in almost every diet.
Collagen Protein: Uses and Benefits
I advocate collagen protein as a fourth macronutrient. It’s different enough from whey and other “regular” proteins, serving a totally different function in the body.
If whey has been the gold standard for the muscle building amino acid profile for 30 years, collagen is the gold standard for supporting collagen-based structures in the body (fascia, ligaments, tendons, cartilage, skin, hair, nails). We don’t get much collagenous material in a normal diet these days, and meat proteins and/or plant proteins and/or milk, eggs, etc. don’t have the collagen peptides nor the ideal ratio of glycine, hydroxyproline, and other amino acids found abundantly in collagen. Furthermore, metabolism of the amino acids present in muscle meat deplete our reserves of glycine, thereby increasing the requirement even further. The more meat you eat, the more collagen you need.
Why We Need Collagen So Much These Days
This (non)relationship with collagen is extremely novel for our species. For millions of years up until very recently we ate nose to tail. We ate the entire animal. To give you an idea of how much collagen we’d have eaten, the average cow is about half muscle meat and half “other stuff,” which includes bones, skin, tendons, ligaments, fascia, and other bits extremely rich in collagen. That’s a ton of glycine and a far cry from eating nothing but ground beef and ribeyes. And more recently, even when we moved toward shrink-wrapped select cuts of meat and away from bones and skin, we still had jello. Then, when jello got maligned, we had nothing. So for the past 20-30 years or so, most Americans have had no appreciable source of collagen peptides in their diet.
Just based on what we know about human biochemistry, this is a disaster. The human body requires at least 16 grams of glycine per day for basic metabolic processes, yet we can only synthesize 3 grams, and the typical omnivorous diet provides just 2-3 grams per day, so we’re looking at an average daily deficit of 10 grams that we need to make up for through diet. Collagen is roughly 1/3 glycine, so that means we need to be eating about 30 grams of collagen per day to hit our 10 gram dosage. And in disease states that disrupt glycine synthesis, like rheumatoid arthritis, or on plant-based diets that provide little to no dietary glycine, we need even more.
I suspect a lot of pro athletes who have connective tissue issues could use even more collagen, especially since they’re exposing their tissues to such incredible stress. I know I did back during my competition days.
What Does Collagen Do For Our Bodies?
It supports our connective tissue and collagen-based structures: fascia, ligaments, tendons, cartilage, skin, hair, and nails.
It improves sleep quality. Human studies show that 3 grams of glycine taken before bed increases the quality of your sleep and reduces daytime sleepiness following sleep restriction. Now that’s isolated glycine rather than collagen, but collagen is the best source of glycine. I can say that a big mug of bone broth or a couple scoops of collagen peptides before bed knock me out and give me great sleep.
It balances your muscle meat intake. I mentioned this earlier, and we see both observational and interventional evidence for it.
- Observational: In one recent observational study, the relationship between red meat and diabetes was abolished after controlling for low-glycine status. People with low glycine levels and high meat intakes were more likely to have diabetes; people with higher glycine levels could have higher meat intakes without any issues. In another study, low circulating levels of glycine predicted diabetes risk.
- Interventional: In both worms and rodents, excessive intake of methionine (the amino acid most abundantly found in muscle meat) reduced longevity, while adding in glycine restored it.
It improves gut health. When I gave up grains and stopped endurance training at age 47 my gut health improved immensely. Like, world-changing for me. But I was still at 90-95%. When I started supplementing with collagen, my gut finally had that last 5% of repair/support/healing it needed to get to 100%.
It’s a great pre-workout. Though maybe not for the reasons most people take “pre-workouts.” I’ve also experienced rapid healing of tendinitis through using pre-workout collagen with vitamin C. I’m not just imagining it because I’ve dealt with a ton of tendon issues over the years, and they never healed that quickly until I introduced pre-workout collagen.
I’ve noticed that my hair and nails grow much faster than before.
Final Answer: Which One?
So, should you use whey or collagen? Let’s get to the bottom line, Sisson.
I made Primal Fuel because I wanted a high quality, low-sugar, moderate-fat meal replacement whey protein.
Personally, I had a need for both.
If I had to choose one, collagen is a better choice for the vast majority of you.
Essential amino acids aren’t a big problem on most ancestral diets, like paleo, Primal, or Primal-keto, and if you’re eating enough animal protein you don’t really need whey. Now, can you benefit from whey despite eating meat? Sure. Necessary does not mean optimal; whey has been shown to improve hypertrophy and muscle recovery from resistance training, plus all the other benefits I already detailed earlier. Almost anyone who does anything in the gym will see benefits from adding 20 grams of whey per day.
But almost no one is getting enough collagen, even the ancestrally-minded eaters who are aware of its importance. And that is a historical aberration on a massive scale. It hasn’t been done before. I wouldn’t recommend testing those waters.
And of course, powders aren’t the only way to get collagen and whey. They both appear in plenty of foods. The powders are just convenient to have on hand when you forget to make the bone broth (chicken, beef, turkey) or throw the oxtails in the crockpot. (Check out those linked recipes if you prefer broth or stew sources.)
Which do you prefer—whey or collagen? What benefits have you noticed from each?
Thanks for reading, everyone. Let me know your thoughts, and take care.
Wodarski KH, Galus R, Brodzikowska A, Wodarski PK, Wojtowicz A. [The importance of lactoferrin in bone regeneration]. Pol Merkur Lekarski. 2014;37(217):65-7.
Markus CR, Olivier B, De haan EH. Whey protein rich in alpha-lactalbumin increases the ratio of plasma tryptophan to the sum of the other large neutral amino acids and improves cognitive performance in stress-vulnerable subjects. Am J Clin Nutr. 2002;75(6):1051-6.
Pal S, Ellis V, Dhaliwal S. Effects of whey protein isolate on body composition, lipids, insulin and glucose in overweight and obese individuals. Br J Nutr. 2010;104(5):716-23.
Hall WL, Millward DJ, Long SJ, Morgan LM. Casein and whey exert different effects on plasma amino acid profiles, gastrointestinal hormone secretion and appetite. Br J Nutr. 2003;89(2):239-48.
Shertzer HG, Krishan M, Genter MB. Dietary whey protein stimulates mitochondrial activity and decreases oxidative stress in mouse female brain. Neurosci Lett. 2013;548:159-64.
Bounous G. Whey protein concentrate (WPC) and glutathione modulation in cancer treatment. Anticancer Res. 2000;20(6C):4785-92.
Meléndez-hevia E, De paz-lugo P, Cornish-bowden A, Cárdenas ML. A weak link in metabolism: the metabolic capacity for glycine biosynthesis does not satisfy the need for collagen synthesis. J Biosci. 2009;34(6):853-72.
The post Collagen vs. Whey: Which Protein is Best For Your Needs? appeared first on Mark’s Daily Apple.
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Last week, I linked to a story about a popular vegan blogger, author, and influencer who found herself going into menopause at the age of 37 despite doing “everything right.” She exercised, she ate raw, she avoided gluten and refined sugar, and, most importantly, she avoided all animal products. Now, this wasn’t a randomized controlled trial. This wasn’t even a case study. But it was a powerful anecdote from someone whose livelihood depended on her remaining a raw vegan. It wasn’t in her interest to make it up.
So, it got me wondering: How do diet and lifestyle influence the timing of menopause?
Now, before I begin, let’s just state the obvious: Menopause isn’t a problem to be avoided. It’s not something to be feared or maligned. It’s not “the end.” I wrote an entire series on menopause last year, and there will always be more to come on the subject because it’s an important time of life with its own questions and possibilities. While it’s a natural, evolutionarily-preserved part of being a woman, it also follows a natural cadence. Menopause at the right time in accordance with your genetics is normal, expected, and healthy. Menopause that occurs earlier than your genetics would direct suggests something is amiss. Sure enough, early or premature menopause—defined in most places as menopause before the age of 40—has a number of troubling links to poor health outcomes.
Early menopause is linked to:
- A shorter life and an increase in the risk of type 2 diabetes.
- Reduced physical function in later years.
- Lower cognitive function.
- Increased heart disease.
Not to mention that all the other things normally associated with menopause, like osteoporosis and changes in mood, also have the potential to occur, only earlier.
Okay, so early menopause can have some health consequences. Is veganism actually linked?
What Research Says About Diet and Menopause Timing
There was one study that found people who’d never been a vegetarian developed menopause at a later age, which is a roundabout way of saying that vegetarianism may increase the risk of early menopause.
Other lifestyle factors linked to later menopause included regular strenuous exercise, never smoking, midlife weight gain, and drinking alcohol. Strange mix of behaviors, both classically healthy and unhealthy.
But then another study in Han Chinese women found the opposite—that vegetarianism was associated with a lower risk of premature menopause.
Those are the only direct (if you can call it that) lines of evidence, and they conflict. No solid answers there. That said, there’s more indirect stuff pointing toward a link between exclusion of animal foods and earlier menopause:
- A high intake of vitamin D and calcium from dietary sources has been linked to a lower risk of premature menopause. Oddly enough, supplemental vitamin D and calcium were not linked to lower risks, suggesting that it’s the food—dairy primarily, but also bone-in small fatty fish like sardines—and not the nutrients alone. So a vegan might not be in the clear simply by supplementing with D and calcium.
- The amount of protein and carbs a woman eats throughout her life seems to predict the age at which menopause occurs. More protein, later menopause. More carbs, earlier menopause. Protein is harder and carbs are easier to come by on a plant-based diet—that’s for sure.
- Another fairly consistent finding is that polyunsaturated fat intake “accelerates” menopause. Women who eat the most PUFA tend to have menopause earlier. High PUFA intakes are pretty unavoidable when your diet is awash in seeds, nuts, and other plant-based fat sources.
Then there was a different connection in another study.
The Nurses Health Study found that women who ate the most plant protein were more likely to avoid premature menopause; animal protein intake had no effect. They even found beneficial links between specific foods and protection against early menopause, including dark bread, cold cereal, and pasta. Those are about as unPrimal as you can get.
How Can We Make Sense of Conflicting Research?
In addition to smoking (which we all know is trouble for almost all markers of health), one thing that keeps appearing in all these observational studies—and they’re all observational studies, unable to prove causation—is that underweight BMIs predict early menopause. In the Nurses Health Study, for example, BMIs under 18.5 were linked to a 30% greater risk of early menopause and BMIs between 25 and 29 were linked to a 30% lower risk. If that’s true, and if that’s actually a causal factor, then the most important thing a woman who wants to avoid early menopause can do is avoid being underweight. In that case, filling up on foods known to cause weight gain in susceptible people like bread, pasta, and cereal would be protective (at least for early menopause).
And that could really explain why the vegan blogger developed premature menopause. In her own words, she “had run out of fuel.”
A big downfall of many plant-based diets is that they starve you. They starve you of vital micronutrients you can really only get in animal foods, like B12, zinc, creatine, cholesterol, and others. They starve you of vital macronutrients, like protein and animal fat. And they starve you of calories. It’s hard to maintain your weight and physical robustness eating a diet of leaves, twigs, and seeds (unless you’re a gorilla). Oddly enough, I think vegans who eat grains and vegan “junk food” like fake burgers and weird nut cheeses are probably better off than the gluten-free ones who live off salads, simply because they’re getting more calories. It’s true that there are many ways to eat vegetarian and even vegan—and some are healthier than others (I’ve written about Primal recommendations for vegetarians and vegans in the past), but the more restrictive a person is with animal products, the trickier it will be to stay well-nourished.
If I had to make a bet, it’d be that any diet that provides sufficient nourishment in the form of micronutrients, macronutrients, and total calories will help stave off early menopause.
What about you? What’s your take on this? Has anyone out there experienced premature/early menopause that didn’t follow natural, familial patterns? What can you recall about the diet and lifestyle leading up to it?
Wang H, Chen H, Qin Y, et al. Risks associated with premature ovarian failure in Han Chinese women. Reprod Biomed Online. 2015;30(4):401-7.
Velez MP, Alvarado BE, Rosendaal N, et al. Age at natural menopause and physical functioning in postmenopausal women: the Canadian Longitudinal Study on Aging. Menopause. 2019;
Sujarwoto S, Tampubolon G. Premature natural menopause and cognitive function among older women in Indonesia. J Women Aging. 2019;:1-15.
Løkkegaard E, Jovanovic Z, Heitmann BL, Keiding N, Ottesen B, Pedersen AT. The association between early menopause and risk of ischaemic heart disease: influence of Hormone Therapy. Maturitas. 2006;53(2):226-33.
Purdue-smithe AC, Whitcomb BW, Szegda KL, et al. Vitamin D and calcium intake and risk of early menopause. Am J Clin Nutr. 2017;105(6):1493-1501.
Sapre S, Thakur R. Lifestyle and dietary factors determine age at natural menopause. J Midlife Health. 2014;5(1):3-5.
Boutot ME, Purdue-smithe A, Whitcomb BW, et al. Dietary Protein Intake and Early Menopause in the Nurses’ Health Study II. Am J Epidemiol. 2018;187(2):270-277.
Szegda KL, Whitcomb BW, Purdue-smithe AC, et al. Adult adiposity and risk of early menopause. Hum Reprod. 2017;32(12):2522-2531.
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The one piece of advice all newcomers to the ketogenic diet receive is to “get enough electrolytes.” It doesn’t matter what flavor of keto diet you’re talking about—paleo, carnivore, Primal, standard, clinical, mainstream, salami-and-cream-cheese. They all mention the importance of getting your electrolytes, particularly during the transition from a higher-carb diet.
I’ve said it. I say it. It really is important. Heck, a major part of the much-maligned “keto flu” can be directly attributed to inadequate intake of sodium, potassium, and magnesium. Oftentimes, increasing your electrolytes stops the flu from happening in the first place.
Why Do Early Stages Of a Ketogenic Diet Trigger an Increase In electrolyte Requirements?
One of the first things that happens when you go keto is you lose a bunch of glycogen from almost everywhere. For one, depletion of liver glycogen—the storage form of carbohydrates in the body—is the trigger for the liver to begin producing ketone bodies. It can’t make ketones if it’s full of glycogen. And, two, since you’ve just removed virtually all the digestible carbohydrates from your diet and your body hasn’t adapted to burning fats directly, it’s going to burn through the stored muscle glycogen and ramp up ketone production to make up for the rest of your energy requirements.
If you’re going keto (and doing it right), you’ll be depleting your glycogen stores. It’s totally normal, but there’s a side effect: water loss.
Each gram of glycogen in the body is stored with four grams of water. Every time you lose a gram of glycogen, you lose four grams of water and a bunch of sodium, magnesium, and potassium. When sodium drops, your kidneys start shedding potassium to maintain the right sodium:potassium ratio. But even though the ratio might be “right,” the absolute amounts of sodium and potassium are inadequate for optimal function.
As you get better at burning fats directly and your body gets acclimated to utilizing them for energy, you won’t have to maintain empty liver glycogen to stimulate massive ketone production. You can use fats for the majority of your energy requirements and can begin storing more glycogen rather than shedding it instantly. As a result, you won’t shed as much water or lose as many electrolytes.
Another factor is that going keto lowers insulin, and low insulin levels reduce sodium retention. This is one reason why low-carb diets are so good for people with salt-sensitive high blood pressure—they help you get rid of excess sodium.
A Few Signs of Low Electrolytes During the Keto Transition
When sodium gets too low, your body will reduce water stores to maintain proper sodium ratios. This creates a vicious cycle of dehydration that can trigger headaches. Luckily, salt repletion will fix most keto headaches.
If you’ve ever felt dizzy and unsteady upon standing up from a seated position, you’ve experienced postural hypotension. Blood pools in the lower half of your body while sitting and the blood pressure is inadequate to adjust in time. Without enough blood in your brain, things don’t work so well. It only lasts for a second or two, but it’s no fun.
Sodium depletion—as occurs in the early stages of keto—is a major risk factor for postural hypotension. Eating more salt is a quick fix. This isn’t keto broscience, either. Standard medical treatment of postural hypotension is to have the patient consume up to a tablespoon and a half of extra salt per day.
Poor Physical Performance
When you go keto, you might notice a drop-off in your physical performance in the gym or on the field. Part of this is a transitory effect of your tissues adapting to a new energy source. But another explanation is that you have low potassium levels.
In the muscle tissue itself, potassium acts as an electrical conduit during muscle contractions—and muscle contractions are what make a muscle “go.”
To some extent, low energy is part and parcel of the keto transition. You’re not great at burning fat and ketones yet. You’re still missing carbs. That’s okay, that’s normal. It’s a necessary evil, and it will pass.
But low energy can also be a symptom of low electrolyte status, as potassium and magnesium are all important co-factors in the production of ATP, the body’s energy currency.
How To Re-establish Optimum Electrolyte Balance During Keto Transitions
The fix is simple. Eat more sodium, potassium, and magnesium.
- Salt your food to taste (your salt appetite is a good barometer of your sodium requirements).
- Drink salty broth (true bone broth is ideal, but good bouillon or store-bought is also acceptable).
- Aim for 3-5 grams of sodium.
- Eat zucchinis, avocados, leafy greens, and medium-rare steak with all the juices (the juice contains tons of potassium).
- Use potassium citrate.
- Aim for 3-5 grams of potassium.
- Eat leafy greens, halibut, dark chocolate, nuts.
- Consider hemp seeds. They’re incredibly high in magnesium, low in phytate, and a little bit goes a long way.
- Use magnesium supplements. The chelated magnesiums (those ending in “-ate,” like citrate, glycinate, or threonate) tend to be the best absorbed. Another option is to use topical magnesium chloride oil.
- Aim for 500 mg of magnesium.
My favorite way to get a big dose of these electrolytes in one fell swoop is to pour a big glass of sparkling mineral water (I like Gerolsteiner) and add juice from 2 limes or lemons, a teaspoon of salt, and a scoop of magnesium powder. Great and incredibly refreshing. Sip on that twice a day, and you’ll be fine.
In my experience, electrolyte loss is the biggest stumbling block for people new to keto. It’s also one of the easiest to avoid. So get after it!
What’s your favorite way to get enough sodium, potassium, and magnesium? Got any great no-sugar electrolyte drink recipes you’d care to share?
Thanks for reading, everyone.
The post Electrolytes and Keto: Why They Matter for the Transition appeared first on Mark’s Daily Apple.
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For today’s edition of Dear Mark, I’ll be answering your CBD questions from the past few weeks. CBD, or cannabidiol, is exploding in popularity, but there are many unknowns. People have a lot of questions and there aren’t many definitive or comprehensive guides, so today I’ll do my best to make sense of it. We’re all piecing things together based on limited data—which, I suppose, is the fundamental human experience.
What’s the difference between hemp and CBD?
Hemp is a (recently legalized) industrial form of cannabis used in the production of paper, textiles, clothing, biodegradable plastics, and overpriced Bob Marley shirts sold along Venice Beach. Hemp seed can be eaten (and is a fantastic source of magnesium, one of the best). Hemp is the plant.
CBD is cannabidiol, a non-psychoactive cannabinoid found in both hemp and cannabis. Unlike THC, CBD won’t get you high.
Due to legal issues, most big name online retailers won’t allow sellers to list “CBD oil” or “CBD” products, let alone CBD content. Descriptions like “full spectrum hemp extract” often mean CBD is present in the hemp oil, but it’s tough to know exactly how much. I recommend investigating the product, searching for the company that makes it, and seeing if they give more explicit details on their website. Even then, make sure the company is the actual seller on Amazon or else you may end up with a counterfeit product sold by wholesalers.
The best bet is to buy directly from the product website.
Is there oil for diabetics??
Although there aren’t any human trials that give CBD to diabetics to see what happens, there are some reasons to think it could be helpful:
Lowering stress. As stated in previous posts, CBD is an effective anti-stress agent. Stress is awful for anyone with diabetes. It increases blood sugar levels. It induces insulin resistance. And if you’re a stress eater, it can increase cravings for high-carb junk food that you really shouldn’t be eating in the first place. In other words, stress exacerbates all the physiological conditions a diabetic is already experiencing.
Improving sleep. Perhaps the most popular use of CBD is to improve poor sleep. Just about the best way to induce some serious glucose intolerance is to get a bad night’s sleep. A diabetic already has poor glucose tolerance; it’s pretty much the defining characteristic of diabetes. What’s worse, a bad night’s sleep has been shown to make a person more susceptible to the allure of junk food.
Inadequate sleep is a strong and independent predictor of type 2 diabetes risk. The less sleep you get, the higher your chance of developing diabetes.
Anything that reduces stress and improves sleep will improve a diabetic’s health. If CBD does that for you, it’ll probably help someone with diabetes. So in a roundabout, not direct way, CBD oil has the potential to help reduce the risk of diabetes and improve the symptoms.
Good MDA folks … does anyone have any experience using CBD oil in lieu of an SSRI to help with anxiety and panic? I’m using CBT techniques to deal with anxiety and panic episodes, and cutting back on my dosage of my SSRI with the intent to eliminate over the next couple of months. I was considering giving CBT oil a try (organic, full spectrum), starting out with just a drop or two and building up to a therapeutic dosage. Also, does CBT oil cause fatigue for anyone? It’s the last thing I want to happen as it’s a big reason I want to eliminate taking the SSRI?
Give it a try, making sure you keep your doctor in the loop.
There are several parallels between anti-depressants and CBD. Both antidepressants and CBD interact with the endocannabinoid receptor systems in the brain. Both antidepressants and CBD can stimulate neurogenesis and counter the depression-related reduction in brain-derived neurotrophic factor.
Any compound that’s used for sleep has the potential to increase fatigue. Sleep is fatigue at the right time. Fatigue is sleep at the wrong time. In an Israeli study of 74 pediatric epilepsy patients using CBD to quell their seizures, 22% reported unwanted levels of fatigue, so it’s a common complaint. Just consider that these were kids taking fairly high dose CBD to quell seizure activity, and that you may not have the same issue taking lower doses at a higher body weight.
Does CBD oil break my fast?
The dosages involved in most CBD oils include at most 1/8 teaspoon of carrier oils, so that’s not enough calories to impact your fast in any meaningful sense.
I haven’t seen any evidence that CBD itself inhibits or impedes ketosis, autophagy, or fat-burning. So, no, there is no indication that CBD oil breaks your fast.
How do I figure out how much cbd is in hemp oil?
As I indicated earlier, it’s impossible to know unless you buy a hemp oil that explicitly states the CBD content.
CBD oil is so expensive. Are there any other options for getting CBD?
You could make your own. It’s actually legal to buy “CBD flower,” which basically looks exactly like the cannabis or weed you’d buy on the street or at a legal dispensary, only it contains little to no THC and tons of CBD. One recipe I saw involved slow-cooking an ounce of the CBD flower in a cup of coconut oil for 8 hours, then straining out the solids. Whatever method you use to cook it, it requires fat, as cannabinoids are fat-soluble.
Here’s a place you can buy CBD flower online. (Note: I don’t have any experience with that company or any other that markets CBD flower or CBD products, so buyer beware.) There are many such places. Just search for them.
CBD is everywhere these days. Should I definitely use it?
Not necessarily. Like anything, it has its uses, there’s great potential, and as new research comes out I foresee the discovery of new modes of action and new applications. However, in all fairness, it’s being overhyped when promoted as a cure-all or panacea.
For what it’s worth, I’m not using it myself. I don’t feel the need, haven’t felt a “CBD deficit.” Don’t assume it’s yet another essential supplement that you simply must have. The basics are the important things—sleep, food, exercise, community, love, micronutrients.
CBD is best used for people who have an established need for it. Chronic pain patient who wants to stop using so many opioids? Great candidate. Kid with epilepsy for whom keto and meds aren’t working? Give it a try. Anxiety and insomnia? Better than just going with narcotics right off the bat. (But as always, work with a physician for any medical issue.)
That’s it for today, folks. If you have any more CBD questions, write them down below and I’ll be sure to answer them!
Rudnicka AR, Nightingale CM, Donin AS, et al. Sleep Duration and Risk of Type 2 Diabetes. Pediatrics. 2017;140(3)
Mcneil J, Forest G, Hintze LJ, et al. The effects of partial sleep restriction and altered sleep timing on appetite and food reward. Appetite. 2017;109:48-56.
Fogaça MV, Galve-roperh I, Guimarães FS, Campos AC. Cannabinoids, Neurogenesis and Antidepressant Drugs: Is there a Link?. Curr Neuropharmacol. 2013;11(3):263-75.
Tzadok M, Uliel-siboni S, Linder I, et al. CBD-enriched medical cannabis for intractable pediatric epilepsy: The current Israeli experience. Seizure. 2016;35:41-4.
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Biological systems are self-maintaining. They have to be. We don’t have maintenance workers, mechanics, troubleshooters that can “take a look inside” and make sure everything’s running smoothly. Doctors perform a kind of biological maintenance, but even they are working blind from the outside.
No, for life to sustain itself, it has to perform automatic maintenance work on its cells, tissues, organs, and biological processes. One of the most important types of biological maintenance is a process called autophagy.
Autophagy: the word comes from the Greek for “self-eating,” and that’s a very accurate description: Autophagy is when a cell consumes the parts of itself that are damaged or malfunctioning. Lysosomes—members of the innate immune system that also degrade pathogens—degrade the damaged cellular material, making it available for energy and other metabolites. It’s cellular pruning, and it’s an important part of staving off the worst parts of the aging process.
In study after study, we find that impairment to or reductions of normal levels of autophagy are linked to almost every age-related degenerative disease and malady you can imagine.
- Cancer: Autophagy can inhibit the establishment of cancer by removing malfunctioning cellular material before it becomes problematic. Once cancer is established, however, autophagy can enhance tumor growth.
- Diabetes: Impaired autophagy enables the progression from obesity to diabetes via pancreatic beta cell degradation and insulin resistance. Impaired autophagy also accompanies the serious complications related to diabetes, like kidney disease and heart failure.
- Heart disease: Autophagy plays an important role in all aspects of heart health.
- Osteoporosis: Both human and animal studies indicate that autophagy dysfunction precedes osteoporosis.
- Alzheimer’s disease: Early stage Alzheimer’s disease is linked to deficits in autophagy.
- Muscle loss: Autophagy preserves muscle tissue; loss of autophagy begins the process of age-related muscle atrophy.
Okay, so autophagy is rather important. It’s fundamental to health.
But how does autophagy happen?
The way it’s supposed to happen is this:
Humans traditionally and historically lived in a very different food environment. Traditionally and historically, humans were feasters and fasters. While I don’t think our paleolithic ancestors were miserable, wretched, perpetually starving creatures scuttling from one rare meal to the next—the fossil records show incredibly robust remains, with powerful bones and healthy teeth and little sign of nutritional deficits—they also couldn’t stroll down to the local Whole Foods for a cart full of ingredients. Going without food from time to time was a fundamental aspect of human ancestral life.
They worked for their food. I don’t mean “sat in a cubicle to get a paycheck to spend on groceries.” I mean they expended calories to obtain food. They hunted—and sometimes came back empty handed. They dug and climbed and rooted around and gathered. They walked, ran, stalked, jumped, lifted. Movement was a necessity.
In short, they experienced energy deficits on a regular basis. And energy deficits, particularly sustained energy deficits, are the primary triggers for autophagy. Without energy deficits, you remain in fed mode and never quite hit the fasted mode required for autophagy.
Now compare that ancestral food environment to the modern food environment:
Almost no one goes hungry. Food is cheap and plentiful, with the tastiest and most calorie-rich stuff tending to be the cheapest and most widely available.
Few people have to physically work for their food. We drive to the store and walk a couple hundred steps, hand over some money, and—BOOM—obtain thirty thousand calories, just like that. Or someone comes to our house and delivers the food directly.
We eat all the time. Unless you set out to do it, chances are you’ll be grazing, snacking, and nibbling throughout the day. We’re in a perpetually fed state.
The average person in a modern society eating a modern industrial diet rarely goes long enough without eating something to trigger autophagy. Nor are they expending enough energy to create an energy deficit from the other end—the output. It’s understandable. If our ancestors were thrust into our current situation, many would fall all over themselves to take advantage of the modern food environment. But that doesn’t make it desirable, or good for you. It just means that figuring out how to trigger autophagy becomes that much more vital for modern humans.
Here are 7 ways to induce autophagy with regular lifestyle choices.
There’s no better way to quickly and reliably induce a large energy deficit than not eating anything at all. There are no definitive studies identifying “optimal” fasting guidelines for autophagy in humans. Longer fasts probably allow deeper levels of autophagy, but shorter fasts are no slouch.
2) Get Keto-Adapted
When you’re keto- and fat-adapted, it takes you less time to hit serious autophagy upon commencing a fast. You’re already halfway there.
3) Train Regularly
With exercise-related autophagy, the biggest effects are seen with lifelong training, not acute. In mice, for example, the mice who are subjected to lifelong exercise see the most autophagy-related benefits. In people, those who have played soccer (football) for their entire lives have far more autophagy-related markers of gene activity than people of the same age who have not trained their whole lives.
4) Train Hard
In studies of acute exercise-induced autophagy, the intensity of the exercise is the biggest predictor of autophagy—even more than whether the athletes are in the fed or fasted state.
5) Drink Coffee
At least in mice, both caffeinated and decaffeinated coffee induce autophagy in the liver, muscle tissue, and heart. This effect persists even when the coffee is given alongside ad libitum food. These mice didn’t have to fast for the coffee to induce autophagy.
Certain nutrients can trigger autophagy, too….
6) Eat Turmeric
Curcumin, the primary phytonutrient in turmeric, is especially effective at inducing autophagy in the mitochondria (mitophagy).
7) Consume Extra Virgin Olive Oil
The anticancer potential of its main antioxidant, oleuropein, likely occurs via autophagy.
Disclaimer: The autophagy/nutrient literature is anything but definitive. Most studies take place in test tube settings, not living humans. Eating some turmeric probably won’t flip a switch and trigger autophagy right away, but it won’t hurt.
Autophagy is a long game.
This can’t be underscored enough: Autophagy is a lifelong pursuit attained by regular doses of exercise and not overeating every time you sit down to a meal. Staying so ketotic your pee tests look like a Prince album cover, doing epic 7-day fasts every month, fasting every other day, making sure you end every day with fully depleted liver glycogen—while these strategies might be “effective,” obsessing over their measures to hit some “optimal” level of constant autophagy isn’t the point and is likely to activate or trigger neurotic behavior.
Besides, we don’t know what “optimal autophagy” looks like. Autophagy isn’t easy to measure in live humans. You can’t order an “autophagy test” from your doc. We don’t even know if more autophagy is necessarily better. There’s the fact that unchecked autophagy can actually increase existing cancer in some cases. There’s the fact that too much autophagy in the wrong place might be bad. We just don’t know very much. Autophagy is important. It’s good to have some happening. That’s what we have to go on.
Putting These Tips Into Practice
Autophagy happens largely when you just live a healthy lifestyle. Get some exercise and daily activity. Go hard every now and then. Sleep deeply. Recover well. Don’t eat carbohydrates you don’t need and haven’t earned (and I don’t just mean “earned through glycogen depleting-exercise”). Reach ketosis sometimes. Don’t eat more food than you need. Drink coffee, even decaf.
All those caveats aside, I see the utility in doing a big “autophagy session” a few times a year. Here’s how mine looks:
- Do a big training session incorporating strength training and sprints. Lots of intense bursts. This will trigger autophagy.
- Fast for two or three days. This will push autophagy even further.
- Stay busy throughout the fast. Take as many walks as possible. This will really ramp up the fat burning and get you quickly into ketosis, another autophagy trigger.
- Drink coffee throughout the fast. Coffee is a nice boost to autophagy. Decaf is fine.
I know people are often skeptical of using “Grok logic,” but it’s likely that most human ancestors experienced similar “perfect storms” of deprivation-induced autophagy on occasion throughout the year. You track an animal for a couple days and come up short, or it takes that long to make the kill. You nibble on various stimulants plucked from the land along the way. You walk a ton and sprint some, then lift heavy. And finally, maybe, you get to eat.
If you find yourself aging well, you’re on the right track. If you’re not progressing from obesity to diabetes, you’re good to go. If you’re maintaining and even building your muscle despite qualifying for the blue plate special, you’ve probably dipping into the autophagy pathway. If you’re thinking clearly, I wouldn’t worry. Obviously, we can’t really see what’s happening on the inside. But if everything you can verify is going well, keep it up.
That’s it for today, folks. If you have any more questions about autophagy, leave them down below and I’ll try to get to all of them in future posts.
Thanks for reading!
Yang ZJ, Chee CE, Huang S, Sinicrope FA. The role of autophagy in cancer: therapeutic implications. Mol Cancer Ther. 2011;10(9):1533-41.
Barlow AD, Thomas DC. Autophagy in diabetes: ?-cell dysfunction, insulin resistance, and complications. DNA Cell Biol. 2015;34(4):252-60.
Sasaki Y, Ikeda Y, Iwabayashi M, Akasaki Y, Ohishi M. The Impact of Autophagy on Cardiovascular Senescence and Diseases. Int Heart J. 2017;58(5):666-673.
Florencio-silva R, Sasso GR, Simões MJ, et al. Osteoporosis and autophagy: What is the relationship?. Rev Assoc Med Bras (1992). 2017;63(2):173-179.
Li Q, Liu Y, Sun M. Autophagy and Alzheimer’s Disease. Cell Mol Neurobiol. 2017;37(3):377-388.
Jiao J, Demontis F. Skeletal muscle autophagy and its role in sarcopenia and organismal aging. Curr Opin Pharmacol. 2017;34:1-6.
Schwalm C, Jamart C, Benoit N, et al. Activation of autophagy in human skeletal muscle is dependent on exercise intensity and AMPK activation. FASEB J. 2015;29(8):3515-26.
De oliveira MR, Jardim FR, Setzer WN, Nabavi SM, Nabavi SF. Curcumin, mitochondrial biogenesis, and mitophagy: Exploring recent data and indicating future needs. Biotechnol Adv. 2016;34(5):813-826.
Przychodzen P, Wyszkowska R, Gorzynik-debicka M, Kostrzewa T, Kuban-jankowska A, Gorska-ponikowska M. Anticancer Potential of Oleuropein, the Polyphenol of Olive Oil, With 2-Methoxyestradiol, Separately or in Combination, in Human Osteosarcoma Cells. Anticancer Res. 2019;39(3):1243-1251.
The post The Definitive Guide To Autophagy (and 7 Ways To Induce 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, 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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The scientific literature is awash in correlations between a person’s health status and various biomarkers, personal characteristics, and measurements. As we hoard more and more data and develop increasingly sophisticated autonomous tools to analyze it, we’ll stumble across new connections between seemingly disparate variables. Some will be spurious, where the correlations are real but the variables don’t affect each other. Others will be useful, where the correlations indicate real causality, or at least a real relationship.
One of my favorite health markers—one that is both modifiable and a good barometer for the conditions it appears to predict—is grip strength.
The Benefits of Grip Strength
In middle-aged and elderly people, grip strength consistently predicts mortality risk from all causes, doing an even better job than blood pressure. In older disabled women, grip strength predicts all-cause mortality, even when controlling for disease status, inflammatory load, depression, nutritional status, and inactivity.
Poor grip strength is also an independent risk factor for type 2 diabetes across all ethnicities, and it can predict the presence of osteoarthritis in the knee. Among Korean adults, those with lower grip strength have a greater risk of clinical depression.
Even when hand grip strength fails to predict a disease, it still predicts the quality of life in people with the disease. The relative rate of grip strength reduction in healthy people is a good marker for the progression of general aging. Faster decline, faster aging. Slower (or no) decline, slower aging. Stronger people—as indicated by their grip strength—are simply better at navigating the physical world and maintaining independence on into old age.
Health and longevity aside, there are other real benefits to a stronger grip.
You command more respect. I don’t care how bad it sounds, because I agree. Historically, a person’s personal worth and legitimacy was judged by the quality of their handshake. Right or wrong, that’s how we’re wired. If you think you feel differently, let me know how you feel the next time you shake hands and the other person has a limp, moist hand. Who are you more likely to respect? To hire? To deem more capable? To befriend? To approach romantically? I’m not saying it’s right. I’m saying it’s simply how it is. We can’t avoid our guttural reaction to a strong—or weak—handshake. To me, that suggests we have a built-in sensitivity to grip for a very good reason.
So, how does one build grip?
10 Exercises To Build Grip Strength
Most people will get a strong-enough grip as long as they’re lifting heavy things on a consistent-enough basis.
Deadlifts are proven grip builders. Wide grip deadlifts are also good and stress your grip across slightly different angles.
2. Pullups and 3. Chinups
Both require a good grip on the bar.
Any exercise where your grip supports either your weight or an external weight (like a barbell, dumbbell, or kettlebell) is going to improve your grip strength. But there are other, more targeted movements you can try to really turn your hand into a vise. Such as:
4. Bar Hangs
This is pretty simple. Just hang from a bar (or branch, or traffic light fixture) with both hands. It’s probably the purest expression of grip strength. As it happens, it’s also a great stretch for your lats, chest, shoulders, and thoracic spine.
Aim to hit one minute. Progress to one-hand hangs if two-handers get too easy. You can use a lower bar and keep one foot on the ground for support as you transition toward a full one-handed hang.
5. Sledgehammer Work
Grab the heaviest sledgehammer you can handle and use it in a variety of ways.
If you had to pick just one sledgehammer movement to target your grip, do the bottoms up. Hold the hammer hanging down pointing toward the ground in your hand, swing it up and catch it with the head of the hammer pointing upward, and hold it there. Handle parallel to your torso, wrist straight, don’t let it fall. The lower you grip the handle, the harder your forearms (and grip) will have to work.
6. Fingertip Pushups
Most people who try fingertip pushups do them one way. They do them with straight fingers, with the palm dipping toward the ground. Like this. Those are great, but there’s another technique as well: the claw. For the claw, make a claw with your hand, like this, as if you’re trying to grab the ground. In fact, do try to grab the ground. This keeps your fingers more active, builds more strength and resilience, and prevents you from resting on your connective tissue.
These are hard for most people. They’re quite hard on the connective tissue, which often goes underutilized in the hands and forearms. Don’t just leap into full fingertip pushups—unless you know you’re able. Start on your knees, gradually pushing your knees further back to add resistance. Once they’re all the way back and you’re comfortable, then progress to full pushups.
7. Active Hands Pushups
These are similar to claw pushups, only with the palm down on the floor. Flat palm, active “claw” fingers. They are easier than fingertip pushups.
8. Farmer’s Walks
The average person these days is not carrying water pails and hay bales and feed bags back and forth across uneven ground like they did when over 30% of the population lived on farms, but the average person can quickly graduate past average by doing farmer’s walks a couple times each week. What is a farmer’s walk?
Grab two heavy weights, stand up, and walk around. They can be dumbbells, barbells, kettlebells, or trap bars. You can walk up hill, down hill, or around in circles. You can throw in some shrugs, or bookend your walks with deadlifts or swings. The point is to use your grip to carry something heavy in both hands.
9. Pinch Grips
Grasp and hold weight plates between your thumb and each finger.
10. Hammer Curls
Next time you do some curls, throw in a few sets of hammer curls. These are identical to normal bicep curls, except you hold the weights in a hammer grip, with palms facing toward each other—like how you hold and swing a hammer. Make sure to keep those wrists as straight as possible.
The thing about grip is it’s hard to work your grip without getting stronger, healthier, and faster all over. Deadlifting builds grip strength, and it also builds back, hip, glute, and torso strength. Fingertip pushups make your hands and forearms strong, but they also work your chest, triceps, abs, and shoulders. That’s why I suspect grip strength is such a good barometer for overall health, wellness, and longevity. Almost every meaningful piece of physical activity requires that you use your hands to manipulate significant amounts of weight and undergo significant amounts of stress.
For that reason, the best way to train your grip is with normal movements. Heavy deadlifts and farmer’s walks are probably more effective than spending half an hour pinch gripping with every possible thumb/finger permutation, because they offer more full-body benefits. But if you have a few extra minutes throughout your workout, throw in some of the dedicated grip training.
Your grip can handle it. The grip muscles in the hands and forearm are mostly slow-twitch fiber dominant, meaning they’re designed to go for long periods of exertion. They’re also gross movers, meaning you use them all the time for all sorts of tasks, and have been doing so for decades. To make them adapt, you need to stress the heck out of them with high weight. Train grip with high reps, heavy weights, and long durations. This is why deadlifts and farmer’s walks are so good for your grip—they force you to maintain that grip on a heavy bar or dumbbell for the entire duration of the set with little to no rest.
Oh, and pick up some Fat Gripz. These attach to dumbbells and barbells and increase the diameter of the bar, giving you less leverage when grabbing and forcing you to adapt to the new grip conditions by getting stronger.
Now, will all this grip training actually protect you from aging, type 2 diabetes, osteoarthritis, and early all-cause mortality? Maybe, maybe not.
But it—and the muscle and fitness you gain doing all these exercises—certainly doesn’t hurt.
How’s your grip? How’s your handshake? How long can you hang from a bar without letting go?
Thanks for reading, everyone. Take care, be well, and go pick up and hold some heavy stuff.
Sasaki H, Kasagi F, Yamada M, Fujita S. Grip strength predicts cause-specific mortality in middle-aged and elderly persons. Am J Med. 2007;120(4):337-42.
Leong DP, Teo KK, Rangarajan S, et al. Prognostic value of grip strength: findings from the Prospective Urban Rural Epidemiology (PURE) study. Lancet. 2015;386(9990):266-73.
Rantanen T, Volpato S, Ferrucci L, Heikkinen E, Fried LP, Guralnik JM. Handgrip strength and cause-specific and total mortality in older disabled women: exploring the mechanism. J Am Geriatr Soc. 2003;51(5):636-41.
Van der kooi AL, Snijder MB, Peters RJ, Van valkengoed IG. The Association of Handgrip Strength and Type 2 Diabetes Mellitus in Six Ethnic Groups: An Analysis of the HELIUS Study. PLoS ONE. 2015;10(9):e0137739.
Wen L, Shin MH, Kang JH, et al. Association between grip strength and hand and knee radiographic osteoarthritis in Korean adults: Data from the Dong-gu study. PLoS ONE. 2017;12(11):e0185343.
Lee MR, Jung SM, Bang H, Kim HS, Kim YB. The association between muscular strength and depression in Korean adults: a cross-sectional analysis of the sixth Korea National Health and Nutrition Examination Survey (KNHANES VI) 2014. BMC Public Health. 2018;18(1):1123.
Lee SH, Kim SJ, Han Y, Ryu YJ, Lee JH, Chang JH. Hand grip strength and chronic obstructive pulmonary disease in Korea: an analysis in KNHANES VI. Int J Chron Obstruct Pulmon Dis. 2017;12:2313-2321.
Iconaru EI, Ciucurel MM, Georgescu L, Ciucurel C. Hand grip strength as a physical biomarker of aging from the perspective of a Fibonacci mathematical modeling. BMC Geriatr. 2018;18(1):296.
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This is a surprisingly common question.
To get it out of the way: Yes, it does. Bone broth contains calories, and true fasts do not allow calorie consumption. You eat calories, you break the fast.
However, most people aren’t fasting to be able to brag about eating no calories for X number of days. They fast for shorter (often intermittent) periods of time for specific health benefits. It’s entirely possible that bone broth “breaks a fast” but allows many of the benefits we associate with fasting to occur.
As is the problem with so many of these specific requests, there aren’t any studies addressing the specific question. The scientific community hasn’t caught up to the current trends sweeping the alternative health community. But we can isolate the most common benefits of fasting and see how bone broth—and the components therein—interact.
Common Benefits of Fasting: Does Bone Broth Help or Hinder?
Fasting is a quick and easy (or simple) way to get into ketosis. You have little choice in the matter. Since you’re not eating anything, and your body requires energy, you break down body fat for energy. And because you’ve only got fat “coming in,” you’ll quickly start generating ketone bodies. If bone broth stops ketosis, it’s probably breaking the fast.
Bone broth doesn’t contain any digestible carbohydrates. Common additions like tomato paste and carrots might add a few tenths of a gram of carbohydrate to your cup of broth, but not enough to throw you out of ketosis.
Bone broth is quite high in protein, especially if you make it right or buy the right kind, but if it’s the only thing you’re consuming during your fast, the overall caloric load won’t be enough for the protein in broth to stop ketosis.
I can’t point to a paper. I know for a fact that I’ve consumed bone broth without affecting my ketones.
Fat-burning is another important aspect of fasting. Since bone broth contains calories, you’ll probably burn slightly less fat drinking broth during a fast. But the calories come from protein, the macronutrient least associated with fat gain and most supportive of lean mass retention. And at any rate, your total calorie intake on a fasting+broth day will be under 100 calories—plenty low enough to promote fat loss.
Over the long term, fasting is an effective way to improve insulin sensitivity and glucose tolerance. Most things that make you better at burning fat and expending, rather than storing, energy—like exercise, low-carb diets, weight loss in general—tend to improve insulin sensitivity over time. But the sometimes counterintuitive piece to all this is that in the short term, fasting can reduce insulin sensitivity. This is a physiological measure the body takes to preserve what little glucose remains for the brain. All the other tissues become insulin resistant so that the parts of the brain that can’t run on ketones and require glucose get enough of the latter to function.
There’s also the matter of sleep, fasting, and insulin sensitivity to consider. Some people report sleep disturbances during fasts, especially longer fasts. This is common. If the body perceives the fast as stressful, or if you aren’t quite adapted to burning fat, you may interpret the depleted liver glycogen as dangerous and be woken up to refuel in the middle of the night. Some people just have trouble sleeping on low-calorie intakes in general, and a fast is about as low as you can get. If that’s you, and your fasting is hurting your sleep, it’s most likely also impairing your insulin sensitivity because a bad night’s sleep is one of the most reliable ways to induce a state of insulin resistance. There’s some indication that total sleep deprivation creates transient type 2 diabetes.
That’s where bone broth comes in. A big mug of broth is one of my favorite ways to ensure a good night’s sleep. It’s a great source of glycine, an amino acid that has been shown in several studies to improve sleep quality and reduce the time it takes to fall asleep. It may “break” the fast by introducing calories, but a broken fast is preferable to bad sleep and the hit to insulin sensitivity that results from it.
Things fall apart. Cars, tools, buildings, toy trucks, civilizations. That’s entropy, which dictates that all things are constantly heading toward disorder. And people aren’t exempt. Our cells and tissues are subject to entropy, too, only we can resist it. One of the ways our bodies resist entropy is through a process of cellular pruning and cleanup called autophagy. There’s always a bit of back and forth between autophagy and our cellular detritus, but it occurs most powerfully in periods of caloric restriction. Fasting enhances autophagy like nothing else because it’s a period of total caloric restriction. If bone broth destroys autophagy, that’d be a big mark against drinking it during a fast.
Amino acids tend to be anti-autophagy signaling agents. When we eat protein, or even consume certain isolated amino acids, autophagy slows. Bone broth is pure protein. It’s almost nothing but amino acids. The key is: Which amino acids are in bone broth, and have they been shown to impede autophagy?
The primary amino acids that make up the gelatin in bone broth are alanine, glycine, proline, hydroxyproline, and glutamine.
Let’s say you’re drinking a mug of strong, really gelatinous bone broth with 15 grams of gelatin protein. How do those amino acids break down?
- 5 grams of glycine. In piglets, dietary glycine activates mTOR, the pathway that triggers autophagy.
- 1.5 grams of alanine.
- 2.4 grams of proline.
- 2 grams of hydroxyproline.
- 1.75 grams of glutamine. 30 grams of glutamine inhibits autophagy.
So it’s a mixed bag. The most prominent amino acid in bone broth—glycine—seems to allow autophagy, but the less proinent amino acids may not. It’s unclear just how much of each amino acid it takes to affect autophagy either way. The absolute amounts found in bone broth are low enough that I’m not too concerned.
What Else To Know…
Okay, so while bone broth technically “breaks” the fast, it may preserve some of the most important benefits. Is there anything else related to bone broth and fasting that deserve mention?
If you’re the type to train in a fasted state and eat right after, you might consider incorporating some bone broth right before the workout. Just like my pre-workout collagen smoothie does, bone broth (plus a little vitamin C to aid the effect) right before a workout improves the adaptations of our connective tissue to the training by increasing collagen deposition in the tendons, ligaments, and cartilage. You’ve already done most of the fast honestly. What’s shaving off a half hour of fasting time by drinking some broth or collagen, especially if you stand to improve your connective tissue in the process? Ask any older athlete and they’ll say they wish they could.
Some spices and herbs that are often added to bone broth can have effects similar to fasting. Take curcumin, found in turmeric. Research shows that it’s an independent activator of mTOR, which in turn can activate autophagy. Ginger and green tea (what, you haven’t tried steeping green tea in bone broth?) are other ones to try. Bone broth with turmeric, green tea, and ginger might actually combine to form a decent autophagy-preserving drink during a fast. Only one way to find out!
That’s about it for bone broth and fasting. If you have any further questions, don’t hesitate to ask down below.
Xu X, Wang X, Wu H, et al. Glycine Relieves Intestinal Injury by Maintaining mTOR Signaling and Suppressing AMPK, TLR4, and NOD Signaling in Weaned Piglets after Lipopolysaccharide Challenge. Int J Mol Sci. 2018;19(7)
De urbina JJO, San-miguel B, Vidal-casariego A, et al. Effects Of Oral Glutamine on Inflammatory and Autophagy Responses in Cancer Patients Treated With Abdominal Radiotherapy: A Pilot Randomized Trial. Int J Med Sci. 2017;14(11):1065-1071.
Shaw G, Lee-barthel A, Ross ML, Wang B, Baar K. Vitamin C-enriched gelatin supplementation before intermittent activity augments collagen synthesis. Am J Clin Nutr. 2017;105(1):136-143.
Zhao G, Han X, Zheng S, et al. Curcumin induces autophagy, inhibits proliferation and invasion by downregulating AKT/mTOR signaling pathway in human melanoma cells. Oncol Rep. 2016;35(2):1065-74.
Hung JY, Hsu YL, Li CT, et al. 6-Shogaol, an active constituent of dietary ginger, induces autophagy by inhibiting the AKT/mTOR pathway in human non-small cell lung cancer A549 cells. J Agric Food Chem. 2009;57(20):9809-16.
Zhou J, Farah BL, Sinha RA, et al. Epigallocatechin-3-gallate (EGCG), a green tea polyphenol, stimulates hepatic autophagy and lipid clearance. PLoS ONE. 2014;9(1):e87161.
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Many of you have asked about prostate health in a Primal context. Men are interested because they know men have a decent chance of getting prostate cancer. Women are interested because they’re worried about the men in their lives getting prostate cancer. Today, I’m going to delve deep into the topic, exploring the utility (or lack thereof) of standard testing, the common types of treatment and their potential efficacy, as well as preventive and unconventional ways of reducing your risk and mitigating the danger of prostate cancer.
First, what does the prostate do, anyway? Most people only think about it in terms of prostate cancer.
It’s a gland about the size of a small apricot that manufactures a fluid called prostatic fluid that combines with sperm cells and other compounds to form semen. Prostatic fluid protects sperm against degradation, improves sperm motility, and preserves sperm genetic stability.
What Goes Wrong With the Prostate?
There are a few things that can happen.
Inflammation of the prostate, usually chronic and non-bacterial. A history of prostatitis is a risk factor for prostate cancer.
Benign Prostatic Hyperplasia
Non-cancerous enlargement of the prostate. As men age, the prostate usually grows in size. This isn’t always cancer but can cause similar symptoms.
What most of us are interested in when we talk about prostate health… After skin cancer, prostate cancer is the most common cancer among men and the sixth most common cause of cancer death among men worldwide. Yet, most men diagnosed with prostate cancer do not die from it; they die with it. The 5-year survival rate in the US is 98%.
That said, there is no monolithic “prostate cancer.” Like all other cancers, there are different grades and stages of prostate cancer. Each grade and stage has a different mortality risk:
- Low-grade prostate cancer grows more slowly and is less likely to spread to other tissues.
- High-grade prostate cancer grows more quickly and is more likely to spread to other tissues.
- Local prostate cancer is confined to the prostate. The 5-year relative survival rate (survival compared to men without prostate cancer) for local prostate cancer is almost 100%.
- Regional prostate cancer has spread to nearby tissues. The 5-year relative survival rate for regional prostate cancer is almost 100%.
- Distant prostate cancer has spread to tissues throughout the body. The 5-year relative survival rate for distant prostate is 29%. Distant prostate cancer explains most of the prostate-related mortality.
What Are Symptoms of Prostate Cancer?
The primary symptom is problems with urination. When the prostate gland grows, it has the potential to obstruct the flow of urine out of the bladder, causing difficulty urinating, weak urine flow, painful urination, or frequent urination. This can also be caused by benign prostatic hyperplasia, a non-cancerous enlargement of the prostate.
What Causes Prostate Cancer?
A big chunk is genetic. People with “knockout” alleles for BRCA, which codes for tumor suppression, have an elevated risk of some forms of prostate cancer. That’s the same one that confers added risks for breast cancer.
Ethnicity matters, too. Men of Sub-Saharan African descent, whether African-Americans in the U.S. or Caribbean men in the U.K., have the highest risk in the world for prostate cancer—about 60% greater than other ethnic groups. White men have moderate risks; South Asian, East Asian, and Pacific Islander men have lower risks.
Testosterone has a confusing relationship with prostate cancer. Conventional wisdom tends to hold that testosterone stimulates prostate cancer growth, and there’s certainly some evidence of a relationship, but it’s not that simple.
In one study, men with low free testosterone levels were less likely to have low-grade (less risk of spreading) prostate cancer but more likely to have high-grade (higher risk of spreading) prostate cancer.
In Chinese men, those who went into treatment with low testosterone were more likely to present with higher-grade localized prostate cancers.
Other studies have arrived at similar results, finding that “hypogonadism represents bad prognosis in prostate cancer.”
Many prostate cancer treatments involve testosterone deprivation, a hormonal reduction of testosterone synthesis. This can reduce symptoms and slow growth of prostate tumors during the metastatic phase, but prostate cancer tends to be highly plastic, with the ability to adapt to changing hormonal environments. These patients often see the cancer return in a form that doesn’t require testosterone to progress.
What About Testing?
If you have a prostate, should you get tested starting at age 40?
Not necessarily. The value of early testing hasn’t been established. Some researchers even question whether early testing is more harmful than ignoring it, and most of the research finds middling to nonexistent evidence in favor of broad testing for everyone. Early testing has a small effect on mortality from prostate cancer, but no effect on all-cause mortality.
PSA testing can also be inaccurate. PSA is prostate specific antigen, a protein produced by the prostate. It’s normal to have low levels of PSA present in the body, and while high levels of PSA are a good sign of prostate cancer—even years before it shows up in imaging or digital probes—they can also represent a false positive. Those two other common yet relatively benign prostate issues—benign hyperplasia and prostatitis—can also raise PSA levels well past the “cancer threshold.”
Other causes of high levels of PSA include:
- Urinary tract infections
- Recent sex or ejaculation
- Recent, vigorous exercise
- Certain medications.
In fact, if you have a PSA reading of 4 (the usual threshold), there’s still just a 30% chance it actually indicates cancer.
What About Treatment?
Let’s say you do have prostate cancer, confirmed by PSA and a biopsy (or two, or three, as needle biopsies often miss cancers). What next? Should you definitely treat it?
It’s unclear whether treatment improves survival outcomes. One study took men aged 50-69 with prostate cancer diagnosed via PSA testing, divided them among three treatment groups, and followed them for ten years. One group got active monitoring—they continued to test and monitor the status of the cancer. One group received radiotherapy—radiation therapy to destroy the tumor. And the last group had the cancer surgically removed. After ten years, there was no difference among the groups for all-cause mortality, even though the active-monitoring group saw higher rates of prostate cancer-specific deaths (8 deaths—in a group of 535 men— vs 5 in the surgery group and 4 in the radiotherapy group), cancer progression, and metastasis.
In another study of men with localized prostate cancer, removing the prostate only improved all-cause mortality rates among men with very high PSAs (more than 10). In men with lower PSAs, “waiting and seeing” produced similar outcomes as surgery.
Prostate removal also carries many unwanted side effects, like incontinence and sexual dysfunction. No one wants prostate cancer, but it’s no small thing to have problems with urination and sex for the rest of your life. Those are major aspects of anyone’s quality of life.
Before you make any decisions, talk to your doctor about your options, the relative mortality risk of your particular cancer’s stage and grade, and how the treatments might affect your quality of life.
How Can You Reduce the Risk of Prostate Cancer?
1. Inflammation is definitely an issue.
For one, there’s the relationship between prostatitis, or inflammation of the prostate, and prostate cancer that I already mentioned above.
Two, there’s the string of evidence linking anti-inflammatory compounds to reductions in prostate cancer incidence. For example, aspirin cuts prostate cancer risk. Low-dose aspirin (under 100 mg) reduces both the incidence of regular old prostate cancer and the risk of metastatic prostate cancer. It’s also associated with longer survival in patients with prostate cancer; other non-steroidal anti-inflammatories are not.
Third, anti-inflammatory omega-3 fatty acids (found in seafood and fish oil) are generally linked to lower rates of prostatic inflammation and a less carcinogenic environment; omega-6 fatty acids can trigger disease progression. A 2001 study of over 6,000 Swedish men found that the folks eating the most fish had drastically lower rates of prostate cancer than those eating the least. Another study from New Zealand found that men with the highest DHA (an omega-3 found in fish) markers slashed their prostate cancer risk by 38% compared to the men with the lowest DHA levels.
2. The phytonutrients you consume make a difference.
A series of studies on phytonutrient intake and prostate cancer incidence in Sicilian men gives a nice glimpse into the potential relationships:
The more polyphenols they ate, the less prostate cancer they got.
The more phytoestrogens they ate, the more prostate cancer they got. Except for genistein, an isoflavone found in soy and fava beans, which was linked to lower rates of prostate cancer. The Sicilians are eating more fava than soy, I’d imagine.
How about coffee, the richest source of polyphenols in many people’s daily diets? It doesn’t appear to reduce the incidence of prostate cancer, but it does predict a lower rate of fatal prostate cancer.
3. Your circadian rhythm and your sleep are important.
Like everything else in life, tumor suppression follows a circadian pattern. Nighttime melatonin—which is suppressed if your sleep hygiene is bad and optimal if your sleep hygiene is great—inhibits the growth of prostate cancer cells and reduces their ability to utilize glucose. One way to enhance nighttime melatonin is by getting plenty of natural, blue light during the day; this actually makes nighttime melatonin more effective at prostate cancer inhibition. On the other hand, getting that blue light at night is a major risk factor for prostate cancer.
4. Get a handle on your fasting blood sugar and insulin.
In one study, having untreated diabetic-level fasting blood sugar was a strong risk factor for prostate cancer. Another study found that insulin-lowering metformin reduced the risk, while an anti-diabetic drug that raised insulin increased the risk of prostate cancer. Metformin actually lowers PSA levels, which, taken together with the previous study, indicates a causal effect.
5. Keep moving, keep playing, keep lifting.
This has a number of pro-prostate effects:
It keeps you insulin sensitive, so neither fasting insulin, nor fasting glucose get into the danger zone.
Oh, and do some deadlifts. Men with prostate cancer who trained post-surgery had better control over their bodily functions, as long as they improved their hip extensor strength. If you don’t know, hip extension is the act of standing up straight, of moving from hip flexion (hip hinging, bending over) to standing tall. It involves hamstrings, glutes, and the entire posterior chain. Deadlifts are the best way to train that movement pattern.
The prostate cancer issue is frightening because it’s so common. Almost all of us probably know someone who has or had it, even unknowingly. But the good news is that most prostate cancers aren’t rapidly lethal. Many aren’t lethal at all. So whatever you do, don’t rush into serious treatments or procedures without discussing the full range of options in a frank, honest discussion with your doctor.
That’s it for today, folks. Thanks for reading. If you have any questions, comments, or concerns about prostate cancer, feel free to chime in down below. I’d love to hear from you.
Perletti G, Monti E, Magri V, et al. The association between prostatitis and prostate cancer. Systematic review and meta-analysis. Arch Ital Urol Androl. 2017;89(4):259-265.
Ilic D, Djulbegovic M, Jung JH, et al. Prostate cancer screening with prostate-specific antigen (PSA) test: a systematic review and meta-analysis. BMJ. 2018;362:k3519.
Brawer MK, Chetner MP, Beatie J, Buchner DM, Vessella RL, Lange PH. Screening for prostatic carcinoma with prostate specific antigen. J Urol. 1992;147(3 Pt 2):841-5.
Castro E, Eeles R. The role of BRCA1 and BRCA2 in prostate cancer. Asian J Androl. 2012;14(3):409-14.
Watts EL, Appleby PN, Perez-cornago A, et al. Low Free Testosterone and Prostate Cancer Risk: A Collaborative Analysis of 20 Prospective Studies. Eur Urol. 2018;
Neuzillet Y, Raynaud JP, Dreyfus JF, et al. Aggressiveness of Localized Prostate Cancer: the Key Value of Testosterone Deficiency Evaluated by Both Total and Bioavailable Testosterone: AndroCan Study Results. Horm Cancer. 2018;
Dai B, Qu Y, Kong Y, et al. Low pretreatment serum total testosterone is associated with a high incidence of Gleason score 8-10 disease in prostatectomy specimens: data from ethnic Chinese patients with localized prostate cancer. BJU Int. 2012;110(11 Pt B):E667-72.
Teloken C, Da ros CT, Caraver F, Weber FA, Cavalheiro AP, Graziottin TM. Low serum testosterone levels are associated with positive surgical margins in radical retropubic prostatectomy: hypogonadism represents bad prognosis in prostate cancer. J Urol. 2005;174(6):2178-80.
Banerjee PP, Banerjee S, Brown TR, Zirkin BR. Androgen action in prostate function and disease. Am J Clin Exp Urol. 2018;6(2):62-77.
Zhou CK, Daugherty SE, Liao LM, et al. Do Aspirin and Other NSAIDs Confer a Survival Benefit in Men Diagnosed with Prostate Cancer? A Pooled Analysis of NIH-AARP and PLCO Cohorts. Cancer Prev Res (Phila). 2017;10(7):410-420.
Russo GI, Campisi D, Di mauro M, et al. Dietary Consumption of Phenolic Acids and Prostate Cancer: A Case-Control Study in Sicily, Southern Italy. Molecules. 2017;22(12)
Russo GI, Di mauro M, Regis F, et al. Association between dietary phytoestrogens intakes and prostate cancer risk in Sicily. Aging Male. 2018;21(1):48-54.
Discacciati A, Orsini N, Wolk A. Coffee consumption and risk of nonaggressive, aggressive and fatal prostate cancer–a dose-response meta-analysis. Ann Oncol. 2014;25(3):584-91.
Dauchy RT, Hoffman AE, Wren-dail MA, et al. Daytime Blue Light Enhances the Nighttime Circadian Melatonin Inhibition of Human Prostate Cancer Growth. Comp Med. 2015;65(6):473-85.
Kim KY, Lee E, Kim YJ, Kim J. The association between artificial light at night and prostate cancer in Gwangju City and South Jeolla Province of South Korea. Chronobiol Int. 2017;34(2):203-211.
Murtola TJ, Vihervuori VJ, Lahtela J, et al. Fasting blood glucose, glycaemic control and prostate cancer risk in the Finnish Randomized Study of Screening for Prostate Cancer. Br J Cancer. 2018;118(9):1248-1254.
Haring A, Murtola TJ, Talala K, Taari K, Tammela TL, Auvinen A. Antidiabetic drug use and prostate cancer risk in the Finnish Randomized Study of Screening for Prostate Cancer. Scand J Urol. 2017;51(1):5-12.
Park JS, Lee KS, Ham WS, Chung BH, Koo KC. Impact of metformin on serum prostate-specific antigen levels: Data from the national health and nutrition examination survey 2007 to 2008. Medicine (Baltimore). 2017;96(51):e9427.
Galvão DA, Taaffe DR, Spry N, Joseph D, Newton RU. Combined resistance and aerobic exercise program reverses muscle loss in men undergoing androgen suppression therapy for prostate cancer without bone metastases: a randomized controlled trial. J Clin Oncol. 2010;28(2):340-7.
Ying M, Zhao R, Jiang D, Gu S, Li M. Lifestyle interventions to alleviate side effects on prostate cancer patients receiving androgen deprivation therapy: a meta-analysis. Jpn J Clin Oncol. 2018;48(9):827-834.
Uth J, Fristrup B, Haahr RD, et al. Football training over 5 years is associated with preserved femoral bone mineral density in men with prostate cancer. Scand J Med Sci Sports. 2018;28 Suppl 1:61-73.
Park J, Yoon DH, Yoo S, et al. Effects of Progressive Resistance Training on Post-Surgery Incontinence in Men with Prostate Cancer. J Clin Med. 2018;7(9)
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