S1: In this episode of the Ben Greenfield Live podcast, we'll
S1: cold water blunt your exercise gains. Is intermittent fasting bad
S1: for you? Low EMF headphones and a whole lot more fitness, nutrition, biohacking, longevity,
S1: life optimization, spirituality, and a whole lot more. Welcome to
S1: the Ben Greenfield Life Show. Are you ready to hack
S1: your life? Let's do this. Well. Hello here I am,
S1: still picking shards of spiraling and cacao nibs out of
S1: my teeth after my usual morning smoothie. You know, I
S1: tried this Ninja Creamy for a while. A lot of
S1: people have been talking about this Ninja creamy ice cream
S1: maker I used for my first recipe. Some goat milk, uh,
S1: some vanilla stevia, the Keihan vanilla whey protein, and a
S1: little bit of cacao powder. Kind of like a chocolate
S1: vanilla ice cream. You freeze the base and then you
S1: take the container that the creamy comes with, and you
S1: put the base back onto the creamy, and it makes
S1: ice cream in like 90s or two minutes with surprisingly, um, uh,
S1: good texture, meaning it mimics the actual texture of ice
S1: cream pretty well. The cooler thing than that is that
S1: similar to cold Stone Creamery, you can dig a little
S1: hole in the ice cream after it's been made. Dump
S1: any toppings you want in there like I used, uh,
S1: some some of the who clean dark chocolate chips. Another
S1: time I use some of the Magic Spoon cereal, and
S1: it kind of gives you this textured ice cream. But
S1: I sent it back because I just found that the
S1: novelty wore off pretty quickly after I tried it about
S1: a month ago, and I didn't really like planning ahead
S1: 24 hours to make my ice cream. What can I say,
S1: I'm lazy, but for smoothie texture, I am still a
S1: huge fan of the Ninja blender because it somehow introduces air.
S1: The nature of the blender, the shape of it introduces
S1: air into the blender jar as you are blending, and
S1: it makes this thick, creamy, nearly fluffy texture that I
S1: find really filling. I think it has great mouthfeel, so
S1: if I had to choose a blender to use for
S1: smoothies because I'm often asked what blender I use, it's
S1: just the basic ninja blender. I think it's like 120
S1: bucks maybe on Amazon works pretty well. I'm curious what
S1: you guys have found though to be your blender of choice.
S1: Now it is important that the blender be large enough.
S1: My smoothies are massive. You know, we're talking like 32oz plus,
S1: so it's got to be a big blender jar. I'm
S1: also curious if anybody's tried this Ninja Creamy. You can
S1: go to the show notes at bengreenfieldlife.com slash 473. Leave
S1: your comments. Let me know. Favorite smoothie recipes? Favorite ice
S1: cream recipes? If you found a good alternative to the
S1: Ninja Creamy, anything like that, let me know. But we
S1: are not here to talk about smoothies till we're blue
S1: in the face. This is the chance for me to
S1: fill you in on all the latest, greatest news flashes.
S1: Occasionally I get to Q and A's. I don't know
S1: if I'll get to any Q and A's today. Uh,
S1: but nonetheless, we're actually here to talk about not eating.
S1: Not eating, but not eating. Uh, and this is because
S1: the internet seemed to break the other day when this
S1: brand new study, if you want to call it that,
S1: came out, indicating that intermittent fasting, which a lot of
S1: people do, it's all the trend. You know, somebody an
S1: intermittent faster when all they do is talk about their
S1: compressed feeding window. Anyways, the the idea here is that
S1: there is all these headlines that are suggesting intermittent fasting
S1: might raise your risk of heart disease. I'll link to
S1: the full paper in the show notes. But basically it's
S1: been drawing a lot of skepticism. What happened was the
S1: American Heart Association, the wonderful Aha, issued a news release,
S1: and it was headlined eight Hour Time Restricted eating linked
S1: to a 91% higher risk of cardiovascular death. That's scary.
S1: That's going to cause a lot of people to put
S1: giant bowls of almonds and dark chocolate and candy on
S1: their counter to make sure that they do not restrict eating,
S1: especially eight hour time restricted eating. All that means is
S1: maybe you start breakfast at 10 a.m. and you shut
S1: off the fire hose into your mouth at about 6 p.m.
S1: that's an eight hour compressed feeding window with typically a
S1: lot of that being an overnight intermittent fast. So they
S1: suggested it might pose risks to your heart or could
S1: lead to a higher risk of death. And that contradicts
S1: a lot of research that has come up before that,
S1: showing that time restricted eating or intermittent fasting could improve
S1: heart health factors like insulin sensitivity or inflammation or obesity
S1: or cholesterol levels. So the Aha news release said that
S1: those with heart disease or cancer saw an increased risk
S1: of cardiovascular death when it was mixed with intermittent fasting.
S1: And in people who have pre-existing heart disease, eating in
S1: a window that's no less than eight but less than
S1: ten hours per day was linked to a 66% higher
S1: risk of death from heart disease or stroke, and fasting
S1: did not reduce the risk of death from any cause. Wow.
S1: This is one of those things that confuses people. I think.
S1: You know, when I sit next to somebody on the airplane,
S1: you know, some sweet old grandma who's like, I.
S2: Just don't know who to trust these days or eggs.
S2: Good for you. Are they bad for you? Is coffee good?
S2: Is coffee bad? We just never know.
S1: You know, that's the issue is these headlines. I've talked
S1: about many similar headlines before. They confuse people because it's
S1: baby talk. It's all or nothing this or that, you know,
S1: bad or good. But here's what you need to know.
S1: First of all, the people who in this study group
S1: consumed all their food in a daily window of eight
S1: hours or fewer had the following a higher percentage of men,
S1: a higher percentage of smokers. A higher percentage of people
S1: with a higher BMI, a body mass index, and any
S1: of those alone could have raised the group's heart disease risk.
S1: They completely lacked data on shift work, on stress, and
S1: a lot of other variables that are confounding variables that
S1: were not adjusted for in this paper, if you want
S1: to call it that. Furthermore, correlation does not necessarily mean causation.
S1: So what I mean by that is just because there's
S1: a link between shorter eating windows and bad health outcomes
S1: in particular, doesn't mean the eating window caused the outcome. Right?
S1: So you could look at the at the, you know,
S1: correlation causation flaw with something like you're more likely to
S1: get bitten by a shark if you've eaten recently eaten
S1: ice cream. Right. And it would be easy to conclude
S1: that eating ice cream somehow leads to increased number of
S1: shark attacks, when in fact, eating ice cream occurs in
S1: warmer weather, during which more people are in the ocean swimming,
S1: thus more exposed to lovely sharks. So ice cream correlates
S1: with shark attacks but doesn't cause shark attacks, and this
S1: is very similar. The other issue is that the study
S1: data for this survey was done by the CDC between
S1: 2003 and 2018. Intermittent fasting wasn't even that popular then.
S1: Even the term was largely not even thrown around. Relatively unknown.
S1: This idea of intermittent fasting. This means that most people
S1: who were skipping meals prior to 2018 weren't necessarily trying
S1: to improve their health because they heard, I don't know,
S1: some podcaster talking about intermittent fasting or saw some documentary
S1: on compressed feeding windows. They were just ignoring what was
S1: the standard dietary guidance at that time. And that means
S1: they could have been far more likely to have poor
S1: eating habits and diets. These were just people who theoretically,
S1: may not have even really been paying that much attention
S1: to their diet and kind of accidentally intermittent fasting as
S1: a part of that. In addition, this study used just
S1: two days of self-reported eating activity to estimate 16 years
S1: of dietary habits and two days of dietary record data
S1: is not at all reflective of an individual's regular eating pattern.
S1: So it's quite sloppy science, really. Um, you know, the
S1: other thing that's important to know is that the people
S1: who restricted eating to eight hours or fewer per day
S1: also had less lean muscle mass than those with longer
S1: eating windows and less lean muscle mass has been linked
S1: to higher risk of cardiovascular mortality. So, long story short,
S1: is it was a highly flawed paper with a lot
S1: of confounding variables, particularly, I think the biggest elephant in
S1: the room here is the people who were intermittent. Fasting
S1: fell into categories like high BMI, poor access to high
S1: quality food, uh, lack of data, or adjusting for shift
S1: work or stress or other variables. Low muscle mass, you know,
S1: it's just a cluster of factors that dictates that if
S1: a compressed feeding window is something that works well for you,
S1: and intermittent fasting helps you stick to a healthy diet
S1: or stuff your face less then all the other more.
S1: Well conducted studies that have been done on intermittent fasting
S1: would indicate that it's going to be better for insulin sensitivity,
S1: for inflammation, for obesity, for cholesterol levels. Now, I do
S1: have to note one thing because I know many people
S1: might note this also. A lot of the benefits of
S1: intermittent fasting appear to be due to the calorie restriction.
S1: What I mean by that is if you take people
S1: eating an isocaloric diet, let's say 2000 calories a day
S1: and one group's eating in a compressed feeding window of
S1: eight hours, and the other group is eating ad libitum
S1: throughout the day whenever they want. At the end of
S1: the day, if the calories are equal, there's not a
S1: huge advantage of fasting. But the advantage of fasting is
S1: that it makes eating fewer calories more reasonable and doable,
S1: because there's simply less time that you've allotted yourself during
S1: the day to be able to snack and eat right.
S1: For example, people who follow an omad diet would be
S1: an extreme example of this, right? One meal a day,
S1: let's say. Let's say you're me, right? My metabolic rate
S1: is screaming high. I got to eat 3500 calories a
S1: day to even maintain weight and not lose weight pretty quickly. Well,
S1: if you tell me I have to eat all of
S1: that at dinner, it's going to be very difficult for
S1: me to shove 3500 calories down the hatch at dinner
S1: without having some pretty significant gut issues. So similar idea
S1: with intermittent fasting, right? If you're a lot of calorie
S1: count is, let's say, 2500 calories per day for weight
S1: maintenance or weight loss or something like that, it's far
S1: easier to reach that allotment or not overreach that allotment.
S1: More specifically, when you're only allowed to eat between like,
S1: I don't know, you know, 10 a.m. and 6 p.m.
S1: or 10 a.m. and 8 p.m.. So that's the idea.
S1: That's where the magic of fasting lies. But ultimately the
S1: biggest focus should be on restricting or at least modulating calories.
S1: Not necessarily fasting, but a fasting makes that easier for
S1: you to do, which it does for a lot of people.
S1: Then don't worry, it's not going to give you heart disease.
S1: So that's the first myth that I wanted to address.
S1: And I have another nutrition myth that's been circulating around
S1: the internet as well that I want to get to
S1: on today's show. So this one is about animal protein
S1: accelerating the atherosclerotic process, animal protein accelerating the atherosclerotic process.
S1: So I realize that's a mouthful. But this study was
S1: titled identification of a leucine mediated threshold effect governing macrophage
S1: mTOR signaling and Cardiovascular risk. Also a mouthful. So what
S1: they suggested was that a high intake of animal protein
S1: could potentially lead to atherosclerosis. So let's look into what
S1: they actually looked at in this particular study. So there
S1: was a rodent component and a human component. And what
S1: they claimed was that they found a protein mediated mechanism
S1: for arterial plaque development, and that it was largely, uh,
S1: an issue with the animal protein that caused the potential
S1: for atherosclerosis to occur. Now, the rodent component of this study,
S1: in which they were fed, animal protein, was divided into
S1: in vitro, which is cell culture, and in vivo, which
S1: is actually inside the animal or inside the rodent, not
S1: in the, you know, petri dish or a test tube.
S1: The in vitro study, right. The test tube study reported
S1: a dose response effect of protein on the reduction of
S1: autophagy in macrophages. And in this case, that would be
S1: a bad thing, right? You're you're not turning over these
S1: inflammatory components of white blood cells adequately. And that was
S1: interpreted as a potential pathway to atherosclerosis. And then they
S1: also did an in vivo trial. This was in the rodents.
S1: And they compared diets that were 7% protein, 21% protein
S1: and 42% protein. They found increased arterial plaque development in
S1: rodents on the 42% protein diet and then in the humans.
S1: And this is super important. I'll get to this in
S1: a second. Humans are not large rodents. Oh, there's a
S1: few politicians and lawyers out there who might fit into
S1: that category, but for the most part, humans are not
S1: large rodents. But what they did was they used strictly
S1: in vitro studies in the human components. They didn't actually
S1: feed humans protein. They took white blood cells in a
S1: petri dish, human white blood cells in a petri dish.
S1: They didn't even look at plaque formation. Basically what they
S1: did was they looked at the effects of a liquid
S1: and a solid food meal, made up of about 450
S1: to 500 calories. And one of the meals was a
S1: higher protein dose when they examined the effects of the
S1: higher protein on the white blood cells in a petri dish,
S1: it resulted in greater activation of what's called monocyte mTORC1, okay.
S1: And these monocytes have the potential to manifest into atherosclerotic plaque.
S1: So they said basically, if we give white blood cells
S1: in a petri dish, more animal based protein, they seem
S1: to turn into something that could potentially in a human cause,
S1: the formation of atherosclerotic plaque. That's it. And then, of course,
S1: all the headlines. I'll read one headline from the New
S1: York Post. This headline from the New York Post says,
S1: you might be eating an artery damaging amount of protein
S1: for breakfast. New study warns. And then the subtitle is
S1: Study discovers molecular mechanism. That could explain why eating too
S1: much protein is bad for your arteries. The paper authors
S1: even said that they found the so-called smoking gun, which
S1: is that these monocytes and macrophages in mice and humans
S1: both experience this issue with escalating doses of leucine from
S1: animal based protein. So anyways, I don't know about the
S1: funding of this study or anything like that. If there was,
S1: you know, plant based protein play or any, any potential influences.
S1: But here's what's important to know. First of all, the
S1: metabolizing of branched chain amino acids, particularly leucine, is way
S1: different in humans versus rodents. So humans and rodents, in
S1: this case rats, they have vastly different distributions of what's
S1: called branched chain amino acid aminotransferase. Realize that's also a mouthful.
S1: But Bcat bcat is an enzyme that catalyzes the breakdown
S1: of these branched chain amino acids that they were using
S1: in the study. Now, this occurs in humans, primarily in
S1: skeletal muscle, and the catabolism of the other essential amino
S1: acids usually occurs in the liver. Now, the bcat activity
S1: in the liver and the muscle of humans and rats
S1: is very different. Rodents have extremely high bcat activity in
S1: their muscle, but very little in the liver. And in
S1: addition to that, they have a much, much higher branched
S1: chain amino acid oxidative capacity in humans. Therefore, it's automatically
S1: false to presume that leucine or protein in general in
S1: rodents is generalizable to humans. And in addition to these
S1: differences in protein and amino acid metabolism, this is important
S1: for you to understand. Any time someone's talking about a
S1: rodent study, you need to understand this stuff. So, for example,
S1: de novo lipogenesis, that's the conversion of carbohydrates to fatty
S1: acids for storage as triglycerides. That contributes to about 60
S1: to 70% of triglycerides in rodents, only about 5% or
S1: less in humans, which means that we can't even extrapolate
S1: carbohydrate and fat research in rodents to humans. In addition
S1: to that, the liver receptors, the so-called lcrs, the liver
S1: X receptors located in liver cells, have way different signaling
S1: activity in response to stimuli from amino acids in rats
S1: versus humans. And that's important because these liver X receptors
S1: are key regulators of genes involved with glucose and fat
S1: metabolizing and homeostasis. So a huge difference in carb and
S1: fat metabolism in rodents. So any, you know, low carb
S1: versus high carb, ketogenic versus non keto, high protein, low
S1: protein studies in rodents versus humans give us almost nothing
S1: that we can extrapolate to humans, especially nothing that can
S1: tell us with a nail in the coffin type of
S1: statement that something like a high protein diet causes cancer,
S1: or that a high amount of animal protein would cause atherosclerosis. Now,
S1: I would say the most significant challenge to the findings
S1: of this paper is the large existing body of human research,
S1: including human in vivo research, not test tube or petri
S1: dish research comparing high protein to low protein diets. For example,
S1: one very recent systematic review and meta analysis of prospective
S1: cohort studies that's a very well conducted body of research,
S1: found that high protein intake in humans is not associated
S1: with increased risk of stroke, increased risk of myocardial infarction,
S1: increased cardiovascular death. Another meta analysis showed that higher protein
S1: diets showed superior benefits for weight loss, for fat loss,
S1: for blood pressure reduction, for lipid profile, for insulin levels.
S1: And the the thing that you must understand here is
S1: that probably a big reason for that is, and this
S1: is related to the recent discussion I had with Doctor
S1: Gabriel Lyons, the muscle centric medicine doctor, that higher protein
S1: intake allows you to maintain or build more muscle, which
S1: has a host of metabolically protective effects. I would hate
S1: for people to read this paper, especially people at risk
S1: for a metabolic issue such as heart disease, and say,
S1: I'm going to eat less protein because protein is going
S1: to give me heart disease. Does the source matter? Absolutely. Right.
S1: A burger, even if you, I don't know, take the
S1: buns off and skip the French fries at McDonald's, is
S1: going to be full of a lot more potential heart
S1: disease risk factors than, say, like a grass fed, grass
S1: finished steak that you might have at home, a whey
S1: protein smoothie that you make at home, and your magical
S1: ninja blender could be far different than some type of sugary,
S1: artificial sweetener infused smoothie that you get from the gym
S1: as you're walking out the door, right? So the source matters.
S1: But ultimately very similar to the intermittent fasting study, you
S1: got to take these things with a grain of salt,
S1: or in this case, a grain of leucine. And I
S1: would not. Say that based on this, despite all the
S1: newspapers reporting that your high intake of animal protein is
S1: going to give you, heart disease tells us anything besides,
S1: rats that are fed a 40 plus percent protein diet
S1: seemed to indicate activation of macrophages that you could theoretically
S1: say would contribute to plaque formation, but the plaque formation
S1: was never actually shown. So there you have it. It's
S1: kind of odd when when I see reports like this,
S1: it's just it's just a head scratcher. So anyways, here's
S1: something that I'm asked a lot about that I definitely
S1: wanted to address. If I get in cold water after
S1: I work out, is it going to blunt my gains? Bro,
S1: this is something that's gone back and forth in research
S1: for a while. It's caused a lot of people to say,
S1: skip the cold shower, skip the cryotherapy, skip the cold
S1: water immersion post workout because it's going to destroy all
S1: that hard work that you did in the gym. So
S1: a brand new, pretty well constructed paper came out called
S1: cold water immersion reduces muscle growth during resistance training. As
S1: you can imagine, that automatically sounds pretty scary. Hey, I'm
S1: reducing muscle growth after I've lifted weights. If I get
S1: into cold water. Let's take a look at what this
S1: actually was, what it said, and what the history of
S1: cold water immersion actually looks like. So this is a
S1: meta analysis of randomized controlled studies on cold therapy. They
S1: reported that cold water immersion after resistance exercise reduced gains
S1: in muscle size compared to resistance training without the cold
S1: water immersion afterwards, though, the effects, admittedly, and even the
S1: paper acknowledges this appeared very small in magnitude, meaning we
S1: might only be really speaking here to like bodybuilders who
S1: are trying to get every last fiber of muscle on
S1: their body, who would even care about this. But anyways,
S1: what they did was they did a meta analysis of
S1: eight randomized controlled studies on cold water immersion. The studies
S1: were all about 4 to 12 weeks in duration. Folks
S1: were lifting weights 2 to 3 times per week. Uh,
S1: one study was using wrist flexor training. I don't know
S1: if I count that as weight training. Another study, a
S1: couple of studies using hand grip training. I don't know
S1: if I count that as weight training either. Three studies
S1: used low body training only, and two studies used a
S1: full body training program, which I think is the most
S1: appropriate approach when we're looking at something like this. Then
S1: all the studies used post-exercise cold water immersion. Okay, three
S1: studies exposed just the upper limbs, two studies exposed the
S1: lower limbs, and three studies used whole body cold water immersion.
S1: Here's what's important to note. These folks were in the
S1: cold water for 10 to 20 minutes, anywhere from 50
S1: to 59°F. Anybody who's jumped into 50 to 59°F water for,
S1: let's say, 15 minutes, let's cut it in the middle
S1: knows that in most cases, unless you're like an Inuit
S1: or a experienced Wim Hof practitioner or something like that,
S1: your teeth are chattering and you're shivering and you're kind
S1: of goosebumpy for hours afterwards. That's a drop in muscle
S1: core temperature that's likely getting close to one degree Celsius, which,
S1: it is true, could impair the natural inflammatory response to
S1: exercise and cause a lack of what would be called
S1: satellite cell proliferation, or an increase in muscle fiber size
S1: or even number in response to resistance training. Folks, this
S1: is way different than you finishing a weight training session
S1: and flipping the cold water on for a minute or
S1: two at the gym, or even jumping in your cold
S1: plunge for 30s because it makes you feel fantastic and
S1: gives you lots of energy after your workout, and keeps
S1: you from pitting out and sweating at work later on. Right?
S1: There's a big, big difference here. The dose is important. Okay,
S1: so understand that the studies and nearly every study that
S1: has looked at cold water immersion and any impairment in exercise,
S1: using 10 to 20 minutes, resulting in a significant drop
S1: in muscle core temperature. Big difference between that and a
S1: cold water, a cold soak, a quick, uh, jump into
S1: a cold plunge, which I do after almost every workout.
S1: So here's what what else is important to know? We
S1: need to talk about what we're analyzing here when it
S1: comes to the effects of cold water, because the effects
S1: go beyond just muscle size and muscle hypertrophy. So traditionally,
S1: cold water immersion has been used as a tool to
S1: help athletes enhance their recovery from exercise and improve their
S1: performance in subsequent exercise sessions or games or competitions or workouts. Now,
S1: cold water immersion has been shown to improve exercise recovery significantly.
S1: For example, there's a few mechanisms why this happens. Cold
S1: water immersion reduces central nervous system fatigue by reducing your
S1: core body temperature and enhancing blood flow and oxygenation, particularly
S1: blood flow, to the brain. That's why it can have
S1: a little bit of a stress reduction response as well,
S1: and make you feel a little bit sharper cognitively the
S1: rest of the day. Cold water immersion reduces cardiovascular strain
S1: when your body temperature goes up. Blood flow. Gets redirected
S1: from your muscles and your core to your skin. That's
S1: how it dissipates heat. Now this reduces blood flow and
S1: oxygen delivery to muscles. It increases heart rate, and it
S1: can impair performance. Cold water immersion redirects the blood flow
S1: to central circulation, because the skin needs less blood to
S1: go out to it to facilitate cooling. That's another way
S1: that it can help with recovery. Cold water can also
S1: result in increased clearance of metabolites that build up during
S1: exercise like lactic acid, potassium, chloride, calcium. A lot of
S1: these things that could contribute to post-exercise soreness or a
S1: little bit of post-exercise swelling or sluggishness, and then finally,
S1: cold water immersion can improve your autonomic nervous system recovery,
S1: not your central nervous system, but your autonomic nervous system.
S1: By inhibiting the sympathetic fight or flight response and activating
S1: the parasympathetic rest or digest or relax response. Anybody who's
S1: gotten into a cold plunge thinks, gosh, I feel like
S1: fighting or fighting the whole time I'm in there. But
S1: when you get out, there is a parasympathetic rebound that
S1: results in you feeling more relaxed later on, which is
S1: why cold water can again be very helpful for something
S1: like stress management. So when they've actually looked at and
S1: then there's been looked at many times cold water immersion post-exercise,
S1: they've found decreased perceived pain after the workout, reduction in
S1: markers of exercise induced muscle damage, a lowered amount of
S1: delayed onset muscle soreness, Doms, lower amount of inflammation, lower
S1: amount of swelling. When we look at endurance. Enhanced endurance
S1: recovery from endurance exercise by reducing cardiovascular and thermal strain,
S1: and lowering levels of perceived soreness, meaning you could actually
S1: have a better workout the next day. Uh, there was
S1: one meta analysis that showed that cold water immersion reduced
S1: delayed onset muscle soreness, reduced ratings of perceived exertion, and
S1: even improved jumping capacity after exercise will decreasing levels of
S1: creatine kinase and lactate 24 to 48 hours after exercise. Now,
S1: there have been some studies that suggest it's not all
S1: rosy when it comes to cold thermogenesis. Post-exercise. For example,
S1: I just named how very long 10 to 20 minutes
S1: of cold post-exercise could inhibit your ability to be able
S1: to gain muscle. Uh, they've also shown that there is
S1: a reduction in muscle power for about 1 to 6
S1: hours after you've done cold water exercise and many studies. Uh,
S1: and they've even compared like a trained limb that is
S1: immersed in cold water post-exercise and a trained limb that
S1: is not immersed in post in water post exercise and
S1: found that the muscle or the limb that's immersed in
S1: cold water has an inhibition in muscle strength. And again,
S1: these are very long immersion periods. We're talking 10 to
S1: 20 minutes. So, uh, what you need to know here
S1: is that if you have a major goal of muscle growth,
S1: hypertrophy i.e. you're trying to get swole, bro, put on
S1: as much size as possible. Don't go get cold for
S1: 10 to 20 minutes after you've worked out. But if
S1: you want to recover faster, feel better, have less stress,
S1: have reduced soreness, potentially increase endurance or even your ability
S1: to perform in the next day's workout or a workout
S1: later on that day. The benefits of cold, particularly briefer
S1: forays into the cold. Again, you know, I my maximum
S1: might be five minutes, you guys maximum. I'm usually in
S1: there for 30s to about two minutes. The drop in
S1: muscle core temperature that occurs with that brief amount of
S1: cold exposure in no way is going to cause these
S1: issues that so many people are talking about when they're
S1: telling you to avoid cold after workout. So that's what's
S1: going on with cold. And as I will do with
S1: all of these studies that I talk about, I'll link
S1: to this in the show notes. If you go to
S1: Bengreenfieldlife.com slash 473. But don't freak out too much about cold,
S1: it's good for you. I think the pros outweigh the cons,
S1: but what is not good for you? Well, that leads
S1: me to the next thing that I wanted to cover.
S1: I've been rewriting my entire book. Boundless. It's going to
S1: come out in January. Boundless 2.0. It's. It's like the
S1: Bible of biohacking. Fully updated. It's going to be fantastic. Uh,
S1: boundless Book.com is where you can check out the old
S1: version as soon as the new version launches, it'll be
S1: available there. But as a part of chapter 20, in
S1: that book, I revisited the idea of air, light, water
S1: and related to this discussion, electricity. And I found some
S1: some very interesting things when it comes to exposure to
S1: radio frequency radiation and 5G. So the first thing, and
S1: this goes way back, I don't know why more people
S1: aren't talking about this way. Back to 2009. Title of
S1: this paper is Increased Blood Brain Barrier Permeability in Mammalian
S1: brains seven days after exposure to the radiation from a.
S1: GSM 900 mobile phone, very similar to the iPhone that
S1: many of us are holding up to our ears, but
S1: way weaker than, say, like a virtual headset like the
S1: Apple Vision Pro, which is subjecting your brain to much
S1: higher amounts, sometimes 4 to 6 more, some 4 to
S1: 6 times more electromagnetic radiation than a cell phone might.
S1: So this study found significant increase in blood brain barrier permeability.
S1: I write about this in chapter two of boundless, this
S1: idea that you can have a leaky, gut permeable gut
S1: lining that allows toxins, compounds, etc. to wind up in
S1: the bloodstream that are supposed to be in the gut very,
S1: very similar with the blood brain barrier. Right? A permeable
S1: leaky blood brain barrier can result in significant neuronal damage.
S1: And this study showed neuronal damage for up to 50 days.
S1: After two hours of radio frequencies from mobile phone exposure
S1: held up next to the head. And this this just
S1: doesn't get talked about. I suspect it's quite inconvenient thing
S1: for phone companies to talk about. It's why I never
S1: hold my phone up to my head, why I use
S1: wired headsets, and why I'm very careful with any type
S1: of electronics, including especially virtual reality headsets around my head.
S1: But it goes on because 5G is obviously something that's
S1: been getting rolled out. And I recently came across a
S1: report that was submitted to the Australian government. So what
S1: happened was in September 2019, uh, in Australia, the Minister
S1: for communications asked a committee to complete and, uh, inquire
S1: into the deployment, adoption and application of 5G in Australia. Now,
S1: I'll link to a document. I recently tweeted this same
S1: document out that was submitted by a guy named Paul Barrett.
S1: He's not a doctor. He's not like a researcher. He's
S1: not a government official. But he did submit a document
S1: chock full of some concerning information about 5G. I'll read
S1: you a little part of this paper says 5G is
S1: dangerous and will harm every living being. Thousands of studies
S1: link low level wireless radio frequency radiation exposures to a
S1: long list of adverse biological effects, including DNA, single and
S1: double strand breaks, oxidative damage, disruption of cellular metabolism, increased
S1: blood brain barrier permeability. What I just got done talking
S1: about melatonin reduction, disruption to brain glucose metabolism, generation of
S1: stress proteins. And let's not also forget that in 2011,
S1: the World Health Organization, the W.H.O., classified radio frequency radiation
S1: as a possible to be carcinogen. Now, more recently, the
S1: $25 million National Toxicology Program concluded that radio frequency radiation
S1: of the type currently used by cell phones can cause cancer.
S1: And it goes on to talk about 5G. So where
S1: does 5G fit into all this? Given that 5G is
S1: set to utilize frequencies both above and below the existing
S1: frequency bands? It sits in the middle of all of this,
S1: but the tendency is for 5G to utilize higher frequency bands,
S1: which brings up specific concerns, namely for eye damage, reduced
S1: immune function, influence on the heart rate variability, and potential
S1: for heart arrhythmias. Increased risk of antibiotic resistant pathogens depress
S1: cell growth rates. Necrosis, particularly has been noted in plants,
S1: meaning that plant foods might become more unsuitable for human consumption,
S1: atmospheric effects, potential for fossil fuel depletion, ecosystem disruption, and
S1: the misleading 5G study results. Can also be related to
S1: the fact that most do not pulse the waves. For example,
S1: research on microwaves shows that pulse waves have more profound
S1: biological effects on the body compared to non pulse waves,
S1: because pulse rates of the frequencies lead to gene toxicity
S1: and DNA strand breaks. And a lot of these 5G signals,
S1: even though they're not pulsed and studies are pulsed when
S1: you're actually exposed to them on your phone, and from
S1: a lot of these towers that are being installed. So
S1: when when you step back and look at 5G, I
S1: think it is something that we need to be concerned about.
S1: But at the same time, and I write about this
S1: in boundless, I give a bunch of tips about what
S1: you can do about it. Because I'm not a Luddite.
S1: I'm not gonna go live with the Amish. I'm not
S1: going to throw out my phone and get one of
S1: those stupid phones, because I like my social media apps,
S1: and I like the ability to be able to ask
S1: Siri or ChatGPT something. It's convenient, but you do need
S1: to be careful. So, for example, uh, I have this
S1: little where is it? I can hold it up for
S1: the camera. It's under my desk. Let me find it here.
S1: I have this little thing underneath my desk, and it
S1: looks like this. If you're watching the video version. Okay.
S1: My phone is hardwired via an Ethernet cable. This is
S1: a USB-C adapter, an Ethernet cable. It's even got a
S1: power adapter on it. So the whole time I'm using
S1: my phone in my office, it's hardwired. Same as my laptop,
S1: same as my computer. Everything's hardwired, so I don't have
S1: to use wireless in my office. A lot of my clients.
S1: They have a digital wall timer. You get a digital
S1: wall timer on Amazon. It's dirt cheap. You plug your
S1: Wi-Fi router into that digital wall timer, which then plugs
S1: into an outlet, and you can set it to automatically
S1: turn your Wi-Fi router off while you're asleep, and then
S1: automatically on when you wake up like you could set
S1: it to do like a 10 p.m. to 5:30 a.m.
S1: sleep wake cycle. This is interesting for anyone who wants
S1: a done for you. Complete bio hacked home. I am
S1: selling my entire tricked out house located on eight and
S1: a half acres of forested land in Spokane, Washington. It
S1: includes a guesthouse, pool house, barn, whole setup for garden goats, chickens, herbs,
S1: fire pit along with a ton of biohacking goodies. The air,
S1: the light, the water, the electricity is all completely tricked
S1: out for optimized human biology. The highest quality air filtration systems,
S1: natural lighting friendly to circadian rhythms, low EMF dirty electricity filters,
S1: EMF blocking equipment throughout. Built to be off grid when
S1: necessary with buried propane and solar grid toxin free and
S1: low VOC construction materials. The most advanced water filtration systems
S1: one can find a massive vegetable garden, greenhouse, herb garden,
S1: outdoor fire pit, goat and chicken grazing pasture and barn
S1: all in a beautiful forest that's about 25 minutes from
S1: the airport and 20 minutes from downtown. This can all
S1: be yours if you're looking for a place to get
S1: away in a safe, natural area and you're looking for
S1: the best of the best biohacks done for you, here's
S1: where you can go to check it out and to
S1: fill out a form with your interest. Bio hacked Spokane home.com.
S1: That's bio hacked. Spokane home.com. Check it out. The number
S1: one place to protect yourself is your bedroom. That's where
S1: your nervous system gets a chance to repair and recover
S1: the entire night while you're asleep. And so you can
S1: walk through your bedroom and get rid of smart appliances,
S1: most of which do not have the ability to disable Wi-Fi.
S1: Like a smart TV, you can unplug things that you
S1: aren't using in the bedroom during the night of sleep.
S1: You can even install dirty electricity filters in the bedroom,
S1: such as greenwave or stetzer or shielded healing. They all
S1: make these dirty electricity filters that reduce the amount of
S1: AC power surges that occur in a room that you
S1: might be sleeping or working in, and you can go
S1: through your entire house and just start to ask yourself,
S1: how many signals am I getting exposed to? Because there's
S1: no biological free pass, folks. How many signals am I
S1: getting exposed to that I don't need to be getting
S1: exposed to? Are you listening to my podcast right now?
S1: We'll take a look at your phone. If it's on.
S1: Why is it on? Are you expecting a call? Are
S1: you texting? Do you need it on? If not, put
S1: it in airplane mode if you need it on. Is
S1: the Wi-Fi disabled? Is the Bluetooth disabled? If not, disable it.
S1: If the Bluetooth is on because you're wearing Bluetooth enabled headphones,
S1: ask yourself why you couldn't just go old school and wire, right?
S1: So I've got a lot more tips in this upcoming
S1: version of boundless, but the last thing I want to
S1: note is a lot of people like, well, Ben, you're
S1: wearing headphones right now while you're recording this. If you're
S1: watching the video, I'm wearing headphones. Even my headphone choice
S1: is pretty specific and intentional. Like right now I'm wearing
S1: Ultrasone headphones for recording this podcast. So the only high quality,
S1: high fidelity set of overear headphones that I could find
S1: that have low EMF. They use what's called ultra low
S1: emission technology, UL technology, to reduce electromagnetic radiation emitted by
S1: the drivers in the headphones. So there's a metal shield
S1: that creates a buffer between the headphone capsule and the
S1: air volume at the ear. And they suggest that this
S1: can reduce magnetic radiation by up to 98% compared to
S1: standard headphones. These are called the Ultra Zone headphones. They're
S1: a little bit more expensive, like, you know, they're like 400,
S1: 500 bucks on Amazon, which for a pair of overear
S1: wired headphones is, in my opinion, pretty spendy. But because
S1: I'm wearing them a lot, you know, things that I
S1: use a lot, I'm pretty intentional about making sure that
S1: I'm not constantly bombarding my body with a lot of
S1: these emfs, including 5G. I'm going to link to a
S1: paper called ten New Studies Detail the Health Risks of 5G.
S1: This is written by somebody who catches a lot of flack.
S1: Doctor Joe Mercola A lot of people think he's a quack.
S1: I think in many cases he's ahead of his time.
S1: He wrote a great book called Emft. I've been to
S1: his house. The guy practices what he preaches. The whole
S1: place is like a dark, safe, quiet cave because he's
S1: cut off so many sources of EMF, similar to what
S1: I'm doing in the new home that I'm building in Idaho,
S1: in the home here in Washington state that I have now.
S1: But basically, you must understand that as inconvenient as these
S1: truths are you. Do need to be aware of the
S1: issues with EMF and do what you can to mitigate exposure. Finally,
S1: I want to throw in there that there are certain
S1: things you can take, like in your body, to help
S1: protect you against the free radicals that are produced in
S1: response to radiation. Uh, for example, molecular hydrogen, like hydrogen tablets,
S1: it's a selective antioxidant that can assist with the radiation
S1: from radio frequency and device exposure. Another would be to
S1: raise your levels of Nerf two. So Nerf two. You
S1: can think about it this way. It's called nuclear factor
S1: erythroid two. Related factor two. It activates the transcription over
S1: 500 genes in the human genome, including many detoxification mechanisms
S1: and a lot of things related to cytoprotection. Now, I
S1: realize that sounds pretty scientific, but the way that you
S1: increase it is pretty easy to wrap your head around
S1: if you're eating a lot of sulfur based compounds, including
S1: molecular hydrogen, by the way, which activates Nerf two very,
S1: very well. But a lot of sulfur based compounds, cruciferous vegetables,
S1: foods high in antioxidants. Uh, you know, garlic, onions, uh,
S1: sprouts are incredible. Like broccoli sprouts, broccoli, cauliflower, cabbage. Any
S1: of these are fantastic for helping boost Nerf two, which
S1: can specifically help you deal with radiation. Then the last
S1: thing I would consider, in addition to molecular hydrogen, sulfur
S1: based compounds and antioxidants, would be the use of magnesium.
S1: Because magnesium can offset a lot of the calcium influx
S1: that occurs into the cell in response to radiofrequency radiation.
S1: So obviously a lot of other things that you could do,
S1: but you could you could start there with magnesium, with
S1: high intake of sulfur based compounds and antioxidants, and then
S1: the use of molecular hydrogen, which I go through a
S1: lot of, for example, when I'm flying on an airplane, right,
S1: I always have antioxidants, I always have magnesium, and I
S1: always have molecular hydrogen. And I throw a fourth in
S1: there that's actually pretty protective and also activates the nerve
S1: two pathway ketones, drinkable ketones when I'm flying. So a
S1: few things to think about. I don't want to scare
S1: you with the tin foil hat, but I'm just saying
S1: you need to be aware of this and understand that
S1: despite them being convenient, the use of wireless devices is
S1: not without risks. Say the same for things like smart appliances. Okay,
S1: I want to get into a few kind of, kind of,
S1: I suppose, funny things. Now, you know, back to the
S1: whole idea of these studies. The power of belief and
S1: placebo is something that I recently became even more aware
S1: of when I came across two new studies that came
S1: out okay. The first was a milkshake milkshake deception study.
S1: This is really interesting. It looked at the effect of
S1: perceived nutritional content of foods on the actual cardiovascular response
S1: to the food intake, meaning this was a randomized controlled
S1: trial in young women. And they found that drinking a
S1: milkshake worsened a marker of vascular function shortly after consumption
S1: of that milkshake. But this effect did not occur if
S1: participants were led to believe that the milkshake was low
S1: in calories, low in fat, and low in sugar. So
S1: what actually happened was they had participants assigned to consume
S1: one of the following three beverages a regular milkshake, right,
S1: 540 calorie milkshake with 80g of sugar, 14g of fat.
S1: Pretty crappy milkshake for you, if you ask me. Then
S1: they had a sham milkshake. Okay, this was identical in
S1: nutritional composition and calories and fat and carbs and sugar
S1: to the regular milkshake. But in this case, they were
S1: told the participants were told that this milkshake only had
S1: 100 calories, three grams of sugar, four grams of fat,
S1: and ten grams of protein. Those dirty, dirty, lying researchers.
S1: But you're allowed to do this ethically in research. And
S1: then they had a third condition that was just basically
S1: a giant glass of water. Right. And then what they
S1: did was they assessed these outcomes, these blood markers, for
S1: up to 90 minutes after the consumption of each milkshake.
S1: And they had to consume each beverage on different days,
S1: separated by at least 48 hours within an eight day period,
S1: so they could assess how different people responded to either
S1: the milkshake, the sham milkshake, or the water. Now, after
S1: drinking the regular milkshake, what's called a flow mediated dilation,
S1: which is a marker of vascular function, even though they
S1: also measured glucose, insulin, triglycerides, cortisol and inflammatory marker called
S1: TNF alpha, the flow mediated dilation seemed to respond the
S1: most significantly to this, meaning that it worsened significantly when
S1: people drank the milkshake that they knew was bad for them,
S1: versus when people drank the same milkshake, but were told
S1: that it, of course, wasn't bad for them because it
S1: was way lower in calories and way lower in sugars, etc..
S1: So what's the practical takeaway from this? Well, first of all,
S1: how much you know about the harmful effects of a
S1: food that you might be eating could actually influence the
S1: deleterious response to that food. This is why if I'm
S1: going out to a fancy restaurant, I sometimes don't ask
S1: what oil was this cooked in? That's partially because I
S1: just don't want people spitting in my food or, you know,
S1: doing something nasty to my food back in the kitchen
S1: because I'm that person. But I don't ask, you know,
S1: what the alcohol, how much sugar in this? Or do
S1: you use canola oil versus olive oil? I don't always
S1: do that because just knowing can cause it to be
S1: worse for you. And frankly, sometimes you just want to
S1: go out and enjoy a meal at the restaurant and
S1: not worry. And this could probably work. I'm guessing I'll
S1: be shocked if it didn't work in reverse. Meaning if
S1: you are making healthy choices and you know those choices
S1: are healthier, even if a meal isn't perfect, you knowing that,
S1: say you chose the skinny option on the margarita, or
S1: you had the milkshake that didn't have quite as much
S1: peanut butter in it, or anything like that could actually
S1: result in you having a less deleterious response to consuming
S1: that particular food or compound. I thought it was very,
S1: very interesting how what you tell someone about the food
S1: that they're eating, whether it's harmful for you or not
S1: harmful for you, actually dictates how harmful it can actually be.
S1: The placebo effect is crazy, isn't it? So the other
S1: one was caffeine ingestion. This was similar. They took recreationally
S1: trained males in long distance running, and then they had
S1: them do a six minute time trial run test. Now
S1: in one they gave them a placebo and they told
S1: them that placebo was caffeine and the other they gave
S1: them the identical placebo. But they didn't tell them that
S1: placebo was caffeinated. You probably can guess where I'm going
S1: with this. The group that got the placebo but that
S1: were told the placebo. Again, those dirty lying researchers, these
S1: participants were told that that placebo contained caffeine. They had
S1: much better six minute time trial running performance. And and
S1: this was simply not because they got caffeine, but they
S1: believed that caffeine ingestion could improve running performance around maximal
S1: aerobic speed. And so even though they didn't have caffeine
S1: in their system, the mere fact that they thought they
S1: did made them faster. So does this mean that before
S1: your child competes in their next soccer or basketball game
S1: or track meet, you should give them a glass of
S1: water and tell them that it contains magical nutrients that
S1: are going to make them faster. I don't endorse lying. Um,
S1: but some of these, some of these mind control tricks
S1: are pretty interesting. You could say when your child sits
S1: down to the dinner table and turns their nose up
S1: at the vegetables, hey, those vegetables are going to help
S1: you perform amazingly in tomorrow's Jiu-Jitsu competition, or in tomorrow
S1: morning's basketball practice, or in your track and field meet
S1: tomorrow afternoon, or your tennis match or whatever. Because technically
S1: that's not lying. It is true. But making your child
S1: or yourself or anyone you know, aware of those truths
S1: and aware of the benefits of what they're consuming, could
S1: make those benefits be even more magnified. That's my takeaway
S1: from from the from studies like this that just imply
S1: the power of the placebo effect. So there you have
S1: it caffeine and milkshakes. All right. Last thing I want
S1: to talk with you about today was a cool study
S1: on enhancing memory in people who are cognitively impaired. So
S1: this was a randomized, double blind, placebo controlled trial conducted
S1: on people who had cognitive impairment to see if they
S1: could somehow improve memory. Now, in this case, what they
S1: did was they gave these people spirulina, they gave them spirulina.
S1: And this was based on the idea that spirulina can
S1: increase mitochondrial membrane potential, can decrease reactive oxygen species build up.
S1: It's something that I've recommended in the past on my podcast.
S1: People consume if they've had a lot of vegetable oil
S1: or a lot of oxidation in their system. Spirulina is
S1: fantastic for that. It can help to scavenge mitochondrial reactive
S1: oxygen species known to cause aging due to protein damage
S1: in cell walls as well as in the mitochondria. And
S1: the memory improvement of spirulina has been reported to be
S1: related to the antioxidant action caused by chlorophyll. I think
S1: it's even more powerful. You combine the chlorophyll in your
S1: bloodstream with red light, but basically when they did this study,
S1: they fed people chlorophyll for 12 weeks and found a
S1: significant improvement in memory. And again, this was a randomized,
S1: double blind, placebo controlled trial on spirulina. So I have
S1: been a spirulina fan for some time. I had it
S1: in my smoothie this morning. I go back and forth
S1: between the blue stuff and the green stuff. But the photo,
S1: CNN's the Chlorella, all of these reactive oxygen species colors
S1: and spirulina dictates that. I think it's actually a pretty
S1: cool thing to have around. And my favorite recipe right now,
S1: I think I talked about in the last podcast, was
S1: to take this blue spirulina. I get it from this
S1: company called a Royal Spirulina. You put a scoop of
S1: that in with a giant scoop of the Keihan Vanilla
S1: whey protein, a little stevia, a little coconut water, a
S1: little salt, and then you mix that up to an
S1: ice cream like texture, and you top it with cacao
S1: nibs and some coconut flakes and any other goodies that
S1: you want on top. And it's incredible. And this company, spirulina,
S1: royal spirulina, they make spirulina pasta, they make spirulina snacks.
S1: They have this blue spirulina. That's fantastic. And this is
S1: really interesting because if you look at it at a
S1: truly alive blue green algae, uh, under a microscope, you
S1: can see the spirulina cells moving. If your kid or
S1: you have a microscope at home, you can do this.
S1: If you get this royal spirulina, I'll put a link
S1: in the show notes. If you go to Bengreenfieldlife.com slash 473,
S1: you can see these little spirulina cells moving around like
S1: they're dancing. Now, if spirulina is frozen or powdered or processed,
S1: it's not alive. It doesn't have that same energy. But
S1: if you look at this royal spiraling, it's a new
S1: find of mine. I'm obsessed with them right now. What
S1: they do is they take this spirulina, they harvest it,
S1: they keep it alive. And it's this extremely rich source
S1: of bioavailable nutrients like B vitamins and minerals, uh, fatty acids.
S1: It's got all the fatty acids in there, like gamma
S1: linoleic acid and alpha linolenic acid and linoleic acid and
S1: serotonergic acid and EPA and DHA and arachidonic acid. The
S1: lipid content is like 8% in spirulina. So it's a
S1: healthy source of fats. The fact that it's so good
S1: for cognition, for sopping up the effects of, say, like
S1: toxins or vegetable oils and the fact that this stuff
S1: is alive, it's pure and alive, and it just tastes fantastic.
S1: So I had to give him a shout out in
S1: today's podcast because I've been going through. Bags and bags
S1: of this stuff. It's not inexpensive. I think of bags
S1: like north of 100 bucks. Uh, but it is incredible.
S1: And if you get the blue stuff, the blue stuff
S1: is super high in antioxidants. And this phycocyanin, which if
S1: you're a fan of red light therapy, can interact with
S1: photons of red light to increase mitochondrial production of ATP.
S1: So spirulina is cool stuff. It's a new find of mine.
S1: And when I saw this research study come up last
S1: week on the effects on memory improvement, I thought, gosh, well,
S1: that's that's another thing to chalk up to spirulina. And
S1: I recommend if you don't yet use it, uh, in
S1: your nutrition. I wouldn't cook with it. You don't want
S1: to degrade it. But, uh, if you put it in
S1: smoothies and stuff like that, it's incredible. So anyways, that
S1: covers just about everything that I wanted to talk with
S1: you about in today's Solusod Q&A. Um, I hope you
S1: enjoy these. I hope they're not too fringe or out there.
S1: I'm telling you to turn off your cell phone if
S1: you're not using the signal, but hopefully this information is
S1: helpful for you and improves your life in some way.
S1: If so, leave me a rating. Wherever you're listening to
S1: this show, uh, go over to the comment section at
S1: bengreenfieldlife.com 473. Let me know what you think. Let me
S1: know what questions you have or studies that you've come across,
S1: or other things that you want to see me address
S1: on this show. And then, uh, finally spread the news,
S1: spread the word to your friends. Any little bit really
S1: helps the podcast out. There's a lot of health podcasts
S1: out there, obviously, and it's a very competitive field. So
S1: the more that you do to help this show out,
S1: spreading the word to your friends, leaving a rating, leaving
S1: a review helps out a ton. So thank you so
S1: much for listening. All the show notes again are going
S1: to be at Bengreenfieldlife.com slash 473 I'm Ben Greenfield. Have
S1: an amazing week. Do you want free access to comprehensive
S1: show notes? My weekly round up newsletter, cutting edge research
S1: and articles. Top recommendations from me for everything that you
S1: need to hack your life, and a whole lot more.
S1: Check out Ben Greenfield Life Comm. It's all there Bengreenfieldlife.com
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