Mark Sisson's Blog, page 381

Why You Should Work Outside

We’ve discussed the “nature-deficit disorder” running rampant throughout contemporary society before. Kids are more likely to control characters in video games who explore vast outdoor worlds (and complain about the graphics “not being realistic enough”) rather than get out and explore the real world themselves (which has excellent graphics, a pretty snazzy physics engine, and killer AI). Adults are likely to go entire days without stopping to smell a flower, pluck a leaf, caress a blade of grass, or even see a shred of foliage. We’ve also written about some of the incredible health benefits that occur once people correct that deficit and go forest bathing, or hiking, or commiserating with animals, or even planting a small garden on their property. In other words, a lack of nature seems to cause physical and mental health problems, while an exposure to nature seems to improve physical and mental health.

What’s going on here?

If you look at things through the lens of evolution, you notice that we’re doing things differently than we’ve ever done before. People live in suburbs or urban centers. Rural communities are shrinking, urban sprawl is widening. Green space is disappearing. And we’re suffering. A lack of nature is incredibly unhealthy. Being in and around leaves and trees and sand and bugs and dirt and desert and all the rest is the natural state of the animal known as man. It’s home. It’s in our blood and in our genes. We might have adapted to spending lots of time indoors, but not completely. The evidence is all around us, if you just pay attention:

The young child who runs around the park like a chicken with his head removed just to do it.

The sullen teen, whose parents drag him kicking and screaming to the redwoods for a hike, who has to leave behind his iPhone, who enjoys himself despite his best efforts to the contrary.

That feeling when you walk through the grass with bare feet as the sun dips below the horizon and you’re hit with a flood of purples and pinks, where if you didn’t know better you wouldn’t be able to tell if it was dawn or dusk.

And finally, the office worker who goes on vacation to Costa Rica, does nothing but sit on the beach at the edge of a jungle teeming with howler monkeys and impossibly brightly-colored birds for two weeks, and comes back healthier, happier, stress-free, and down ten pounds.

Yeah, for a great many people, work stinks. Actually, let’s put that a little differently: For a great many people, indoor work stinks. What if it didn’t have to be like that? What if you could work outside, commune with nature as you typed, feel the grass underfoot as you brainstorm, and hear not the drone of the overhead lighting but rather the chirp of the bird, the caw of the crow, and the overpowering stillness of the outdoors? There’s very little direct research dealing with the effect of working outside versus indoors, but I think we can make some predictions based on the considerable evidence for the benefits of being outside in general.

Unfortunately, the benefits of working outdoors aren’t always obvious. What does your boss care if you feel more relaxed when you take your work outside? If it doesn’t translate to improved earnings, the higher-ups generally aren’t going to take it into account. They might care on a personal level, but there is no way to accurately or reliably quantify the benefits to the business. Or if you’re the boss, either of employees or yourself, why should you want to switch everything up and start working outside? What’s in it for you, besides feeling better and some random health benefits? How will it affect a person’s ability to work?

Stress Alleviation

The clear-cut, most obvious problem with work is job-related stress. We’re pushed too hard for too little pay. This can be stressful. We’re doing something we’d rather not, rather than doing something we actually enjoy. This is stressful as well. We’re competing with our workmates for promotions, pay raises, or even just to keep our jobs. Such competition, especially prolonged competition, can be stressful. We’re looking over our shoulders, worrying about layoffs and mergers and fluctuations in other markets that affect our employment. This can be stressful, especially because so much is ultimately out of our immediate control. It’s no wonder, then, that people assume that the stress comes entirely from the actual work. Doing anything for eight hours at a time, especially when you don’t particularly care for it and particularly when you sit down the entire time with nary a break, can be draining and stressful. You toss in a long commute and a boss you hate, and things get even worse.

But I think there’s much more to job-related stress than the job. I think the physical work environment – the office, the cubicle, the indoor lighting, the walls boxing you in, the uniform sameness of it all – also plays a role, perhaps even the primary role. After all, evidence is mounting that nearly all lab animals are perpetually stressed, primarily because their natural habitats are vastly different than the lab habitat. If we’re in a similar position, spending a third of our days in physical environments that are wholly alien to our genes, subject to lighting that’s not as bright as the sun, windows that only some of the UV rays through, walls that keep us penned in, chairs that keep us immobile, and a distinct lack of greenery, dirt, sand, silt, mud, muck, bugs, and trees, increased stress is a likely result.

As to why we should want to improve our experience at work and reduce stress, job-related stress isn’t just unpleasant and, well, stressful. It can also complicate, complement, and exacerbate metabolic syndrome, raising triglycerides, blood pressure, and the risk of renal and heart disease. Pretty hard to get those TPS reports done with a failing kidney. Oh, and happier and less stressed workers are also better workers. Overall, occupational stress is a huge target. If we can reduce that by working outside, we’ll probably have mitigated a big portion of the stress in our lives.

Attention Restoration

For all intents and purposes, humans have two “types” of attention: voluntary, or active attention; and involuntary, or passive attention. When we’re working (or reading, or writing, or watching a TV show, or trying to remember a phone number), we are using voluntary attention. We have chosen to direct our attention toward this task, this task demands our full and sustained attention, and we are actively attending to it. An artist, a craftsman, a teacher, a golfer, an insurance broker, a copywriter – they all use voluntary attention to do their thing. Everyone who does anything does. Of course, voluntary attention takes a lot out of us. It’s tiring. It must be sustained, but it’s not indefinitely sustainable. We need a break from it.

Involuntary attention refers to “soft fascination.” It’s watching two birds in flight, an ant carrying food back to the nest, a leaf fluttering down from the tree, carried by the wind. It’s hearing a child’s cry, a trickling creek, a distant waterfall. It’s a respite from voluntary attention, because it doesn’t really require active engagement. It’s just there, and we’re observing it, almost like we’re “meant” to see this type of stuff on a regular basis without it occupying too much brain power.

If voluntary attention is like an intense workout, involuntary attention is the low-intensity active recovery, the walking, the mobility work, the cool down. We need both to be whole and healthy and attentive. If we spend all our time engaged in voluntary, active attention – like 10 hour days at work, 2 hour commutes, and 2 hours of late night TV – our performance declines, we get mental fatigue, and we’re less able to respond to novel situations and plan ahead. In short, we get overtrained.

Research shows that nature exposure is a way to foster involuntary attention, since walking in the woods doesn’t require us to “be on.” And if we move our work outside, to even just a small sliver of nature like a garden or a park, research shows that we can restore our attentional capacity, our balance between voluntary and involuntary attention. Our voluntary attention is the precious, finite resource that allows us to excel at work-related pursuits, and going into nature can replenish our stores of voluntary attention and, subsequently, our ability to work smarter and better. Why, it’s like using your laptop while it’s plugged in – you can operate at full screen brightness, have three browsers with tons of tabs open, watch videos, render graphics, edit photos, and play music, all at the same time. Okay, so that’s probably a bit of an exaggeration, but it will almost certainly help your performance.

There’s this idea that dallying in nature is wasteful, or that it’s time that could be better spent being productive, making money (especially for someone else!). I’m not buying it. For hundreds of thousands of years, people have been making tools, setting traps, building homes, butchering beasts, discovering math, science, physics, and astronomy, all while living in or near nature. Until recently, the wild was all around most of us. Even if you lived in the city or a village, nature was waiting outside the walls. Still we worked, and worked well. Why not now? Why not today?

As John Muir once said, ”Thousands of tired, nerve-shaken, over civilised people are beginning to find out that going to the mountains is going home; that wildness is a necessity; that mountain parks and reservations are useful not only as fountains of timber and irrigating rivers, but as fountains of life.” Going outside is “going home.” Now just imagine if you could work from home, too.

That’s the “why.” Next week, I’ll discuss the “how.” In the meantime, go outside, will ya?

Thanks for reading, folks. Thoughts, comments, and concerns are welcome, as always.

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Top 7 Most Common Reactions to Your High-Fat Diet (and How to Respond)

A couple weeks back, I wrote about the top 8 most common reactions you get when people hear you don’t eat grains, and I offered up some concise responses to those reactions. It was well received, so I thought I’d do the same thing for “your high-fat diet.” If you thought having to explain your grain-free diet was tough, explaining a high-fat diet – in particular, a high-animal fat diet – may seem even harder. At least with a grain-free diet, you’re merely removing something that many hold near and dear to their hearts. It’s “healthy” and “delicious,” sure, but at least you’re not adding something that will actively kill you. Fat is that deadly thing, for many people. It’s “fat,” for crying out loud. It’s bad for you, practically a poison. Everyone knows it. I mean, have you seen what fat down the kitchen drain does to your plumbing?

Actually, like the grain-free diet, explaining the high-fat diet is not that hard. I’ll even promise you that there are ways to do it, explanations and answers that don’t make you seem like a crazy person who hates his heart (I make no such promises for those of you with a stick of butter with bite marks and a tub of coconut oil with a greasy spoon beside it on your office desk, however). Now let’s get right to their questions and responses you can use:

“Isn’t all that fat gonna glom onto your arteries?”

That isn’t how it works. Atherosclerosis is caused by oxidized LDL particles penetrating the arterial wall, inciting inflammation, and damaging the arterial tissue. It is not caused by fat mechanistically attaching itself to the surface of the arteries like fat in a kitchen pipe. Also, it’s not like you eat some butter and that butter gets directed straight into your bloodstream. Your blood doesn’t have oil slicks running through it, or congealed droplets of grease gumming up the passageways. You are the product of millions upon millions of years of evolution, and I think our bodies can do better than trying to ape modern plumbing.

Response: “My arteries are not pipes. Fat is not solidifying in my blood like it can in the plumbing. Atherosclerosis is a complex process with dozens of factors beyond what’s in your diet, let alone the fat content.”

“Isn’t all that cholesterol gonna raise your cholesterol?”

If I were a rabbit, sure. When you feed cholesterol to an herbivorous animal, like a rabbit, whose only encounters with dietary cholesterol occur in a lab setting, their blood lipids will increase and they will usually develop atherosclerosis. For many years, the “cholesterol-fed rabbit” was a popular model for studying heart disease and gave rise to the now-popular idea that dietary cholesterol also elevates blood lipids in humans (thus immediately condemning them to a heart attack, naturally). Except it isn’t the case. Save for a select few who are “hyper-responders,” the vast majority of people can eat cholesterol without it affecting their cholesterol levels. And even when dietary cholesterol affects blood lipids, it’s usually an improvement, increasing HDL and the HDL:TC ratio while leaving LDL mostly unchanged. As for where all that blood cholesterol comes from, we make pretty much all the cholesterol in our blood in-house, and dietary cholesterol tends to suppress endogenous cholesterol synthesis. Boy, between “staying local” and “only making as much as we need,” our livers are downright green. I bet our HDL is GMO-free and organic to boot (not so sure about those sneaky LDL particles, though).

Response: “Dietary cholesterol does not affect total blood cholesterol. In fact, when we do eat cholesterol, our bodies make less of it to keep our blood levels in balance.”

“Isn’t all that fat gonna make you fat?”

Fat doesn’t make you fat. While you can technically overeat enough fat calories to accumulate adipose tissue, thus getting fat, this is a difficult feat, for two primary reasons:

Fat is very satiating, especially when paired with low-carb eating. Grass-fed pot roast, ribbed with yellow fat, connective tissue, and ample protein is far more filling than some crusty bread spread with butter. You’ll eat a decent slice of the former and be done, but you could easily polish off half a loaf of the latter with half a stick of butter and still be hungry. Fat gain requires a caloric excess, and it’s difficult to achieve one going on a high-fat, low-carb diet.

Dietary fat in the presence of large amounts of dietary carbohydrates can make it difficult to access fat for energy, while dietary fat in the presence of low levels of dietary carbohydrates makes it easier to access fat for energy. Couple that with the fact that fat and carbs are easier to overeat together, and you have your explanation. In fact, studies have shown that low-carb, high-fat diets not only reduce weight, they also retain or even increase lean mass. That means it’s fat that’s being lost (rather than the nebulous “weight”), which is what we’re ultimately after.

Response: “No. Caloric excess determines fat accumulation, and eating a high-fat, low-carb diet is the easiest way to inadvertently reduce calories without sacrificing satiation or satisfaction. It also improves your ability to access stored body fat rather than lean mass, which is helpful for fat loss.”

“But Dean Ornish/my mom/Walter Willet/the AHA/my doctor said saturated fat will give you heart attacks.”

They all may say that, and sound pretty convincing as they say it, but the science says differently. I tend to listen to the science, rather than what I think the science is saying:

A 2011 study found that “reducing the intake of CHO with high glycaemic index is more effective in the prevention of CVD than reducing SAFA intake per se.”
From a 2010 study out of Japan, saturated fat intake “was inversely associated with mortality from total stroke.”
A 2010 meta-analysis found “that there is no significant evidence for concluding that dietary saturated fat is associated with an increased risk of CHD or CVD.”

That looks pretty clear cut to me.

Response: “The most recent studies have concluded that saturated fat intake likely has no relation to heart disease, contrary to popular opinion.”

“Where do you get your energy?”

I get my energy from fat, both dietary and stored body fat. At 9 calories per gram, fat is the densest source of energy. I’m not sure if you’ve noticed, but humans tend to store it on their bodies. That’s not just for show, you know. We actually store it in our bodies as energy for later, for leaner times, for when food isn’t available. Fat is the ideal energy source for life’s daily activities; walking, working, even going for a hike or a light jog all access the oxidative, or fat-based energy pathway. Carbs only really come into play when you’re doing repeated bouts of intense exercise, like sprint intervals or high-intensity endurance training. But for just about everything else? Fat is king.

Response: “Fat is the body’s preferred and most reliable form of energy, which is why we store excess energy as fat on our bodies. Unless you think we accumulate body fat just to make pants fit tighter.”

“But isn’t fat totally free of nutrients? How do you get your vitamins if you’re eating all that fat?”

The richest source of natural tocotrienols (vitamin E), potent antioxidants, is red palm oil – a fat.

One of the richest sources of choline, a vital micronutrient for liver function, is egg yolk – a fat.

One of the better sources of vitamin K2, an oft-ignored nutrient involved in cancer prevention, arterial health, and bone metabolism, is grass-fed butter – a fat.

The best dietary source of vitamin D, a nutrient most people are deficient in, is cod liver oil – a fat.

See what I mean? Also, even when you’re cooking with a fat that doesn’t contain many vitamins, that fat is still going to improve the bioavailability of the fat-soluble vitamins (like A, D, E, K, K2) in the food you’re cooking.

Response: “Certain fats, like egg yolks, palm oil, extra virgin olive oil, cod liver oil, and grass-fed butter, are some of the most nutritious foods in existence. And without fat in your meals, you often won’t absorb all the nutrients that are present in other foods like leafy greens, since many of them require fat for full absorption.”

“Doesn’t the brain run on carbs, not fat?”

Yes, the brain requires glucose. That is true. However, the brain is more of a gas/diesel hybrid. It can run on both fat and glucose. Ketones, derived from fatty acids, can satisfy the majority of the brain’s energy needs, sparing the need for so much glucose. You’ll still need some glucose, as the brain can’t run purely on ketone bodies, but you won’t need nearly as much. And, best of all, your brain will run more efficiently on a combination of ketones and glucose than on glucose alone.

That improved efficiency means you can actually function without food. Since you have ample brain energy stores on your body (even the lean among us have enough body fat to last for weeks), and a high-fat diet allows you to access that body fat for brain energy, you’ll no longer suffer brain fog just because your afternoon meeting went a little long and you missed lunch. Instead, you’ll enjoy steadier, more even energy in mind and body.

Additionally, your body, through a process know as gluconeogenesis, can make up to 150 grams of glucose a day – more than the brain even needs (roughly 120 grams/day).

Response: “While it’s true that the brain requires some glucose for energy, using fat-derived ketones as well can make the brain run more efficiently and reduce its glucose requirements. On top of that, your body can probably create more glucose than your brain even requires.”

Compared to last week’s grains post, there were fewer entries today, the simple reason being that while grains are hyped beyond belief, people have but a few scant – albeit robustly defended – justifications for fearing dietary fat. The backlash almost always revolves around the visceral fear of “fat.” It’s a scary word, after all, but it shouldn’t be. No one should fear something so vital to life, so crucial for nutrient absorption and hormonal function, and so delicious with roasted vegetables.

Hopefully, these responses will help curb some of that fear.

So, what’d I miss? What else have you heard, and how did you respond? Let me and everyone know in the comments!

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How to Conduct a Personal Experiment: Cold Water Plunges

I’ve always been a self-experimenter, even when I didn’t realize it. Back when I raced competitively, I logged – compulsively – all my training routes, times, and distances. My logging didn’t begin as a grand self-experiment. It was just a way to authenticate my hard work. See, races were their own reward. Beating the other guys? Nothing sweeter. But those were few and far between. To get to those races, I had to train, day in and day out, with nothing tangible to show for it save for sore joints and a bottomless pit for a stomach. Filling those blank spaces with numbers made what I’d done somehow tangible, and the agony of training day in, day out became more bearable.

Of course, patterns emerged in those logs. I’d notice a string of particularly strong training days and think to myself, “What was different that week?” Had I eaten a particular something? Had I not eaten a particular something? If a weak sequence appeared, I’d wonder the same thing and explore my past. “Oh yeah, that was the week I had friends in town and I stayed up late every night” – maybe sleep does matter! Or, “I trained fewer days that week and my times actually improved” – could less possibly be more? And so from the practical, the numbers, the data, the objectivity, I gleaned the intuition, the insight, the lessons to be learned.

Now that I’ve internalized all those training lessons learned from my accidental self-experimentation, I don’t have to log it. I just do it. Same goes for eating. I don’t calorie or carb or protein count; I just eat. You can get there, too, and I suspect many of you have with regards to certain aspects of your diet or your training. But before you get there, before you’re dialed in, you have to experiment. You have to start with an idea, give it an honest shot, and see it through to the end. Though making your experiment air-tight enough to pass peer review isn’t necessary, try to be as systematic and scientific as you can. It will pay off and your results will have that much more meaning.

I hear people getting up to leave. I know, I know. We’re all about the ease of Primal eating, exercising, and listening to one’s body while looking at calorie-counting with suspicion and often barely veiled scorn – “just follow these basic rules and everything will fall into place like so” –  but logging data, analyzing data, and drawing conclusions from said data is really about honing your intuition. It’d be nice if we all maintained that Primal connection to our bodies, but most of us have not. Most of us have lived lives divorced from our bodies, eating weird pseudo-foods, strapped several inches of rubber to our feet, sitting in the same place for ten hours a day, staring at one electronic screen or another instead of the wide world around us, sleeping in rooms with bright blue green blinking shards of light filling our dreams, and we’re all a little confused. That’s okay. That’s to be expected. We can come back from this to reclaim our intuition, and data logs, journals, and self-experiments are how we get there.

You know how people say you go to college to learn how to learn? This is kinda like that.

What’s cool is that we can all learn something from a self-experiment. No matter what you know or think you know, you have a weak spot that can be identified and hammered out by systematically logging, journaling and testing. I know this because I have plenty of them myself. Ever since I wrote that first post on self-experimentation, I’ve been playing around with my own experiments, and I have an effective, simple methodology for testing. Also since that blog post I’ve quietly been putting the finishing touches on a new book, a 90-Day Primal Journal that will contain this methodology and deals with precisely this subject. It drops later this month.

Thus, this post marks the start of a new self-experimentation series on MDA. In the coming weeks, I’ll introduce new concepts to try, parameters to track, and experiments to run, but today, we’re going to cover cold water plunges.

Why cold plunges? A few reasons. First, cold water immersion is sort of a hot topic these days around the Primal and ancestral health community. It’s on people’s minds, so they’re already primed to consider it. If I had just come out of the blue with a random charge – “try plunging your mostly-naked body into cold water!” – you might write me off. This way, it’s not such a foreign concept.

Second, the weather’s warming up (at least for those of us living where summer is approaching). You’re more likely to try something as physically unappealing and discomforting as a cold plunge when it’s warm out. When it’s cold out? Not so much. For many people, the winter months are traditionally associated with hot mugs of coffee, hearty soups, and raging fireplaces, not feed troughs full of hose water doubling as immersion baths. This is a good time to ease into the practice of plunges. And who knows – maybe you’ll dig ‘em so much that you consider employing them in winter, too.

Third, for all the negative (and positive) stuff surrounding cold plunges, I think there’s real merit in them. They aren’t faddish, they aren’t (necessarily) dangerous, and though they’re not magical, brief exposure to cold can serve as a potent hormetic stressor that can induce positive adaptations.

Fourth, I’ve been incorporating them into my own routine for a few years now, and I’ve noticed a big difference. I think you guys will, too, and I think a community-wide push to systematically test the effect of cold plunges will give us a lot of data.

Okay, so how do I do it?

Come up with a goal that cold plunges may help realize. The link between your goal and the plunges should be plausible, of course. People make a lot of fantastical claims about the benefits of cold water plunges. Some say it’ll make you immune to the ravages of even the most pernicious pathogens. Some folks claim that cold water plunges will fine tune your metabolism. And some people swear that there’s no better hangover cure than a few minutes in some really cold water. While I have little doubt that there are kernels of truth hidden within most of these claims, the bulk of the established research has hitherto focused on workout recovery and fat loss.

Here are a couple ideas, but you can definitely come up with your own:

I want to improve workout recovery.
I want to lose body fat.

Then, come up with a hypothesis:

Post-workout cold plunges will improve recovery, reduce soreness, and increase subsequent performance.
Daily cold plunges will reduce body fat without affecting lean mass.

Let’s choose “workout recovery.” Identify the variables and note how they may affect the outcome:

Water temperature – Is colder better? Is there such a thing as “too cold”?
Time spent plunging – Is five minutes better than three? Is there such a thing as “too long”?
Frequency – Every day or every other day?
Contrast – Is cold/hot contrast water immersion better?
Body parts immersed – Is full body necessary? What if I just stick the legs in? Do I need to dunk my head? Do I only need to dunk the body parts I just worked out?
Time of day – Does it matter how far post-workout I take the plunge?
Workout intensity and volume – The intensity and volume of the workout itself are obviously huge determinants of how well you recover.

Test one variable at a time. If you change more than one variable from one plunge to the next you won’t be able to attribute the positive or negative results to the accurate variable.

Then, decide what you’ll be measuring in order to quantify “workout recovery”:

Subjective perception of soreness, ranked 1-10.
Heart rate upon waking, indicative of “recovery.” Overtrained individuals will often wake with elevated heart rates.
Weight lifted, reps hit, sprint times, mile times, and other markers of performance.

Oh, and if you want really strong results, be sure to introduce a period where you remove the cold plunges and note the change (or lack thereof) in workout recovery.

There are inherent limits to this brand of personal science, but so what?

Again, you are not a team of objective scientists, slavishly eliminating confounding variables (or trying your best) to test a single, solitary change and get published. You’re the scientist, the subject, and the reviewer. Ultimately, you’re just trying to help yourself and improve your health, not get published. You can cut corners. You won’t be able to eliminate confounders. Your diet won’t be completely static throughout, nor will your workouts, or the weather, or your sleep, or your stress levels. Things may have changed without the introduction of the variable, since working out consistently will generally produce improved performance, with or without a cold plunge. These things and more will affect the results of what you test, but that’s okay. After all, that’s life.

Okay. I’ve said my piece. Now, it’s your turn to get out there and get into some cold water. Shoot for around 60 degrees F, which will feel cold but not shockingly so. Stay in for as long as you can handle to start. Be sure to let me know how it goes!

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Dear Mark: Swimming Pool Chemicals, Washing Veggies, and Carb Blockers

Who doesn’t like a lovely day at the pool? Unless you can’t swim, there’s no reason not to love the cool water, the bright sun, the ping pong (every swimming club worth a dime has a ping pong table, or several of them), the face dunking, the high dive, and the chicken fights. But what if something sinister churned within the depths of the chlorinated water? What if by entering that pool you were risking life, limb, and the pristine alabaster of your eyeball? In today’s edition of Dear Mark, I’ve gone back to the roundup format. I begin with the question of swimming pool chemical safety, follow with a query about washing vegetables, and I finish the post with a short section on carb blocking agents. Sound good?

Let’s go:

Dear Mark,

I was wondering about possible negative effects of pool water. I enjoy a good sprint workout in the pool, especially when traveling and staying in a hotel. Could the chlorine or other chemicals be harmful since they do sometimes make me itch a little afterwards and burns my eyes (especially if I open them underwater)?

Thanks and Grok on,

Andrew

I hate to be the bearer of potentially bad news, but there’s probably something to this. Most pools use chlorine as a disinfectant, to keep the water clear of bacteria and other microbes, and it’s darn good at that. Reason? Chlorine, in its pure form, is toxic. The chlorine in the pool is obviously diluted, so it’s not going to burn or kill you outright, nor are you a microbe, but toxicity concerns remain. Your first clues that it might be doing something untoward, of course, are the burning eyes and itching skin. That’s pretty normal, albeit disconcerting. As a kid, I used to get red, burning eyes when I’d spend the day at the pool. Nowadays, I think back to that and wonder…

Anyway, red eyes clear up and itchiness subsides, but could other problems be lurking beneath the surface? Maybe. Chlorine reacts with other substances, including bodily fluids and various organic matter, to form disinfection byproducts (DBPs), which may have novel – and unwanted – health effects. Let’s take a look at some evidence:

When chlorinated pool water meets dimethylamine (found in urine and sweat), nitrosamine carcinogens (the same type of compound that forms when we overcook bacon) form, and appear in pools at concentrations up to 500-fold higher than drinking water. Though it’s unclear whether or not these particular nitrosamines are absorbed by pool users, some nitrosamines are absorbed through (rat) skin. Why should you care? Well, nitrosamines are used to induce bladder cancer in rodents, and chlorinated pool and bathing water usage have been linked to bladder cancer in humans (though it’s just observational).
Chloramine, another DBP, has been linked to asthma in pool workers and elite swimmers.
A recent study found over 100 chemical byproducts in swimming pools, many of them toxic. Before and after 40 minutes of swimming laps in such a pool, healthy subjects’ biomarkers were tracked and recorded. One marker suggested increased lung permeability and inflammation, while another marker indicated a kind of DNA damage that, if unchecked, might lead to cancer. Subjects had also accumulated elevated levels of four of the most common DBPs after 40 minutes in the pool.

The good news is that you’re probably okay. Problems may arise when we absorb and uptake these DBPs (like chloroform) via inhalation, dermal absorption, and the ingestion of affected water on a regular basis. The populations that seem to suffer most from pool-related maladies are the ones who spend significant amounts of time at, in and around the pool – competitive swimmers (with their infamously long daily workouts), lifeguards, and other pool workers – and it doesn’t sound like you’re living in the water. If you stick to short, intense sprints, performed only when you have access to a pool on business or vacation, I wouldn’t worry.

Hello Mark,

Can I wash my veggies with dish washing solutions? Or must I use special vegetable washing solutions?

Thank you for your time,

Mindaugas

Actually, you don’t have to use either. Tap water will work just as well. But don’t take my word for it. Check out the results of this study that explored this exact question. They used tap water, Palmolive, and four different vegetable washes to process unwashed, pesticide-laden produce and found no differences in pesticide residues when all was said and done. Luckily, washing the produce – whatever the solution used – took care of most of the surface pesticide residues (not all of them, though, not to mention the pesticides that are integrated within the produce).

So, yes, dish washing solution will work just as well as special vegetable washing solution, but so what? Water does the job, too.

Hi Mark,

Whats the deal the Carb-inhibitor/blocker pills, do they work? Are they safe? If so, which ones do you recommend? Thanks.

Ashley

Carb blockers use an extract of the white kidney bean that inhibits alpha-amylase, a digestive enzyme that breaks down starch. Without alpha-amylase doing its work, we can’t effectively digest starches, and they pass through to the small bowel to be fermented by gut flora. Sounds great, right? You get to eat carbs and you don’t digest them. They don’t turn into glucose, they don’t get absorbed, and insulin stays low.

I kid, but actually, a study shows that this is pretty much what happens. On the first day, subjects ate 50 grams of rice starch. On the second day, they were administered an amylase-inhibitor that inhibited 95% of amylase activity and fed another 50 grams of rice starch. Postprandial (post-meal) delivery of carbohydrate to the small bowel was increased after eating the carb blocker, meaning less was absorbed. Blood glucose spike was reduced by 85%. Insulin was “abolished.” What’s not to like?

I’m a little suspicious of something that “blocks” a normal physiological function. Just because I think we should reduce our reliance on carbohydrates as energy sources doesn’t mean I no longer value our natural, inherent ability to digest them. I’m also suspicious of shuttling all those fermentable carbohydrates to our gut flora. Giving some soluble prebiotic fiber? Cool, that’s great and we evolved eating fibrous vegetable sources, so our “normal” gut flora is likely used to it. But it sounds like providing a massive dose of something like sweet potato starch to our eager gut flora is a potential recipe for small intestine bacterial overgrowth (SIBO), which we definitely don’t want. There’s evidence that blocking amylase action indeed increases short chain fatty acid production by our gut flora, a marker for gut flora activity, but instead of absorbing the healthful fatty acids, those with impaired amylase activity excrete most of them. That tells me that maybe the gut flora are biting off more than they can chew, that maybe providing all that cheap starch to our small bowels is too much of a good thing.

But that’s just speculation off of a few related studies. We can’t know for sure, of course. Still, if you want to block carbs, just don’t eat so many of them. That’s certainly safer than messing with a vital, inherent part of our physiology, don’t you think?

Thanks for reading, folks. Let me know what you think in the comment board. Grok on!

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Weekend Link Love

Is elevated cholesterol just a marker for sunlight deficiency?

How to shop for kids’ shoes (video), featuring KStarr.

Paleo bumperstickers have officially been released. Go get yours today.

The FDA recently the Corn Refiners Association, saying that its petition to change the name of “high-fructose corn syrup” to “corn sugar” would confuse the public and fail to reflect reality.

“We were surprised to find the proportion of retractions due to scientific misconduct in the drug literature is higher than in general biomedical literature.”

Cancer researchers turn their eyes toward red palm oil, the most potent source of tocotrienols, in the hopes that a supplement derived from the oil could help prevent and stave off cancer cells. Instead of waiting, you know, you could just eat the oil.

A recent study has “definitively” linked irritable bowel syndrome, or IBS, to small intestinal bacterial overgrowth, or SIBO.

“Regardless of their fussiness,” kids served water were more likely to desire and eat vegetables than kids served soda.

Kids will be kids. Despite less time for unstructured play, children these days use more imagination during playtime than kids surveyed twenty years ago.

Cupcakes: the new cocaine?

Swimming coach inadvertently employs Primal training principles (play, less volume), produces a likely Olympic contender in the process.

Recipe Corner

Saag paneer, only this time with kale. Genius (if you like dairy).
Forget loaves of bread, standard meatloaf, and Meatloaf. Try Lebanese lamb loaf.

Time Capsule

One year ago (June 3 – June 9)

Vacations: Are They Good For Your Health? – The Worker Bees certainly think so. Find out the truth inside.
How to Wake Up and Feel Alert – For some, it’s not the sleeping that’s the problem. It’s the waking.

Comment of the Week

I had never heard of this before, but thank you for a wonky article as a means of introducing me to something I ultimately don’t need to worry about.

Sorry if that came off as sarcastic as it wasn’t my intention.

- I expect every post has this effect on at least one person.

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Roasted Cactus Salad with Shrimp

Familiar to some, exotic to others, cactus paddles (or nopales) have a mild but tart flavor and are surprisingly easy to cook. If you’ve been deterred from eating cactus because of the rumor that it has a slimy texture you should know that this rumor’s only half true. When cut into, raw cactus paddles do ooze a clear, tasteless and odorless gel that has a sticky, slimy texture (similar to aloe vera gel). When cooked, however, the gel disappears and the cactus paddles are crisp but tender.

Recipes often suggest boiling the slime away, but skipping this step and throwing the paddles directly onto a hot grill or pan works just as well. The direct heat evaporates the gel pretty quickly. While nopales that haven’t been boiled are a little bit chewier, they have a fresh, vibrant flavor. This flavor, which tastes a little bit like a green bean or tart green pepper, is great when tossed in with other ingredients like tomatoes, onions, garlic, peppers and radishes.

In this refreshing salad, roasted cactus paddles are combined with raw tomatoes, red onion and cilantro and then tossed with tender shrimp. The salad can be served as a main dish for lunch or dinner or as an omelet filling for breakfast (with or without the shrimp). Roasted cactus salad is also quite good with thin strips of steak instead of shrimp.

Refreshing, light and flavorful, cactus paddles are an interesting and versatile ingredient. For best results, roast, grill or sauté the cactus paddles alone to get rid of the slime factor, then combine them with other veggies, meat or seafood. The combinations really are endless.

Servings: Approximately 4-6

Ingredients:

1 pound of cactus paddles (about 4), cleaned and trimmed
2 tablespoons olive oil or coconut oil
1 pound of shrimp, shelled and cleaned
2 tomatoes, chopped
2 tablespoons finely chopped red onion
1/4 cup chopped cilantro
Lime or lemon juice to taste (optional)
Sliced jalapeno or hot sauce (optional)
Sea salt to taste

Instructions:

Preheat oven to 375 degrees Fahrenheit.

Some markets sell trimmed and cleaned paddles, others sell paddles that still have thorns. If the cactus paddles still have thorns, use a pair of tongs or a thick towel to hold a paddle steady on a cutting board. Use a sharp knife or vegetable peeler to scrape the thorns off both sides of the paddle. Then use kitchen shears or a knife to trim a little bit of the edge off the entire perimeter of the paddle.

When all the paddles are trimmed, rinse them then cut into 1/2-inch squares.

Put the cactus pieces in a single layer on a rimmed baking sheet – it’s important not to overcrowd the pan or there will be too much moisture and the gel won’t evaporate.

Drizzle with oil. Roast for about 20-30 minutes, stirring occasionally, until the cactus pieces are tender and most of the gel and liquid in the pan has evaporated.

While the cactus is roasting, bring a pot of water to a boil. Add shrimp, and boil 3 minutes until pink all the way through. Drain.

Remove the cactus from the oven and toss with shrimp, tomatoes, red onion and cilantro. Add the remaining ingredients to taste. The salad can be served warm or chilled.

To sauté cactus instead of roasting it, sauté the pieces in oil over medium heat for a few minutes then reduce heat to low and cover, stirring occasionally, until the cactus has released liquid, about 5 minutes. Increase heat back to medium and cook, uncovered, stirring occasionally, until all the liquid is evaporated.

To grill cactus paddles, clean and trim the paddles but leave them whole. Brush with oil, then grill for around 6 to 10 minutes, slice and serve.

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I Cannot Imagine Living Any Other Way

It’s Friday, everyone! And that means another Primal Blueprint Real Life Story from a Mark’s Daily Apple reader. If you have your own success story and would like to share it with me and the Mark’s Daily Apple community please contact me here. I’ll continue to publish these each Friday as long as they keep coming in. Thank you for reading!

Dear Mark,

I just wanted to thank you for your hard work and dedication to your blog.

I discovered Primal living during my recovery from anorexia. I didn’t give it a real shot until 5 months into recovery. I was just too afraid of all of that fat was going to make me fat!

During those 5 months, I gained up to an ideal weight for myself eating 3000-3500 calories a day. Oh, and lots and lots of carbs and lean protein – you know, that bodybuilding stuff. I still had no menstrual cycle and had a night eating problem. I was still depressed, anxious, and was still drooling over food I saw on the Food Network. I was getting really scared because I literally could not stop eating. I didn’t want to gain any more weight. I had decided I nothing to lose, so took a plunge into Primal living.

I obviously didn’t go cold turkey with the carbs. It took about a week to cut my carbs in half and eliminate most grains. (I swear carbs are like crack). I started eating lots of egg and cheese omelets, BEEF, whole avocados, some bacon. I was so excited eating cheeseburgers at my favorite burger place where they have grass-fed beef burgers…YUM. I knew if I didn’t eat enough fat and too much carbs at a meal, my cravings returned. I quickly learned this and became very consistent with my Primal choices.

About a month into the diet change, I noticed some changes. My anxiety after a meal decreased, and I was able to concentrate on school and my son more.  I started to feel my sex drive returning, was less hungry, was able to go longer periods without eating.

Then about a week ago, BAM, my period finally returned! I was so, so relieved and felt like I was back to my old self, but a more improved version.

I know this is not a typical success story, but I feel that my mental success is equally as important as my physical success. I am finally looking forward to movies, meeting new people, completing my school work, and playing with my 17 month old. I now eat to live instead of living to eat/binge by myself.

Don’t get me wrong, I am very pleased with my appearance. And I am glad that I don’t have to spend mindless hours running on the treadmill – how depressing! I have fallen in love with resistance training and have gained lots of strength.

Although I am sure there is no proof, I believe that the lack of saturated fats and too many carbs completely messed up my mental health. (It wasn’t until I turned vegan that my anorexia really peaked). I see so many people devote years to their eating disorder and sometimes even never recover. I feel very fortunate that I got out of that hell in a relatively short amount of time and am healthy again.

I found what lifestyle works for me and simply cannot imagine living any other way. I am so grateful that I discovered Primal living and happy that I am living life again!

Thanks, Mark!

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A Primal Primer: Brown Adipose Tissue

Last week’s Dear Mark discussing cold thermogenesis got some of you asking about brown adipose tissue. It’s a topic that deserves a full-fledged Primal Primer, especially since the idea of “good” body fat, a term many use to describe brown adipose tissue (BAT), is a foreign one. I mean, we’re talking about body fat here. Who wants it? Everyone I know is trying to get rid of their adipose tissue, not obtain more. It’s what brings many to this blog and what initiates this grand journey toward health and wellness. Even the people who say they “don’t care” about how they look would rather not have excess body fat, if only because it’s a marker of poor health or hormonal disregulation. We might acknowledge that we technically “need” some body fat to survive, but most of us will pass on any more than is absolutely necessary, thank you very much.

So whenever brown adipose tissue is invoked as the “good” kind of body fat, a body fat that cannibalizes other body fat, flabbers audibly gast. Is such a thing even possible?

Yes. Brown adipose tissue is very different than white adipose tissue. While white body fat can be regarded as an endocrine organ involved in the release of hormones, it doesn’t “do” all that much. It leads a pretty sedentary existence. Brown adipose tissue is metabolically active, however, consuming fat and glucose, increasing metabolism, and generating warmth for the organism as needed. Animals without the ability to shiver or tie scarves around their necks – like rodents and newborns – have lots of brown fat, because that’s how they stay warm – through “non-shivering thermogenesis.” Brown fat is dense with mitochondria, the power plants of cells which normally use fat and glucose to produce ATP. BAT mitochondria use fat and glucose to produce heat, rather than ATP. Thermogenin, or UCP1, is the uncoupling protein within the mitochondria that enables BAT to oxidize fat without producing much ATP.

Until quite recently, researchers assumed brown fat was mostly absent in adult humans. And if adults did have any, it was probably just a vestige from childhood with little actual functionality. In actuality, recent studies show that men and women can and do have significant amounts of brown fat, usually located near the neck, the chest, and the upper back, with women tending to have more than men. Rather than being inert, this adult brown adipose tissue is metabolically active with some interesting potential effects:

If “cold exposure” is indeed a proxy for “brown adipose tissue activity,” as I suspect, it clears triglycerides from the blood once the fat in the BAT has been depleted.
It is inversely correlated with obesity. The more body fat you have, the less BAT you have and the less activity you show in the BAT you do have.
It is correlated with bone mineral density. Low, or nonexistent levels of brown fat are strongly linked to low bone mineral density.
It is inversely correlated with fatty liver.

That all sounds pretty good, but how do we act on this knowledge? Is there anything we can do to start utilizing brown adipose tissue in our pursuit of health, leanness, and general Primal awesomeness? Maybe.

If you want to activate BAT, you have to get cold. Seeing as how brown adipose tissue’s primary function is to maintain body temperature, cold exposure activates existing brown fat – it presents the necessary environmental stressor to tell brown fat to start burning triglycerides for energy. A recent study (PDF) found that while exposing both lean and overweight men to “mild cold exposure” (61 degrees F, or 16 degrees C) activated brown adipose tissue in 23 out of 24 of them, thermoneutral temperatures resulted in zero BAT activity. Your brown adipose tissue doesn’t have much to do on a nice, warm day – nor, for that matter, on a miserably cold day so long as you’ve got the heater on inside.

Get cold, but not so cold that you can’t stand it without breaking down into a shivering mess. Brown fat keeps us warm up until the point of shivering, after which the physical act of trembling warms us and brown fat is deactivated (or down-regulated; it’s not clear whether it gets flipped off or gradually fades away). If you want to activate your BAT and only your BAT, don’t get so cold that you begin to shiver. Eventually, of course, your “shiver set point” will improve, you’ll get used to the cooler temperatures, and you’ll be able to tap into your BAT at lower and lower temperatures. Shivering also burns calories in its own way, but, well, shivering is kind of unpleasant and awful and it requires far lower temperatures. Go for goosebumps.

Although cold exposure is definitely the best way to activate brown fat, there’s also evidence that a person’s brown fat stores mediate the amount of energy they store after eating. Whenever you eat something, heat is generated, both from the physical and enzymatic breakdown of the food and from “diet-induced thermogenesis.” In patients with lower UCP1 expression (remember, UCP1 is the protein that enables combustion in the brown adipose tissue), the thermogenic response to a meal is lessened; and patients with confirmed brown adipose tissue generate more heat in response to a meal than patients without brown adipose tissue. Since that heat comes from energy that is not being stored, a greater thermogenic response to food means less (bad) body fat accumulation.

All this revolves around the activation of existing brown adipose tissue. While that’s important, what about creating new BAT? There are two candidates – chronic cold exposure and exercise.

In rodents, temperature to which the animal is chronically exposed determines the total amount of BAT on the body. Rats in a heated lab will have less brown fat than rats living outdoors. Humans, even those living in cold climates, are rarely exposed to the cold weather. They sleep in heated homes, drive in heated cars, shop in heated department stores, and bundle up with multiple layers for those fleeting moments spent outdoors. It’s even been proposed that the advent of central heating is related to obesity. I suspect that the total amount of human BAT also depends on chronic exposure to cold, especially since one study (PDF) showed that outdoor workers have more BAT than indoor workers. Acute exposure activates, chronic exposure creates.

Irisin, the “exercise hormone,” appears to convert white adipose tissue to brown adipose tissue. As irisin increases in a rodent’s blood, energy expenditure increases without an increase in movement or food intake, suggesting an increase in thermogenesis mediated by the converted WAT. Humans also make irisin in response to exercise, so this could work for us, too.

I don’t think we can ignore brown adipose tissue as a partial player in the metabolic mess we’re in. It’s not the one key to solving the obesity epidemic, but neither is anything else. It’s a piece of the puzzle, a contribution to the whole mess, and it’s completely plausible to think that people are fatter than they have to be because they’re too dang warm all the time. Sure, people have always avoided the cold, whether through central heating or animal pelt, but the way we avoid it today is way different – and far more effective. At any rate, it can’t hurt to give it a shot.

Hopefully, one of these Saturdays I’ll be able to include a recipe for stir-fried veggies in the rendered brown fat of pasture-raised hamster (sorry, hamster lovers; I had to pick a rodent). Until then, let’s hash things out in the comments. Tell me about your experiences with cold exposure, brown fat, and weight loss, or weight gain, or your plans to experiment. Take care!

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The Tall Tail of Telomeres

For years now, it’s been said that telomeres – the tips of your chromosomes – are the key to cancer and aging. The shorter they are, the worse off you are – so the story goes. But what do we really know about them? Can the length of your telomeres help predict how long you’ll live? Could telomere research unlock a modern fountain of youth? Could humans one day live to be hundreds of years old?

Dr. Ron Rosedale of DrRosedale.com and The Rosedale Diet is here to answer some of these questions in this special guest post. In it he will introduce you to these little bits of genetic sequences, and provide his expert commentary on the state of telomere science. It will get somewhat technical in parts, but it’s well worth the read.

Now, Dr. Rosedale…

Summary – The Good, the Bad, and the Ugly

The Good: With considerably more research in the control of telomere length specific to different issues, it may be a new and powerful therapeutic tool to improve health.

The Bad: It is not likely a modality to extend maximal lifespan. It is far from the fountain of youth.

The Ugly: Without proper and exact knowledge of when and where to control telomere length, it will likely greatly increase one’s risk of cancer. In other words, it may very well increase healthspan as it reduces lifespan.

Introduction

Can the length of very simple, short genetic sequences at the tips of chromosomes called telomeres determine how healthy you are and how fast you will age? This has become a popular idea in paleo blogs and in the lay world of “anti-aging medicine”, especially now that telomere length (TL) can be relatively easily measured.

First, let’s examine very briefly the history of that idea. In 1961 Leonard Hayflick discovered that cells in a petri dish could only divide a limited number of times before cell division would cease permanently. This famously became known as the “Hayflick limit”. 10 years later Olovnikov, a Russian researcher, linked the tails of chromosomes to this cell division arrest. It was found that the enzymes that duplicate the DNA of chromosomes cannot continue this duplication all the way to the ends of linear chromosomes. If cells were to divide without telomeres, with each cell division they would lose a chunk of critical and functional DNA. The telomeres act as sacrificial lambs for DNA duplication. They are repeating nucleotide segments (TTAGGG) of relatively meaningless segments of chromosomes such that the loss of a small chunk of these when cells divide is genetically harmless… up to a point. If a cell divides too much, and its telomeres become too short, at best it can no longer divide. Worse, genetic harm befalls that cell. A process is initiated within the cell causing it to self-destruct (called apoptosis). Later, it was found that a natural enzyme that some cells manufacture called telomerase is capable of lengthening telomeres and potentially immortalizing that cell. The finding that telomeres shorten with increasing age has led to the theory that telomeres are at least a biomarker of aging, if not at least partially causative of the damage associated with aging (called senescence). It was, and still is in some circles, thought that increasing telomere length slows, if not reverses, aging. The telomere theory of aging was born. Should it continue to live, or die a peaceful apoptotic death as shortened telomeres themselves are apt to cause?

A full discourse on telomeres and the biology of aging would consume an excessive amount of all of our already telomere challenged lives. I will instead focus on telomeres as a potential biomarker and/or “anti-aging” therapy and the deeper meaning of this.

First, let’s get our terms straight. What is mean by “anti-aging”. The word itself is controversial. In the more scientific, biology of aging community where researchers are genetically manipulating specific (i.e. insulin) metabolic pathways and extending lifespan a hundred or more percent in some animals, that word has a negative connotation. To them, it conjures up images of modern day snake oil salesmen promising longevity treatments such as growth hormone therapy, that if anything, might likely shorten lifespan. To them, a slowing down of the typical aging process results in a lengthening of maximal lifespan as opposed to average lifespan. The two are quite different. The maximum human life span (that has been well-documented) is considered to be 122 years that Jean Calment, a French woman lived before dying in 1997. The average lifespan in the United States is roughly 78 years. If one greatly increased the health of the general population, one might increase average lifespan to be hypothetically 85 years. However, if no one still lived over 122 years, the maximal known human lifespan would continue to remain unchanged.

A treatment such as lengthening telomeres might well improve some, and possibly many, symptoms of aging and even the average or median lifespan, while leaving maximum lifespan unchanged…or perhaps even shortening it. It would not and should not then be considered an “anti-aging” treatment though possibly a good therapeutic modality.

On the other hand, biology of aging experts such as a friend of mine, Andrzej Bartke, past president of the American Aging Association, are able to extend the maximum lifespan in laboratory animals such as mice…a lot. He is the last recipient of one of the most prestigious and lucrative awards in aging research, the Methuselah Prize. He did this by genetically suppressing the growth hormone receptor in a strain of mouse such that it lived about twice as long as usual; the equivalent of a human living to be approximately 180 years old. In the published study that won the prize he states, “We propose that mechanisms linking GH [growth hormone] deficiency and GH resistance with delayed aging include reduced hepatic synthesis of insulin-­like growth factor 1 (IGF­-1), reduced secretion of insulin, increased hepatic sensitivity to insulin actions, reduced plasma glucose…An important role of IGF­1 and insulin in the control of mammalian longevity is consistent with the well­-documented actions of homologous signaling pathways in invertebrates.” (Life extension in the dwarf mouse; Curr Top Dev Biol. 2004;63). I mention this also, since a similarly hyped and very popular “anti-aging” treatment is growth hormone therapy, whereby growth hormone is regularly injected with supposed rejuvenating properties…exactly opposite to what was done to win the coveted Methuselah Prize… Caveat emptor.

Many so-called experts on health and longevity talk a lot about increasing telomere length as proof of efficacy of some sort of diet or other health modality. Let’s look at that statement. What do they mean by increasing their telomeres? They have about 15 trillion cells. Did they increase the telomere length of all chromosomes in all cells? Were they all measured? Was a representative sample measured? Is telomere length even indicative of health, or aging? Is it even a biomarker of aging, and if so, is that relevant?

One of several major problems with all this; less than 1% of a person’s cells have the enzyme telomerase and thus are even capable of increasing their chromosome’s telomere length. The other 99% are incapable of doing so. What about neurons, and heart cells that typically do not divide and where their telomeres do not shorten with age? The large majority of liver and kidney cells can’t lengthen telomeres, etc., etc. Perhaps the 1% that can are the most critical. They include white blood cells (WBCs) and many stem cells. We will examine that a bit more later.

Is it even good to increase telomere length? Maybe not. 90% of cancer cells do it. The fact that telomeres shorten may actually allow us to live longer, as it may reduce the risk of cancer. The good news is that the telomeres in almost all the cells other than WBCs and stem cells do not increase, for if they did, dying of cancer would be all but certain.

The chromosomes of nearly all multicellular life are linear; they have a beginning and an end. As such, for these cells, telomeres are essential to life. The exception are bacteria whose chromosomes are circular. They do not have a beginning or an end and thus telomeres are a moot point. Thus, there are no telomeric restrictions on bacterial reproduction. They continue to reproduce as often and as fast as they can; like cancer, that seems to be their singular goal. The purpose of linear chromosomes and telomeres is often thought to be secondary to our evolution from single celled bacteria to large, complex, multicellular individuals such that their now linear chromosomes with telomeres prevent cells from easily reverting back to their ancestral bacterial ways, i.e. the singular purpose of reproduction, that in multicellular life is cancer. It is a must to continually lengthen telomeres to lift the restriction on cell division if a cell hopes to stay a cancer cell.

Another major problem with the telomere theory of aging; if anything there is a negative correlation between telomere length and lifespan of different species. For instance, mice have much longer telomeres than humans but live a small fraction as long.

However, numerous studies have shown a correlation within a particular species between telomere length and length of life. This has therefore been used as strong evidence that length is a good biomarker of aging within a particular species and even that telomere attrition causes aging itself. Hopefully they mean the damage associated with aging. It is unlikely that you would not be a day older tomorrow.

A major mistake made so frequently in medicine, but rarely in other sciences, is the confusion and interchange between correlation and cause. An example is the consistent reference to cholesterol being a cause of heart disease, when in fact it is an association, and even a weak one at that. An entire industry and economy has been built over that “mistake”. I digress; that is a story for another day (or you can read on the web what I have already said about that long ago).

Getting wrinkles is far more correlated, and is therefore a far better biomarker for aging than telomere length, however undergoing a dermabrasion is not likely to extend lifespan. Once again, it is science 101 to not confuse correlation with cause. It could very well be, and in fact is likely, that reduced telomere length is a byproduct of the cell damage and turnover associated with aging, rather than a prime cause of it, though it likely does have some adverse repercussions especially to the immune system and possibly stem cells.

How about current laboratory testing for telomere length? It merely requires a tube of blood since one of the very few cell types that is easily accessible and where telomerase is present such that telomere length can increase are white blood cells. Is the test meaningful? Probably not very. The rate of telomere attrition, the rate of decrease in telomere length that may be more important than absolute length, will increase with increased cellular damage and turnover such as that caused by oxidation, free radical damage, glycation, and inflammation. In other words, all that a higher rate of telomere shortening of any kind might indicate is an increased rate of cellular damage, but it doesn’t tell you what is causing the damage. Glucose perhaps?

Many, including myself, believe that all shortening of WBC telomere length in particular reflects, is the state of inflammation. There are many other much simpler and less expensive, albeit less glamorous markers for this such as a C-peptide or even the sedimentation rate. Furthermore, both a healthy, though at the time less active immune system, and an overly stressed or suppressed immune system might, at least theoretically, lead to less telomere attrition due to less cellular proliferation.

Though the rate of white blood cell TL shortening has been shown to decrease and may even increase with certain changes in lifestyle such as exercise and diet (that might just reflect improved immune response), TL also has been shown to oscillate even if you don’t do anything; not change your diet, nor exercise, take antioxidants, or think positively about your TL.

However, the biggest problem in measuring TL in WBC’s is that there are many different telomeres of different lengths in many different kinds of cells with differing rates of attrition. An increase in white blood cell TL or reduced rate of shortening does not necessarily reflect a change in other telomeres, especially from other cell types. For instance, in cells that don’t divide, such as heart and nerve cells, TL is somewhat meaningless. Telomere length even varies depending on the kind of white blood cells.

Robust evidence also shows that it is not the length of telomeres, or even the rate of telomere reduction with age that matters, but rather that telomeres must get to a critically short length for adverse genetic repercussions to take place. Measuring WBC TL only measures average WBC telomere length and not the number of critically short telomeres.

For all of the above reasons, I feel that current measurement of WBC TL is not a very good biomarker of aging and is virtually meaningless as an important independent indicator of the rate of aging.

What about the other major cell type that produces telomerase and is capable of increasing telomere length? What about measuring stem cell TL? This is done, but currently only in research laboratories and generally only in animals. Not very many people would volunteer for heart biopsies, for instance. A jilted lover might volunteer their ex perhaps. However, stem cell TL is actually where the rubber meets the road. Stem cells are very important as is their preservation. They are certainly capable of regenerating many tissues, including those not producing telomerase. Unfortunately, WBC TL does not necessarily reflect stem cell TL, nor does it reflect telomere attrition, especially since there are so many different types of stem cells from so many different types of tissue with so many different rates of cellular turnover and damage. I discuss this more below when I show excerpts from some studies that are quite revealing.

Telomere length is correlated with rate of cellular replication, and cellular replication is increased with increasing mTOR, IGF-I and inflammation. Therefore, it very well could be that the correlation between telomere length and longevity is only just that, a correlation, and not a cause, and the underlying mechanism of aging has much more to do with levels of glucose, mTOR, IGF-I…and insulin and leptin. That is likely true. Indeed, telomere length, has been shown to be highly (negatively) correlated with leptin levels (see below).

As I was actually writing this article, one of the most significant studies to be published pertaining to telomeres in recent years came out of Maria Basco’s lab from Spain. I will discuss it more at length below. It shows just how important it is to orchestrate telomere length and telomerase. It must be turned on, or off, at a certain time and place for there to be any chance at significantly improved health without increasing cancer risk.

Conclusion

The telomere theory as a cause of aging was hotly debated over a decade ago in many biology of aging conferences where university researchers got together to discuss their latest findings. Now, this is barely discussed outside of pseudoscientific circles… Perhaps the latest Basco study will reinvigorate this debate.

I believe that lengthening telomeres, most specifically in stem cells, and then only temporarily to mitigate against increasing cancer risk, may offer potential to increase health span and delay the onset and even treat certain chronic diseases of aging. However, this is not the same or as powerful as increasing maximal lifespan and stretching out youth that research into genetic pathways of aging regulated by nutrient sensors (insulin, leptin, and mTOR) offer, as illustrated by the increase in maximal lifespan of many species by 200% and more when insulin, IGF-I, and mTOR are genetically suppressed.

One must accurately define health before directions to be healthy are given and just like health is not low cholesterol, health is not defined or synonymous with long telomeres.

Life is dependent on the coordination of its constituent parts. This is especially true pertaining to the length of telomeres of the various cells and organs to maintain health but prevent a high risk of cancer.

As I have said so frequently in the past, we are 15 trillion cells and 90 trillion bacteria that must work harmoniously as one for us to be healthy and remain alive. This requires an intricate orchestration of communication between the different parts. That includes the genes, telomeres, and telomerase. It is where, when, and how much they are played, like the keys of a piano playing an infinite variety of music from the same keys, that determine who we are, diabetic or not, and if we stay alive or die.

What we do want to do is slow down the reduction in the length of our telomeres in an organ and tissue-specific manner that can be orchestrated only through proper genetic expression. Leptin and insulin are among the most, if not the most powerful influences of this. And these in turn are controlled by what you eat.

Review of Telomere Literature

Need more convincing? Confused? Have insomnia? Quotes from various references with brief discussions will follow. (Paper titles are bolded and hyperlinked, quotes from the papers are in the quote boxes, and my comments follow each box).

Telomere biology in healthy aging and disease , Hisko Oeseburg, Eur J Physiol (2010) 459:259–268

In contrast to the similarity of the sequence, the telomere length is highly variable among species, within species, within an organism, and even between chromosomes.

Telomere length of a few different species;

Humans 5–15 kb [kilobase; 1000 base pairs]

Mice Up to 150 kb

Rats 20–100 kb

Birds 5–20 kb

Ants 9–13 kb

…mice strains with longer telomeres do not seem to have an increased lifespan compared to mice strains with shorter telomeres…in African Americans telomeres generally are longer than in White Americans.

Rosedale: …yet have shorter average lifespans. All of this well known data will tell you immediately that telomere length, per se, is not critical to biological aging.

Telomere length [is] highly variable between organs from one subject. This may be explained by variable telomere attrition rate.

Rosedale: One could postulate that rather than absolute telomere length, telomere attrition rate might be significant. However, this could and indeed likely is a reflection of the rate of cellular damage, death, and degree of cellular multiplication to replace that damage. In other words, telomere length would be secondary to aging rather than a cause of it. Measuring telomere attrition rate would, of course, necessitate the measurement of telomere length over time.

The major disadvantage of using leukocyte telomere length is that it is a measure of the activity state of the immune system and one might argue that leukocyte telomere length is rather a representation of increased inflammation than of aging.

Rosedale: The state of inflammation is quite variable over time. A strep throat, upset stomach, and a scraped knee could increase your general state of inflammation for weeks and this could reflect in variably lower WBC telomere length secondary to a healthy immune system.

Blood Cell Telomere Length Is a Dynamic Feature, Ulrika Svenson, PLoS ONE June 2011 Volume 6 Issue 6

Irrespective of the biological background, leukocyte telomeres appear to oscillate in length over time [months].

Rosedale: Therefore many measurements over time in a single individual would be necessary to know if a change in TL was due to normal oscillation or not.

Shortening telomeres are more secondary to aging and disease than a cause of it.

Telomere length and cardiovascular aging: The means to the ends?, Tim De Meyer, Aging Research Reviews, Vol 10, #2 April 2011, Pages 297–303

Conclusion: Shorter inherited telomeres do not appear to predispose to early atherosclerosis. Atherosclerosis related factors accelerate telomere attrition.

Rosedale: Shortening telomeres may have a huge evolutionary advantage, especially for larger animals…

Telomerase activity coevolves with body mass, not lifespan, Andrei Seluanov, Aging Cell. 2007 February ; 6(1): 45–52

Here we show that telomerase activity does not coevolve with lifespan but instead coevolves with body mass: larger rodents repress telomerase activity in somatic cells. These results suggest that large body mass presents a greater risk of cancer than long lifespan, and large animals evolve repression of telomerase activity to mitigate that risk.

Rosedale: What about the potential of increasing telomere length?…

Telomere length, stem cells and aging, Maria A Blasco, Volume 3 Number 10 October 2007 Nature Chemical Biology

The fact that the vast majority of human tumors seem to depend on telomerase reactivation to prevent critical telomere loss and to divide indefinitely suggests that telomerase inhibition could be an effective way to abolish tumor growth.

The fact that telomerase deficiency only results in loss of organismal viability when telomeres reach a critically short length is an important point when considering possible secondary effects of these therapies.

In particular, this predicts that putative anticancer therapies based on temporary telomerase inhibition will only trigger loss of viability in those cells with short telomeres that depend on telomerase activity. Presumably, these include tumor cells but not healthy tissues, which generally lack telomerase activity and have sufficiently long telomeres to maintain viability during the human lifetime, thus providing a window of opportunity for intervention.

Therapeutic agents that could be designed to [re-activate telomerase temporary] would preferentially target those cell types that normally divide to maintain organ homeostasis—such as stem cells, which, although telomerase-proficient, do not have sufficient telomerase activity to maintain telomere length over time.

Rosedale: As in all disease, especially having to do with genes, it is where, when, and how they are read that determines their contribution to health, disease, and even who you are.

Telomere Length of Circulating Leukocyte Subpopulations and Buccal Cells in Patients with Ischemic Heart Failure and Their Offspring, Wong LSM, PLoS ONE 6(8) August 18, 2011

For instance, it has been shown that vascular endothelial cells that endure more hemodynamic sheer stress have shorter telomeres than endothelial cells in low pressure arteries [secondary to a greater rate of turnover]

Rosedale: i.e. TL is a secondary byproduct of aging, not a primary cause of it.

To further dissect the association of ischemic heart disease with mean overall leukocyte TL we need to establish whether mean overall leukocyte TL is a reflection of TL in different cell types or whether it is more or less specific for leukocytes. Of particular interest in this regard are the CD34 positive (CD34+) cells as it is thought that these cells might be cardiovascular progenitor [stem] cells and play a role in cardiovascular repair…Furthermore, mean leukocyte telomere length has not been compared to non-circulating non-vascular cells and it is unknown whether leukocytes might merely be a reflection of overall TL of the whole body… One of the aims of this study was determining whether telomere length of CD34+ cells is different in IHF patients compared to healthy controls. We did not find a difference in TL between IHF patients and controls in CD34+ cells. These results clearly indicate that there is no significant difference in CD34+ cell TL between IHF patients and controls.

The major difference in telomere length between IHF patients and controls was observed in the overall leukocyte pool, not specifically in CD34+, MNCs or buccal cells as a source of non-blood derived cells.

The comparable TL of CD34+ cells in cases and controls strongly suggest that telomere shortening of CD34+ cells is not a major player in the pathophysiology of IHD…In the elderly, specific immune responses might be diminished, but many other functions are unchanged or even augmented compared to young persons.

Rosedale: This study is important for several reasons, the main one being to illustrate that even though WBC TL may correlate with a disease state such as ischemic heart failure (secondary to correlating with cellular damage and turnover), WBC TL did not correlate, at least in this study, with representative cells of the only major cell group that may have significant therapeutic potential, stem cells. One cannot extrapolate WBC telomere length to other tissues.

Telomerase, senescence and ageing., Shawi M, Autexier C., Mech Ageing Dev. 2008 Jan-Feb;129(1-2):3-10. Epub 2007 Dec 14

Paradoxically, the introduction of telomerase is proposed as a method to combat ageing via cell therapy and a possible method to regenerate tissue, while telomerase inhibition and telomere shortening is suggested as a possible therapy to defeat cancers..

Rosedale; In other words, telomerase must be turned on and turned off at the appropriate time and location, i.e. it must be orchestrated.

Rosedale: And again, one cannot extrapolate WBC telomere length to other tissues.

Measuring relative telomere length: Is tissue an issue?, Monica M. Gramatges and Alison A. Bertuch. AGING, November 2010, Vol 2 N 11

Although the number of subjects was small, strong correlations between blood, buccal cells, and fibroblasts were observed in the study population as a whole. When taken individually, however, only cells from subjects with DC demonstrated significant correlation. [dyskeratosis congenita (DC). DC is a rare genetic disorder stemming from a defect in telomere maintenance.]

Rosedale: Can TL predict centenarians? Not in the following study. Also, WBC TL was again not correlated with another representative tissue type.

Telomere length in fibroblasts and blood cells from healthy centenarians., Mondello C, Exp Cell Res. 1999 Apr 10;248(1):234-42.

In this paper we analyzed the mean length of the terminal restriction fragments (TRF) [frequently how TL is measured] in fibroblast strains from 4 healthy centenarians, that is, in cells aged in vivo, and from 11 individuals of different ages. No correlation between mean TRF length and donor age was found.

…chromosome analysis did not show the presence of telomeric associations in early passage centenarian fibroblasts. In blood cells from various individuals, the expected inverse correlation between mean TRF length and donor age was found. In particular, a substantial difference (about 2 kb) between telomere length in the two cell types was observed in the same centenarian.

No Association Between Telomere Length and Survival Among the Elderly and Oldest Old, Bischoff C, Epidemiology: March 2006 – Volume 17 – Issue 2 – pp 190-194

This longitudinal study of the elderly and oldest old does not support the hypothesis that telomere length is a predictor for remaining lifespan once age is controlled for.

Rosedale: We have lots of telomeres. We have at least 500 trillion of them and measuring a select few from one cell type is not necessarily going to tell you what the other telomeres are doing…

Ageing and telomeres: a study into organ and gender-specific telomere shortening, H. Cherif*, 1576±1583 Nucleic Acids Research, 2003, Vol. 31, No. 5

In humans, telomere length is relatively short, highly variable between tissues and individuals and, with regard to replicating somatic cells, inversely related to donor age

We show clearly in this study that the mean TRF length method is unable to detect small changes in telomere size or to visualise the length of individual short telomeres in a distribution of TRFs. There is increasing evidence suggesting that it is not average telomere length, but rather individual critically short telomeres that trigger cellular responses to the loss of telomere function

The latest study and the most promising to show health benefits in telomerase expressed mammals was published last week…

Telomerase gene therapy in adult and old mice delays aging and increases longevity without increasing cancer, Bruno Bernardes de Jesus, Maria Blasco, EMBO Mol Med march 16, 2012 4, 1–14

Importantly, telomerase-treated mice did not develop more cancer than their control littermates, suggesting that the known tumorigenic activity of telomerase is severely decreased when expressed in adult or old organisms using AAV vectors telomerase treated mice, both at 1-year and at 2-year of age, had an increase in median lifespan of 24 and 13%, respectively.

Owing to its ability to confer with unlimited proliferative potential, over-expression of the telomerase reverse transcriptase (TERT) is a common feature of human cancers and can increase cancer incidence in the context of classical mouse TERT transgenesis.

A drawback of mTERT over-expression in transgenic mouse studies has been an increased cancer incidence, except for cancer-resistant backgrounds.

Telomerase expression late in life leads to overall telomere lengthening and decreased abundance of short telomeres in various tissues.

…telomerase activation can delay normal mouse aging in cancer resistant mice…

However, with the exception of mice genetically engineered to be cancer resistant, increased telomerase expression is associated with a higher susceptibility to develop cancer both in mice and humans…

Notably, in these studies increased TERT expression is forced since early embryo development through germ line modifications, which may favour the expansion of cancerous cells and the development of cancer later in life…Here, we show that increased TERT expression later in life (adult and old mice) by using a gene therapy strategy has rejuvenating effects without increasing cancer risk…the known tumorigenic activity of telomerase is severely decreased when expressed in adult or old organisms. Finally, re-introduction of mTERT in both 1- and 2-year old mice increased significantly its median lifespan (24 and 13%, respectively).

Rosedale: It generally takes at least several years for cancer to reveal itself. These mice only live 2 to 3 years. Therefore expressing telomerase when these mice only had one or less years to live likely did not give cancer cells enough time to manifest themselves. This would not be the case when using this sort of therapy in humans with more than 1 to 2 years to live. Note further that it is median lifespan that was modestly increased rather than maximal lifespan.] Also note that humans have much more body mass than mice, and therefore artificially activating telomerase in humans may have significantly greater negative consequences especially relative to cancer rate as compared to mice. See study above.

A commentary to the above article in the same journal:

Telomerase gene therapy: a novel approach to combat aging, Virginia Boccardi, Utz Herbig, EMBO Molecular Medicine 4, 1–3

…numerous studies using mouse models have demonstrated that critically short and dysfunctional telomeres indeed present a powerful barrier to cancer growth.

A question that has therefore intrigued researchers for many years is whether it is possible to slow aging and improve health span by re-activating telomerase in all of our cells. Constitutive expression of telomerase, unfortunately, is a characteristic of almost all cancer cells. It is therefore no surprise that transgenic animals over-expressing the catalytic subunit of mouse telomerase (mTERT), develop cancers earlier in life, thereby masking the potential beneficial lifespan extending properties of telomerase.

While these studies provide a proof-of-principle that telomerase gene therapy is a feasible and generally safe approach to improve healthspan and treat disorders associated with short telomeres [in mice], a clinical application in humans is likely still some time away. Low levels of integration of rAAV vectors into genomic DNA have been observed, raising the possibility that rare integration events of constitutively overexpressed TERT into genomes of long lived species might eventually promote cancer growth.

Furthermore, as with other gene therapeutic approaches, targeting the virus to specific cells in the body remains an obstacle. Also uncertain is specifically which cells should be targeted using a telomerase gene therapy.

Rosedale: Conclusions?

Association Between Telomere Length, Specific Causes of Death, and Years of Healthy Life in Health, Aging, and Body Composition, a Population-Based Cohort Study, Omer T. Njajou, J Gerontol A Biol Sci Med Sci 2009. Vol. 64A, No. 8, 860–864

In conclusion, we did not find any evidence of association between [WBC] TL [telomere length] and overall survival or between TL and specific causes of death. We also report for the first time that longer TL is associated with self-reported health status and greater YHL. Findings suggest that TL, although not a strong biomarker of survival in older individuals, may be an informative biomarker of healthy aging.

Is Telomere Length a Biomarker of Aging? A Review, Karen Anne Mather, J Gerontol A Biol Sci Med Sci. 2011 February; 66A(2):202–213

The observation that telomeres shorten with increasing age and are implicated in cellular aging has led to the proposal that telomere length is a biomarker of aging.

Currently, telomere length does not fully meet American Federation of Aging Research criteria that telomere length is (a) a better predictor of life span than chronological age (Criterion 1) and that (b) it monitors a basic process underlying normal aging at the pop-ulation level (Criterion 2).

Interestingly, an increase in intra-individual telomere length for a minority of participants at follow-up (ie, with increasing chronological age) has also been observed in three independent studies (27,39,78). However, this may not represent an increase in overall telomere length but rather could reflect the loss of cells with shorter telomeres.

Rosedale: It has been found that likely only cells with extremely short telomeres are so adversely affected that the process of apoptosis is initiated.

Could the significance of TL be secondary to leptin levels? TL is inversely correlated with leptin levels.

Obesity may accelerate the ageing process., Rowan Hooper, New Scientist 14 June 2005

But animal studies have failed to reveal any simple relationship between telomere length and lifespan… the youngest women had telomeres that were around 7500 base pairs long. Their length declined with age at an average rate of 27 base pairs per year.

When lifestyle factors were taken into account, however, dramatic differences emerged. The difference between being obese and being lean corresponds to 8.8 years of extra aging…

Smoking was the other big factor… Obesity accelerates the ageing process even more than smoking. Intriguingly, the link between high leptin concentrations and telomere shortening was even stronger than the link with obesity…The damage to telomeres is probably done by free radicals. Smoking causes oxidative stress ­ a source of free radicals ­as does obesity [and high leptin]

Free radicals can cause mutations in DNA, and there is some evidence that mutations in telomeres cause larger chunks than normal to be lost during cell division. In other words, it is a byproduct of aging that results in cellular turnover and molecular damage and therefore shortening of telomeres and not the other way around.

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Caveman Blogger Fights for Free Speech and Internet Freedom

You may have heard that Steve Cooksey of Diabetes-Warrior.net received a letter back in January from the North Carolina Board of Dietetics and Nutritionists explaining to him that he and his website were being investigated. What was Steve doing wrong, you ask? Well, Steve was sharing his story with his readers and suggesting that they might benefit from following a similar path. And he was doing it without a license! You can read all about it here.

Apparently, Steve sharing advice about diet – whether he offered it for free or charged for it – was a crime and they could take a him to court over it. After he made some changes to his website Steve was told he was in “substantial compliance” with North Carolina law and they closed the investigation. You can read more about that here.

While the North Carolina Board appears to be finished, Steve isn’t. Steve is launching a major battle for Internet freedom and free speech that could impact the millions of people that share advice online everyday, in places like blogs, Facebook, Twitter and Reddit. He’s joined the Institute for Justice in filing a lawsuit that challenges the government’s authority to censor ordinary advice and, as a memo I received from the Institute of Justice states, “seeks to answer one of the most important unresolved questions in First Amendment law: When does the government’s power to license occupations trump free speech?”

I helped Steve get started on his journey a few years ago and was proud of not only his progress, but the track he took in helping people, so it was astounding to hear that he could get shut down for offering his opinion about which foods to buy at the grocery store. Check out the Institute of Justice’s YouTube video (above), case launch page, and case backgrounder page. Needless to say, this is an important case, and one I will be following closely.

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