S1: In this episode of the Ben Greenfield Life podcast. The
S1: ban on nicotine pouches which fruits are best for cancer prevention?
S1: A Q&A on ozempic alternatives and much 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, folks, welcome once again
S1: to another solo sode. I am sore as a chimpanzee
S1: with rhabdomyolysis. It's crazy. What happened was, you may have
S1: heard me interview this guy who has done all this
S1: research on the ancient Spartan training programs and Chinese training programs,
S1: and an ancient Indian warrior programs and wrestlers and old
S1: American presidents. And he's put together all these crazy fitness routines.
S1: His name is James Purat. I'll put a link to
S1: the show notes. The show notes for this episode, by
S1: the way, are Bengreenfieldlife.com 476. It's Bengreenfieldlife.com For 76. Anyways,
S1: after I interviewed James, he sent me up a few
S1: sample protocols. Everything from like a tar mahara crazy running
S1: program all the way down to these secret Soviet kettlebell
S1: training routines that he had researched and developed. While I
S1: convinced my twin 16 year old sons to join me
S1: in eight week Soviet kettlebell training program. I'm three days
S1: in and holy cow, I've got muscles sore that I
S1: don't think I've ever used before in my life. It's
S1: been a been a rough morning. Lots of sauna and
S1: cold plunging this morning, I'll tell you that. Got a
S1: great show for you today. A little special announcement towards
S1: the end related to my relocation to the beautiful woods
S1: of Idaho. Uh, but we'll save that for the end.
S1: And today, we're just going to jump right in to
S1: some news flashes. Got some great questions. If you have
S1: a question for the podcast, you can surf on over
S1: to Bengreenfieldlife.com slash 476 and leave your question over there. But, uh, anyways,
S1: I had another podcast guest who I interviewed, and I
S1: figured I'd bring this up right away. Just, uh, basically
S1: get this elephant out of the room. You may have
S1: heard me interview the mass spec guy Ben Katz, the
S1: mass spec guy, Ben Katz. And in our interview, he
S1: talked about how some of these nicotine pouches, Zyn in particular,
S1: was the one that he talked about, use synthetic cooling agents.
S1: And unfortunately, it turns out that these cooling agents also
S1: enhance the flavor of the nicotine pouches as a result
S1: of some of Ben's work, his Instagram channel. I don't
S1: know if our podcast had anything to do with this
S1: or not. I'm not going to narcissistically pretend that it did.
S1: But yeah, I think this is interesting. It happened, you know,
S1: shortly after our podcast was released was Zane got banned.
S1: I'm sure the person most pissed off about this is
S1: Tucker Carlson, who I think goes through probably 4 or
S1: 5 zins during the average interview that he does. But anyways,
S1: zyn nicotine pouches got banned. So the idea here is
S1: that Philip Morris international, who just so happens to own
S1: and produce Zyn, uh, came under the regulatory eye of
S1: regulatory authorities and the Senate, uh, because the vaping and cigarettes,
S1: I would say, are far less healthy than something like
S1: a zyn nicotine pouch. The problem is that you're not
S1: supposed to flavor tobacco. You're not supposed to make tobacco
S1: even more of a vice than it already is, even
S1: more addictive than it already is by adding a bunch
S1: of flavoring agents. And the way that I understand this
S1: ban is that even though Zyn isn't using flavoring agents,
S1: some of the other chemicals or molecules that they're adding
S1: to Zinn has resulted in them stepping over the boundaries
S1: of a 2022 ban on all sale of flavored tobacco
S1: that was actually in in D.C., the District of Columbia.
S1: So anyways, the idea here is that apparently they are
S1: recalling and removing Zinn from shelves, and you can't get
S1: your nicotine patches as easily now. And it's actually a really,
S1: really interesting development in the realm of nicotine stimulating, addictive
S1: product that I will admit doesn't prove focus. And I
S1: probably chew on, uh, I'll probably go through about a
S1: pack of Lucy nicotine gum a week just chewing on
S1: on nicotine gum here and there. I'm pretty careful and
S1: cognizant about how I use it and how often I
S1: use it. I know some people who are literally go
S1: through a whole pouch of Zin. You know, one of
S1: these entire pouches designed for maybe a week or two
S1: weeks of use in a single morning. Uh, but anyways,
S1: Zin has yet to be authorized by the FDA in
S1: a similar way that nicotine gum and lozenges are authorized
S1: by the FDA. Isn't that funny? A pouch is something
S1: that is banned as far as a flavoring agent, but
S1: companies that are producing gum and lozenges can get away
S1: from it. So if the FDA decides to ban zyn altogether,
S1: it will become illegal in the states. Uh, right now,
S1: as far as I know, they're undergoing a lawsuit for
S1: false and what is called malicious advertising. And, uh, as
S1: far as the actual ban goes, I think the idea
S1: is that it's happening in multiple states. I don't think
S1: it's nationwide, but it is going to be more and
S1: more difficult to get your hands on these in pouches.
S1: So I suppose stock up if you're a Zen fan
S1: or switch to gum or lozenges or, I don't know,
S1: just maybe grab a pipe or a cigar. Either way,
S1: I think you do need to proceed with caution with nicotine,
S1: but you would actually really enjoy this podcast that I
S1: did with with Ben Katz, the guy who used mass
S1: spectrometer equipment to test all sorts of things, energy drinks
S1: and chocolate and candy and kratom and nicotine and all these,
S1: you know, common vices that we use. Uh, I'll link
S1: to that one in the show notes at Bengreenfieldlife.com slash 476.
S1: But if you're a zyn user, be careful. You might
S1: not be around much longer. The next thing is, a
S1: lot of people are sleeping less this time of year.
S1: A lot of people are sleeping less this time of year.
S1: And the BBC did a pretty interesting review on why
S1: that might be, why many of us are familiar with
S1: this struggle to muster the energy to leave bed in
S1: the morning during winter, but sometimes we often have difficulty
S1: staying in bed during the summer in the warmer months. Well,
S1: new research suggests that humans may need more sleep during
S1: the dark, cold winter months than we do during the summer,
S1: and this seems to even occur in people living in
S1: cities where artificial lights would be expected to interfere with
S1: the natural influence of daylight on our sleeping patterns. Right?
S1: You'd think that we could just, like, artificially create summer,
S1: which I think in some cases we kind of do
S1: with constant exposure to bright, blaring overhead LED fluorescent lights
S1: and malls and indoor areas and cars and the like,
S1: but yet still, even while living in an urban environment.
S1: This latest study found that that with artificial light included,
S1: humans still experience seasonal sleep. Maybe it doesn't just have
S1: to do with the light. Maybe it has to do with,
S1: for example, the temperature. Now, now, previous studies have found
S1: exposure to artificial light before bedtime, and I've talked about
S1: this on the podcast before. Can suppress the secretion of melatonin,
S1: which is the hormone produced by your pineal gland that
S1: regulates your circadian clock, that natural sleep wake cycle that
S1: repeats every 24 hours and makes you feel sleepy. But
S1: this latest German study that I wanted to get out
S1: in today's news, flashes used detailed sleep recordings of about
S1: almost 200 patients who lived in urban settings and yet
S1: suffered from disturbed sleeping patterns. They found that even when
S1: exposed primarily to artificial lights, these people experience seasonal variations
S1: in REM sleep, which is directly linked to circadian rhythm.
S1: In fact, these people slept on average an hour longer
S1: in December compared to June. And this, this REM, this
S1: rapid eye movement sleep, which is the most active stage
S1: of sleep during which you dream, during which your heart
S1: rate increases. It was 30 minutes longer. The REM sleep
S1: phase was in the winter, then during the summer. And
S1: REM sleep is highly regulated by your circadian clock, so
S1: the fact that it goes parallel with seasonality makes pretty
S1: good sense. But this study also had some other surprising results.
S1: They found that there were also seasonal changes when it
S1: came to slow wave sleep, also known as deep sleep
S1: or slow wave sleep. And they found that specific changes
S1: in not just REM sleep, but also deep sleep. The
S1: two major stages in sleep occurred during the year. Now,
S1: slow wave sleep. Just so you know, deep sleep occurs
S1: during the final stage of non-rapid eye movement sleep of
S1: non-REM sleep, and REM sleep. That's when your body repairs
S1: and regrows tissues and builds muscle and strengthens the immune system.
S1: It's important for the consolidation of long term memory and
S1: processing newly acquired information. It's very important that you get
S1: this non-rapid eye movement sleep. It's one of the reasons
S1: I'm not a fan of using like THC gummies prior
S1: to sleep. If you care about memory and learning consolidations
S1: because THC can suppress that non-rapid eye movement. Sleep CBD
S1: not quite so much thc marijuana. Yes. So the slow
S1: wave sleep of the study participants was 30 minutes shorter
S1: in September than in February. So basically what they showed
S1: there was a seasonality of deep sleep as well. So
S1: this means that basically you need less deep sleep in
S1: the autumn than in the winter. You need less REM
S1: sleep in the summer compared to the winter. And interestingly,
S1: and here, here's what I think is kind of fascinating.
S1: We also know that a good night's sleep is dependent
S1: on temperature. Your body requires a temperature between about 31
S1: and 35°C, which is about 87, close to 88 to 95°F,
S1: which is conducive to ideal sleep. Now, in the summer,
S1: when higher temperatures are more common, that can be harder
S1: to control, especially during heat waves. So this means that
S1: if you want to avoid the the jet lag esque
S1: symptoms that you can sometimes experience as the seasons change
S1: and as you know, you experience temperature fluctuations. My number
S1: one tips for you are a be careful with artificial light,
S1: especially in the evening. I think most of you already
S1: know that. And it's something that that's you know, unless
S1: you've been living under a rock, a lot of people
S1: know to avoid light at night now. And they're even
S1: now programming our TVs and our computer monitors and our
S1: phones that take advantage of that fact. But b engage
S1: with cooling mechanisms. Also, like if you find yourself sleeping
S1: in in the winter, consider using something like a bed
S1: jet or a lot of people like this eight sleep mattress.
S1: Even though from what I understand, it kicks off a
S1: little bit more EMF than what I'm comfortable with. Uh,
S1: or for a long time, even though I think the
S1: company is now becoming defunct. Another company called Chilly Sleep
S1: had the ability to increase not just the cooling mechanism
S1: to help you to fall asleep, but can also produce
S1: heat to help you wake up. So you could use
S1: that in the winter. And then of course, in the
S1: summer you keep the bedroom environment as cool as possible.
S1: A lot of people ask me what I use now. Uh,
S1: my chilly sleep broke. I think they were having chip issues.
S1: They couldn't repair it. The chilly sleep is the one
S1: that that circulates cold water underneath your your top sheet
S1: at night. And that can also that water temperature can
S1: also be increased, for example, to help you wake up
S1: alarm clock free in the morning. Now I use one
S1: called a bed jet. It's pretty cool. I have a
S1: little remote control. I can set it for anywhere from
S1: 65 up to 80°F. I can I can set it
S1: to switch to warmer air as the morning approaches. I
S1: can set it for cooler air during the night. It
S1: does a really good job cooling the bed. It's like
S1: an air conditioning unit for my bed. It even has
S1: special sheets that allow the air to move more slowly,
S1: or to to move more freely underneath the sheets for
S1: your sleep. So when I use now, it's called the
S1: bed jet. Uh, and again, the eight sleep is the
S1: one that I know a lot of people are comfortable
S1: with and have success with, but I thought this was
S1: just very interesting how much the seasons change your sleep.
S1: And if you are one of those people who hay
S1: year round based on work life, etc., you know you
S1: want to sleep 10 p.m. to 6 a.m., you don't
S1: want to sleep, you know, 9 p.m. to 7 a.m.
S1: in the winter and 11 p.m. to 5 a.m. in
S1: the summer, and so you can tweak light and tweak
S1: temperature to to take advantage of that fact. I should mention,
S1: by the way, when I'm talking about all these things, light, temperature, etc.,
S1: these are called uh, zeitgebers or zeitgeist, uh, German word
S1: for time keepers. And you can use this when you're traveling.
S1: You know, the same type of facts. For example, you
S1: can limit light exposure when you travel until the actual
S1: sun has risen in the area of the world that
S1: you happen to be in. To allow yourself to adjust
S1: to that time zone more easily. You can. I use
S1: this for jet lag a lot. Getting a cold body
S1: of water or take a cold shower, especially in the morning,
S1: to jump start that that drop in adenosine or that, uh,
S1: that that adjustment in adenosine. Maybe I'll get to a
S1: denizen later on. I think I will in this podcast. Uh,
S1: you can also use protein, a protein rich meal, to
S1: jump start the circadian rhythm. So light temperature or protein
S1: rich meal and then physical movement. Those are the four
S1: best ways to beat jet lag. So get bright light
S1: in the morning. Avoid bright light at night. Uh, get
S1: the body nice and cool in the morning if you can,
S1: and then repeat that in the evening. And then also
S1: get about 30g of protein with breakfast. Don't skip breakfast
S1: those first few mornings when you're traveling to get over
S1: jet lag a little bit more easily, and then finally exercise. Exercise,
S1: preferably when the morning has come around, whatever area of
S1: the world that you happen to be in. So anyways, uh,
S1: and I actually do want to talk about caffeine a
S1: little bit because a lot of people are under the
S1: impression that, uh, to, uh, to, to not throw off
S1: your sleep, you're supposed to not drink caffeine for the
S1: first 60 to 90 minutes after wakening, because it's going
S1: to shove your sleep, drive forward, and make you feel
S1: tired earlier in the day. Not necessarily true. I'm going
S1: to get to caffeine later on in this podcast, but
S1: I'm just going to leave that there. As a teaser
S1: for you and all these studies I talk about, you
S1: can access if you go to Bengreenfieldlife.com slash 476. All right.
S1: Next up just published on my website, very interesting article,
S1: the unique anti-cancer strategies of one of Finland's healthiest and
S1: fittest 73 year old men. A guy named Vessi. I
S1: first met Vessi eight years ago at a biohacking summit
S1: in Finland. He turned out to be a very eccentric inventor,
S1: one of the most athletically talented old guys I've ever
S1: met in my life. Very smart. He had competed in
S1: several sports on a national and competitive level, including. Shooting.
S1: Military three. Skill. sport, diving, sprinting. He rides horses and
S1: plays left handed and right handed, tennis and swims and
S1: skis and skin dives and walks, long distances and swing dances,
S1: and took us out in a giant Viking ship that
S1: he built to go camp on an island. Very interesting guy.
S1: When I met him, he could crank out 25 pull ups,
S1: speak multiple languages, I own several multinational corporations and is
S1: an inventor, and he looks remarkably well preserved and young
S1: for 73 years old. Well, he wrote me an email
S1: a few weeks ago about some of the unique anti-cancer
S1: strategies that he has implemented with friends, with people who
S1: he advises, and he's not a doctor. I don't want
S1: you to misconstrue any of this as medical advice, but
S1: one of the things that that is in that article,
S1: which is very comprehensive, I'll link to it in the
S1: show notes. But he wrote me a super long email,
S1: and I wound up editing it and turning it into
S1: an article, just getting into all of his anti-cancer strategies.
S1: And one of the things that he really harps on
S1: is the idea of berry consumption. Uh, specifically, there's a
S1: whole range of different berries that are used in northern
S1: European medicine, particularly in Finland, that have supposedly anti-cancer properties.
S1: And he gets into a lot of them from black
S1: chokeberry for colon cancer to, uh, to blueberry, for many cancers,
S1: to lingonberry, for endocrine based cancers, to grapes for different
S1: types of lung cancers. And so anyways, I dug into
S1: this a little bit because I have been seeing a
S1: few other articles that have come out lately about, uh,
S1: cancer and specifically cancer and fruit consumption. I would definitely
S1: put berries into the category of fruit consumption. So the
S1: first one was a paper that looked into whether fruit
S1: intake protects against colon colorectal cancer. It was what's called
S1: a Mendelian randomisation study, a Mendelian randomization study. So what
S1: that means is they actually look at common genetic variations
S1: associated with fruit intake. So in this case they looked
S1: at almost 65,000 participants. They looked at these specific genetic variations,
S1: and they were able to examine the relationship between genetically
S1: predicted fruit intake and colorectal cancer risk. Now, this is
S1: very interesting. I interviewed Doctor Matt Dawson recently about this
S1: idea of using genetic proxies. Meaning if you have enough
S1: big data and you know that a certain gene or
S1: a certain blood marker is associated in a very large
S1: population with a certain lifestyle factor like smoking or alcohol intake,
S1: or in this case, fruit consumption, or a certain amount
S1: of fitness, or VO2 max or grip strength or vitamin
S1: D levels. You can actually, using big data, produce some
S1: very accurate predictions about causal relationships between certain lifestyle or
S1: dietary or exercise factors and certain disease risks, and in
S1: this case, they use this Mendelian randomization tactic to look
S1: at the causal relationship between fruit consumption and colorectal cancer risk. Now,
S1: in a nutshell, I guess I should say in a
S1: melon rind, uh, higher genetically predicted fruit intake was indeed
S1: associated with reduced colorectal cancer risk. Um, and this was specifically, uh, very,
S1: very significant when it came to men. So then I
S1: looked at another recent study that came out that actually
S1: dug into what kind of fruits could actually reduce colorectal
S1: cancer risk. And this is a big issue. I mean,
S1: we're even seeing children now coming down with colorectal cancer.
S1: I think it could be a combination of everything from
S1: from herbicides to pesticides to toxins to ultra processed foods,
S1: to a host of factors, including microbiome based factors. And
S1: I think that my friend doctor McCullough's new book coming
S1: up soon on cellular health, he gets deep into the
S1: colon and and aerobic and anaerobic bacteria in the colon
S1: and a whole host of factors related to this. But regardless,
S1: this is important. I think, you know, even if you're
S1: not some, you know, uh, you know, 70 year old
S1: person who's at a high risk of colorectal cancer, this
S1: is important even for your kids to know. So what
S1: this meta analysis of observational studies looked at was what
S1: fruits were actually associated with reduced risk of colorectal cancer.
S1: It turns out that any citrus fruit. Right. So lemon, orange, mango, etc.. Apples,
S1: watermelon and kiwi. So citrus fruits, apples, watermelon and kiwi
S1: are the four that are the most associated with decreased
S1: risk of colorectal cancer. I think it's also interesting because
S1: if you look at kiwi in particular a kiwi fruit extract,
S1: you can actually buy that on Amazon. It's fantastic for
S1: constipation as well. Uh, but this was a total of
S1: over a million participants under the age of 80 in
S1: this meta analysis of observational studies. And that's what is found. Citrus, apples,
S1: watermelon and kiwi are the ones associated with the lower
S1: risk or the lowest risk of colorectal cancer. Now, I
S1: still think that based on data that I've seen, I'm
S1: going to link to a few papers in the show
S1: notes on the antioxidant and anti-cancer properties of berries, which
S1: is what got me talking about in the first place.
S1: I think that berries still are the most powerful when
S1: it comes to the lowest in fructose and sugar, but
S1: the highest in a lot of these cancer fighting compounds.
S1: So as a matter of fact, one of these studies
S1: and if you want to read the full paper, I'll
S1: link to it. It's called, um, it's called the protective
S1: Role of dietary Berries and cancer. It's a it's a
S1: pretty comprehensive 2016 paper. So it begins by highlighting the
S1: significant impact of colon cancer globally and specifically treats colorectal cancer. And,
S1: you know, this is a topic near and dear to
S1: my heart because my father several months ago actually passed
S1: away of colorectal cancer. And so I'm actually pretty motivated
S1: to get information out there to people about prevention. And
S1: of course, you know, because I'm genetically related to my father,
S1: this is also information that's near and dear to my heart.
S1: So basically, berries are very rich in a lot of compounds.
S1: You're no doubt familiar with antioxidants, polyphenols, flavonoids, and a
S1: host of different vitamins that play a critical role in
S1: combating oxidative stress and inflammation, which are key contributors to
S1: cancer development, oxidative stress and inflammation not just cancer, but
S1: a host of chronic diseases. You control oxidative stress and inflammation,
S1: and you are going to be well equipped to fight
S1: a lot of diseases. And there is a Goldilocks effect, right?
S1: You want every single day to create oxidative stress in
S1: your body from herbs and plants and spices and sauna
S1: and exercise and cold and sunlight, radiation and grounding, etc.
S1: but there is a Goldilocks zone to oxidative stress, you know,
S1: the same can be said for inflammation exercise. Allow your
S1: body to mount an inflammatory response. Don't take a bunch
S1: of antioxidants after exercise. Don't go to a long cold soak.
S1: But in general, rampant chronic oxidative stress and inflammation are
S1: definitely associated with cancer development. So the high antioxidant content
S1: in berries helps to neutralize those free radicals. While a
S1: lot of the plant defense compounds in berries produce this
S1: so-called xeno hormetic effect, which allows your body to be
S1: able to better mount its own antioxidant response. So it's
S1: kind of operating on a on A12 combo punch here.
S1: So the anti-cancer properties of berries this paper gets into
S1: are attributed to their ability to modulate some signaling pathways
S1: associated with cancer progression. The signaling pathways have very long
S1: complex names like NF kappa B and the wind pathway
S1: and the Akt mTOR pathway and the Erk mAPK pathway.
S1: But basically, the long story short is that these are
S1: pathways critical in regulating cellular proliferation, programmed cell death, aka
S1: apoptosis and angiogenesis, or the formation of new blood vessels.
S1: And by influencing each of these pathways, berries can inhibit
S1: tumor growth and tumor spread. There's actually a great book
S1: by a guy I interviewed named Doctor William Li called
S1: Eat to Beat Disease. If you want to get more
S1: in especially the the anti or pro angiogenesis properties of
S1: different foods, check that book out eat to beat disease.
S1: You may start eating black squid ink pasta after reading
S1: that book. I'm just going to warn you or listen
S1: to the podcast interview that I did with him. Fantastic
S1: book Eat to Beat Disease. Anyway, so this study concludes
S1: that incorporating berries into the diet is a powerful strategy
S1: in cancer prevention and treatment, particularly for colorectal cancer. You know,
S1: backing up a lot of what Vesey wrote in this
S1: article on my website about the anti-cancer effects of some
S1: of these northern European approaches to managing cancer, both preventively
S1: and then also treating it acutely with high berry intake.
S1: So I don't necessarily expect you to go out and
S1: hunt down sea buckthorn berries and cloudberries and lingonberries and
S1: some of the berries that, you know, I've had a
S1: chance to personally forage for in Finland. They have a
S1: biohacking summit in Helsinki, Finland every year. Shout out to
S1: my friends from the Biohacker summit. And usually we go
S1: foraging for berries during this summit, but just the average
S1: berries that you can find, uh, in the average American
S1: grocery store or European grocery store work just fine. Now, remember,
S1: berries are included amongst the dirty dozen, right? Like like
S1: fruits that tend to be sprayed, that contain edible skin.
S1: Or the ones you need to be more careful with, right?
S1: Avocados and bananas. You don't necessarily have to break the
S1: bank to buy organic berries. Absolutely. Apples, lettuce, etc. so
S1: some of the best ones. Blueberries. Yay! Anthocyanins. Resveratrol. Blueberries
S1: are fantastic. Always have a few frozen ones for making
S1: my morning smoothies. I like to toss a few in there. Strawberries.
S1: Very rich in vitamin C and antioxidants, strawberries can also
S1: help lower the risk of esophageal cancer. Raspberries, high in
S1: fiber and something called ellagic acid, also talked about in
S1: that book, Eat to Beat Disease, linked to a wide
S1: variety of cancer preventions, and then blackberries, which also have
S1: a very, very high amount of anthocyanins in them. So anyways,
S1: the idea of fruits and fructose being poison is something
S1: that I know somebody's going to mention or bring up.
S1: And here's the deal. Yes, excess fructose consumption in fruit
S1: can increase triglycerides. It can increase your risk of non-alcoholic
S1: fatty liver disease. It can cause accumulation of visceral fat,
S1: which can churn out inflammatory cytokines. But any study that
S1: has shown fructose or high fruit intake or high fructose
S1: corn syrup intake to be able to do that has
S1: only demonstrated that that's the case in the state of
S1: caloric excess. And what I mean by that is, if
S1: I'm burning 2000 calories a day, I can comfortably tell
S1: you that I could drink 2000 calories of Coca-Cola a
S1: day and my liver would be just fine. Now I
S1: might experience micronutrient deficiencies and vitamin deficiencies, etc. I could
S1: also eat a couple of pounds of apple a day,
S1: and as long as I'm not exceeding my my total
S1: calorie burn, that excess fructose is not going to spill
S1: over and create any kind of issues in my body. Now, yes,
S1: some people have things like fructose intolerance and fructose allergies
S1: and get bloating. Some people are sensitive to FODMAPs, which
S1: are found in things like apples, these fermentable carbohydrates that
S1: can cause bloating and gas. But those issues aside, fructose
S1: is not a problem at all unless you're overeating. The
S1: problem is, most people who are eating a lot of,
S1: let's say, dried apple chips and sodas and Coke and
S1: high fructose corn syrup, etc. they're also eating to excess.
S1: But put me on a desert island with a bunch
S1: of blueberries. I'll sit there and eat them all day long.
S1: You know, as long as I'm not exceeding the number
S1: of calories that I'm burning and have no issues or
S1: concerns about, you know, about high triglycerides or nonalcoholic fatty
S1: liver disease or anything of the like. So just understand
S1: the actual caloric dose of the fructose is the issue,
S1: not the fructose in and of itself. And yes, I
S1: know there are some there are some exceptions to this fact,
S1: like the harsh toxins or chemicals that might be used
S1: for extractions, used to create, say, like high fructose corn syrup.
S1: I don't think that a Coca-Cola 2000 calories of Coke
S1: is the same as 2000 calories of blueberries. I'm not
S1: a total calorie and calorie out kind of guy. I
S1: think the quality of the food does matter. But nonetheless,
S1: the major takeaway that I want to give you here
S1: is that eating fruit is a good idea for cancer prevention.
S1: Berries are probably the top of the totem pole. And
S1: then secondarily apples, kiwis, citrus fruits and gosh darn it,
S1: if I'm not forgetting what the last one was. Anyways though,
S1: eat your fruits. All right, so let's go ahead and
S1: move on to the next topic that I want to discuss.
S1: The world's most popular drug. You guessed it caffeine aka
S1: 137 trimethyl xanthine. And I'm drinking paraxanthine right now in
S1: this update. Energy drink. But caffeine is 137 trimethyl xanthine,
S1: one of the most widely consumed substances in the world,
S1: and the Journal of the International Society of Sports Nutrition.
S1: I love this journal. Uh, their most recent edition got
S1: into common questions and misconceptions about caffeine supplementation, so let's
S1: get into what they looked at and what they found.
S1: So um, first of all, a little bit of a
S1: background here. Um, let's let's talk a little bit about
S1: what caffeine actually does when you consume it. So caffeine
S1: in most people is 99% absorbed within 45 minutes of
S1: ingesting it. And peak plasma concentrations occur between about 15
S1: minutes and two hours after ingestion. That can depend on genetics,
S1: whether or not you're a fast caffeine metabolizer, or a
S1: slow caffeine metabolizer. If you're a slow caffeine metabolizer, it's
S1: going to take a longer time to show up in
S1: your bloodstream. And this is why people who are slow
S1: caffeine metabolizers if they have an affogato espresso with ice
S1: cream after dinner at the Italian restaurant can be up
S1: until 2 a.m., while a fast caffeine oxidizer can be
S1: slumbering peacefully by 10 p.m.. So, uh, and caffeine's elimination
S1: half life can range between one and a half and
S1: 9.5 hours, and again ranges from individual to individual. And
S1: this is why some people can have a cup of
S1: coffee at 4 p.m. in the afternoon, and other people
S1: are totally screwed by that. So anyways, once caffeine is absorbed,
S1: your body converts about 70 to 80% of it into
S1: actually what I'm drinking right now. Paraxanthine. And uh, the
S1: formation of Paraxanthine and the subsequent excretion in the urine
S1: is the major pathway for caffeine metabolism and clearance. Now,
S1: the way that caffeine actually keeps you awake is mechanistically,
S1: it binds to adenosine receptors. It blocks the binding of
S1: adenosine to its receptor, and that directly affects the release
S1: of neurotransmitters like norepinephrine and dopamine and serotonin and gamma
S1: aminobutyric acid. And by binding to those receptors, it keeps
S1: adenosine from causing sleep drive to be enhanced, thus keeping
S1: you awake for longer periods of time. It's blocking the
S1: effects of adenosine. Now, another mechanism of action lesser known
S1: for caffeine is that it inhibits something called phosphodiesterase, and
S1: that prevents another molecule called Camp from being enzymatically degraded. Now,
S1: the accumulation of Camp, because it's not getting broken down
S1: as much when you are consuming caffeine, then stimulates the
S1: release of dopamine, epinephrine, and norepinephrine, and that can cause
S1: not only wakefulness, but also this is kind of cool.
S1: Adipose tissue, lipolysis breaking down of fat and subsequent fatty
S1: acid oxidation. That's why in some studies, caffeine has been
S1: shown to increase metabolism and cause you to burn more fat.
S1: But there's lots of questions about caffeine. Like, can it
S1: dehydrate you? Uh, you know, can it actually burn an
S1: appreciable amount of fat, how much caffeine could kill you, etc..
S1: And that's what this great paper from the Journal of
S1: the International Society of Sports Nutrition got into. I'll link
S1: to the whole thing in the show notes at bengreenfieldlife.com.
S1: Slash 476. But I wanted to get into some of
S1: the highlights for you, uh, today. So first of all,
S1: can caffeine dehydrate you if you are not exercising just
S1: at rest, drinking caffeine at the office during the day.
S1: Some people say it's such a profound diuretic that it
S1: can dehydrate you. Now, the most up to date research
S1: shows that in habitual drinkers who are used to caffeine,
S1: not someone who's having their first cup of coffee for
S1: the first time anywhere, up to around 300mg does not
S1: produce a significant enough amount of diuresis to actually dehydrate you. Now,
S1: that means that you're not going to start to experience
S1: the dehydrating effects of caffeine until you're exceeding about three
S1: cups or more, and even then, some of the volume
S1: of the fluid associated with your caffeine intake is going
S1: to affect this meaning if you're drinking a grande iced
S1: Americano with a shot of espresso that's maybe slightly less
S1: than 100mg, the amount of fluid that you're getting in
S1: a grande is like 2020 four ounces. That's more than
S1: enough to offset the diuretic, p inducing or so-called dehydrating
S1: effects of caffeine. But then if you're having, like, I
S1: don't know, four espresso shots that are just a tiny
S1: 1.5oz espresso shots without much fluid volume in them, it's
S1: a different story altogether. so kind of depends. But you
S1: got to drink at least three servings of coffee or,
S1: you know, 300mg plus of caffeine to start to get
S1: to the dehydrating effects. Now, when they look at the
S1: potential for caffeine to dehydrate you during exercise, it's a
S1: little bit similar. The if you're drinking caffeine and it's
S1: part of some kind of a fluid substance that you're
S1: consuming during exercise. As long as hydration is managed, it
S1: does not appear that caffeine intake during exercise results in
S1: any significant differences in things like fluid retention or urine output.
S1: If you're using concentrated sources of caffeine like nodoz tablets
S1: or caffeine tablets, or some pre-workout that doesn't have fluid
S1: in it, but that is a high amount of concentrated caffeine.
S1: That's where there could be some diuretic dehydrating effects of
S1: caffeine during exercises. I mean, uh, per so I talked
S1: about this on the podcast recently. I recently formulated a pre-workout.
S1: It's got about 80mg of caffeine in it for a
S1: company called Vita Boom. You can check it out at
S1: Vita boom Vita Vita boom.com/ben, me and my sons all
S1: had that pre-workout before our kettlebell training session yesterday, and
S1: we were sweating buckets way more than we had the
S1: other days when we hadn't had the pre-workout. And I
S1: know it was because of the caffeine and some of
S1: the blood flow enhancers in that pre-workout. But if we
S1: hadn't been paying attention to fluid balance, our bodies would
S1: be more dehydrated from that versus having an energy drink
S1: that contained 80mg of caffeine. Because the energy drink includes
S1: sometimes 16, 20, 24oz of fluid with it, whereas a
S1: pill does not. So it kind of depends on the
S1: delivery mechanism when it comes to caffeine during exercise. So
S1: the next question is does caffeine significantly or appreciably decrease
S1: body weight and fat mass? I already explained to you
S1: how caffeine can enhance fat oxidation both at rest and
S1: during exercise. But the question is, is that appreciable enough
S1: that so-called thermogenic effect to actually cause meaningful body fat reduction? Well,
S1: it turns out that if you are an untrained person
S1: just starting to drink caffeine or energy drinks pre-exercise, there
S1: is a big enough effect, a big enough thermogenic effect
S1: of caffeine to cause a significant amount of fat oxidation
S1: that would allow you to burn more fat and lose
S1: more weight, caffeinated and exercising than if you weren't caffeinated. However,
S1: if you are trained and you're also habituated to caffeine intake,
S1: then in that case, you're not going to see a
S1: huge impact of caffeine on weight loss energy. Yes, which
S1: could indirectly result to more weight loss because you're more
S1: likely to hit the gym or hit the gym harder
S1: because you have more energy. But if you're used to
S1: drinking caffeine and you're already a pretty trained person, you're
S1: not going to see a huge amount of fat loss. Now,
S1: I should note that in many of the clients I coach,
S1: I actually have them do fasted workouts with caffeine in
S1: their system. And anecdotally, I see better weight loss than
S1: everyone from Hollywood celebs who I train to athletes to
S1: executives who are trying to burn a few extra pounds
S1: for swimsuit season. One of the protocols I have them
S1: do is go out in the morning, fasted exercise, post
S1: a cup of coffee or green tea without calories and
S1: creamer added to it, and then we finish that up
S1: with 2 to 5 minutes of cold. And I can
S1: literally just see fat melt off a body when I'm
S1: using that approach. But I haven't seen any studies that
S1: have actually looked into the fat oxidizing or weight loss
S1: inducing effects of caffeine when it's combined with fasted exercise versus, say,
S1: fad exercise. So that's not something that's been studied. But
S1: I can say anecdotally, I think there's something to the
S1: idea of consuming a thermogenic agent fasted in the morning
S1: doing aerobic exercise and then preferably even chasing that with cold.
S1: So you get some white adipose to metabolically brown active
S1: fat conversion. But anyways, uh, might be getting into the
S1: weeds there. But it is an interesting strategy that I
S1: think works really well. Uh, another another question that they
S1: looked at in this study was how much caffeine could
S1: kill you. How much caffeine could kill you? Now, this
S1: might seem like a ridiculous question, but if you go
S1: to Amazon, you can buy caffeine powder and like, you
S1: can buy like, like a 10,000 plus milligram canister of
S1: caffeine powder. Well, it turns out that the potentially lethal
S1: dose of caffeine is about five grams, right? So if
S1: you weren't doing things right or if you were taking
S1: excess energy compounds, the the so-called median lethal dose, the
S1: Ld50 of caffeine is actually not quite as high as
S1: what you would estimate. As a matter of fact, the
S1: toxic effects like seizures for example, not death, but seizures,
S1: heart palpitations, etc. can be observed with rapid consumption of
S1: around 1200 milligrams of caffeine. And there are some energy
S1: drinks that get pretty close to that. As a matter
S1: of fact, back to that mass spec guy who I interviewed, uh,
S1: Ben Katz. He's even done mass spectrometry studies on energy drinks,
S1: showing sometimes they're at 2 to 3 times higher the
S1: amount of caffeine than is actually advertised on the label.
S1: So it's important to think about. But yeah, five grams
S1: of caffeine, you could die. And again, remember the average
S1: cup of coffee has like 100mg or so depending on,
S1: you know, whether it's an orange mocha Frappuccino or a
S1: double espresso or a triple Red bull. But, you know,
S1: that means you have to drink like 50 cups of
S1: coffee to get close to that, that lethal dose. Yet
S1: it can be done, especially with some of these concentrated
S1: caffeine extract. So something to think about, something to think about.
S1: Don't don't miscalculate your caffeine dose. Uh, sex differences regarding
S1: caffeine's effect. It also looked into this. Right. So there's
S1: literature showing that there are factors like your estrogen level
S1: or even the use of oral contraceptives, which can decrease
S1: the CYP activity that breaks down caffeine. So if you're
S1: on the pill, you're going to be more sensitive to caffeine. Uh,
S1: you're not going to metabolize it quite as quickly. Uh, menstruation,
S1: time of month, periods that can all influence your ability
S1: to metabolize caffeine more quickly or more slowly. Also, Uh,
S1: but it looks like overall, the most important thing when
S1: it comes to sex differences with caffeine is that males
S1: seem to respond much better to the ergogenic performance enhancing
S1: effects of caffeine than females do, and that probably is
S1: due to some type of estrogen interplay in the female population.
S1: And therefore that could also mean that in a postmenopausal female,
S1: they might actually respond to caffeine just as well as
S1: a man might when it comes to the ability to
S1: be able to increase exercise performance. But it turns out
S1: caffeine helps men more than women exercise harder or improve performance.
S1: So the next question that they looked into was when
S1: it comes to performance, and this is something that's interesting
S1: because I'll tell you a story. When I used to
S1: do Ironman Triathlon, I would abstain from caffeine for two
S1: weeks leading up to the race, and then I would
S1: have caffeine before the race and during the race. And
S1: like little energy gel packets, I would do the same
S1: thing with carbohydrates. I would go very, very low carb
S1: for about a week leading up to the race, and
S1: then starting about four days prior to the race, I'd
S1: begin to carb load with the idea very similar to
S1: what I used to do in my bodybuilding days, that
S1: if you restrict carbohydrates, you upregulate the enzymes responsible for
S1: taking carbohydrates into muscle, and therefore you ramp up the
S1: amount of carbohydrate that you can store away as storage glycogen.
S1: And there actually is something to that approach. But the
S1: idea behind the caffeine was that if you abstain from it, the, the,
S1: the notion is that you're going to be more sensitized
S1: to it versus if you're a habitual caffeine drinker and
S1: you're consuming caffeine, I say drinker. Obviously, caffeine can be
S1: consumed in many delivery mechanisms beyond just coffee. I'm just
S1: going with the world's favorite way to consume caffeine. Uh,
S1: if you are habitually consuming caffeine, does it negatively impact
S1: the ability to be able to use caffeine as an
S1: ergogenic aid? Well, if you would have asked me a
S1: few years ago, I would have said yes. But more
S1: and more studies seem to indicate that unless you are
S1: on massive doses of caffeine, specifically 6mg/kg per day, right?
S1: So if I weigh 80kg, rough math, that's four. So
S1: if I'm having 480mg of caffeine per day, like almost
S1: five cups of coffee per day, then if I want
S1: to use caffeine as a performance enhancing aid, I would
S1: indeed need to abstain from caffeine usage or lower caffeine
S1: usage prior to whatever event or workout or performance for
S1: which I wanted the ergogenic effects of caffeine. But unless
S1: you're having a massive amount of caffeine, it turns out
S1: that you don't need to, like, restrict caffeine to be
S1: able to reintroduce it and see a performance enhancing effect.
S1: That's kind of like old school knowledge, But nowadays it
S1: appears that caffeine is ergogenic, irrespective of the user's typical
S1: caffeine consumption habits. I'll say that again, caffeine is ergogenic
S1: performance enhancing irrespective of the typical caffeine consuming habits. Now,
S1: another question this paper looked into was whether or not
S1: caffeine actually works for everyone for for wakefulness, for exercise performance.
S1: muscular endurance, power, strength, sprinting, jumping, throwing, you name it. Well,
S1: this probably comes as no surprise to you that that
S1: you can test your caffeine metabolizing genetics. Caffeine is metabolized
S1: in your liver pretty rapidly, as we've already established via
S1: the cytochrome P450 enzyme pathway. And that's your that's your
S1: Cyp1a2 gene. It's responsible for about 90% of caffeine metabolism.
S1: Genetic variations in that gene can influence the rate of
S1: caffeine breakdown. For example, individuals who are homozygous alleles of
S1: that particular gene are fast caffeine metabolizers, whereas people who
S1: are who are heterozygous and AC or actually a CC.
S1: Those are also known as slow metabolizers. So yes, certain
S1: people can definitely have a large amount of variability when
S1: it comes to the ergogenic response to caffeine ingestion. And
S1: it turns out that if you are a slow caffeine metabolizer,
S1: your overall going to be more sensitive to caffeine, and
S1: it's going to be more likely to induce a performance
S1: enhancing effect. So, uh, it might not just be genetic factors, right?
S1: There could be other factors, such as, you know, how
S1: quickly you absorb it and your habitual usage, etc. but
S1: it turns out that in the majority of cases, slow
S1: metabolizers appear to be more responsive than fast metabolizers as
S1: far as feeling the effects of caffeine more, although the
S1: research does go back and forth, there's some research that
S1: says fast metabolizers do better with caffeine, so I think
S1: we need more research on this. But, you know, all
S1: we can say is that, yes, different people will respond
S1: to caffeine differently. Uh, next up, you know, related to
S1: caffeine causing death, some people wonder, well, could caffeine influence
S1: my cardiovascular health? Uh, we know that acute ingestion of
S1: caffeine has been consistently demonstrated to improve cognitive performance, particularly
S1: in the realms of attention and vigilance and improved cognitive function,
S1: can indirectly contribute to cardiovascular wellbeing by promoting healthier lifestyle
S1: choices like increasing spontaneous physical activity or the motivation to
S1: go to the gym. Now, we also know that caffeine
S1: can promote nitric oxide production, which can lead to improvements
S1: in your endothelial function. And that's important because endothelial dysfunction
S1: is a well-established precursor to atherosclerosis, one of the primary
S1: underlying causes of a variety of cardiovascular diseases. Now, many
S1: epidemiological studies have indicated long term caffeine consumption can protect
S1: against specific cardiovascular conditions. Habitual caffeine use has been inversely
S1: related to the incidence of stroke and heart failure. It's
S1: been associated with lower risk of developing type two diabetes,
S1: a major cardiovascular risk factor. Uh, however, acute ingestion of caffeine,
S1: especially in people who aren't habituated to it, like your,
S1: I don't know, eight year old son who happened to to,
S1: you know, sneak a few sips of your quad, uh,
S1: chocolate orange Frappuccino. Uh, that can cause a transient increase
S1: in heart rate and a systolic and diastolic blood pressure increase.
S1: And it can elevate what's called myocardial oxygen demand, which
S1: could trigger myocardial ischemia. And someone who has preexisting cardiovascular conditions,
S1: which your six year old son may not have, but
S1: which could be an issue in some people. And so
S1: even high caffeine intake has been associated with increased arterial
S1: stiffness or another risk factor for cardiovascular disease and atrial fibrillation.
S1: A cardiac arrhythmia has been reported amongst heavy caffeine users. However,
S1: if you actually step back and look at the research,
S1: you got to get again pretty high for you to
S1: have heart problems from caffeine, more than 400mg a day
S1: is where you start to see the Goldilocks zone jump in,
S1: and caffeine does not appear to improve heart health and
S1: may actually decrease heart health once you exceed about 400mg daily. Okay,
S1: 400mg daily. If you're exercising and you're using a bunch
S1: of energy drinks and some of those compounds we talked
S1: about earlier, you might exceed 400mg, in which case, proceed
S1: with caution, especially you have a high risk for for
S1: cardiovascular disorders. But it's about 400mg where you do need
S1: to start getting concerned about the potential effects on the heart. Uh, next,
S1: the study looked at at bone loss, right. Could caffeine
S1: actually cause you to lose bone or cause osteoporosis or osteopenia? Well,
S1: it turns out that high coffee consumption is actually associated
S1: with a lower risk of osteoporosis and the overall consumption
S1: of coffee and fractures bone fractures is non-significant. However, there
S1: is a certain amount of coffee consumption that can lead
S1: to a decrease in osteoblastic activity, which are the cells
S1: involved in bone formation and high caffeine intake has also
S1: been shown to suppress vitamin D function and alter the
S1: expression of vitamin D receptors, which can also adversely affect
S1: bone mineral density. So when it comes to coffee and
S1: your bones, it's actually very close to coffee and your heart.
S1: It turns out that threshold is also about 400mg. So
S1: if you're concerned about your bones or you're concerned about
S1: your heart, 400mg is the the amount of coffee to
S1: stop at when it comes to health or the amount
S1: of caffeine to stop at, I keep using those terms synonymously.
S1: I realize their difference. But but no, no more than
S1: 400mg of caffeine per day. Preferably. I think in most cases,
S1: especially for bone and heart is something that's important. Pregnancy, man.
S1: I mean, if you look at caffeine, it's lipophilic. It
S1: can transfer across the blood brain barrier and the blood
S1: placental barrier. Right. And neither the fetus nor the placenta
S1: have enzymes for caffeine's metabolism. It can accumulate in the
S1: oviductal and uterine fluid environments. Right. Which which means both
S1: pre and post birth your child could be absorbing caffeine
S1: and multiple multiple studies have shown that daily doses of
S1: even less than 300mg of caffeine can increase the risk
S1: of pregnancy failure, and daily intake. As low as 100
S1: to 200mg per day is associated with increased risk of
S1: miscarriage and fetal growth restriction. Low birth weight, increased risk
S1: to the offspring, including cognitive impairments and overweight and obesity implications. Uh,
S1: if I knew anyone in my life who was pregnant,
S1: I would highly recommend them based on the cumulative scientific
S1: evidence to avoid caffeine. I'm sorry, but the Starbucks drive
S1: thru is just not going to be an option for
S1: those nine months. And I think that's very important and
S1: something that could be one of the more important parts
S1: of what I'm telling you about caffeine is don't have
S1: it if you are pregnant. Absolutely. So, um, so that's
S1: another thing that was discussed, almost done going through this,
S1: I realize a lot of information on caffeine, but it's
S1: actually very, very interesting. Um, is caffeine addictive? Is caffeine addictive?
S1: There seems to be a common assumption that caffeine is
S1: an addictive, um, substance. Now, if you look at the
S1: Diagnostic and Statistical Manual of Mental Disorders, the DSM five
S1: caffeine withdrawal is an officially recognized diagnosis, as are caffeine
S1: induced disorders and caffeine intoxication. But in order for something
S1: to be considered for a criteria for caffeine use disorder,
S1: there has to be a persistent desire or unsuccessful effort
S1: to limit use. Continued use despite knowledge of potential harm
S1: and then withdrawal symptoms. This might sound like you after
S1: going one morning without a cup of Joe. Uh. However,
S1: it actually is pretty weak when it comes to its
S1: addictive potential. Now, caffeine can have an impact on some
S1: neurotransmitters related to addiction. It does have the potential to
S1: be abused by some. There are some established withdrawal symptoms,
S1: but if you actually look at caffeine for the current
S1: mechanistic evidence and the criteria, according to the American Psychiatric Association,
S1: for something to be associated as addictive, caffeine is actually
S1: pretty weak on that. And believe it or not, I
S1: think it's pretty easy to stop caffeine. I keep decaf
S1: on hand all the time I have about 2 to
S1: 3 cups of coffee a week. When I am at home.
S1: I have 1 to 2 cups of coffee a day
S1: when I travel, usually just because when I'm at home,
S1: I got all sorts of teas and mushroom teas and
S1: all sorts of fancy little things to try when I travel.
S1: It's just like a cup of coffee from the hotel lobby,
S1: you know? And I realize that's not mold and mycotoxin
S1: free and blah blah blah. But, you know, sometimes you
S1: just got to take one for the team. So anyways,
S1: I drink a lot more coffee when I travel, but
S1: if if I get home from travel, even if I
S1: feel a higher urge for caffeine than I normally would,
S1: I find it's often just the taste and the black
S1: substance and the desire for something to induce a morning
S1: bowel movement. And I can literally just do decaf and
S1: be fine. I think often it's the taste, it's the habit.
S1: It's the neural association with something in the morning that
S1: you do caffeine with, like reading a book or meditating
S1: or journaling that can result in it feeling addictive. But
S1: it's not as addictive as you would actually think. So.
S1: One last thing, and this is important, does waiting one
S1: and a half to two hours after waking to consume
S1: your first cup of coffee, or any form of caffeine
S1: help you avoid the afternoon crash. And there's been a
S1: trend of a lot of podcasters and people on social
S1: media who recommend delaying your coffee ingestion in the morning
S1: by anywhere from 30 to 60 minutes to as much
S1: as 90 to 120 minutes after waking, with the rationale
S1: being that you want to prevent prolonging your waking cortisol
S1: response because your adenosine levels are still going down during
S1: that time. And remember that adenosine is responsible for inducing
S1: the sleep drive. And so if you prolong that waking
S1: cortisol peak, then you would actually potentially, uh, produce an
S1: afternoon crash based on speeding up your sleep drive. Now,
S1: here's the thing. Cortisol does have a circadian rhythm, right?
S1: Circulating levels of cortisol are lowest at sleep onset. They
S1: begin to increase during sleep, and then they peak within
S1: about an hour of waking. And then they start to
S1: decline across the day. And that's all regulated by what's
S1: called your HPA axis. The fact is that the elevation
S1: in cortisol secretion, when you have that first cup of
S1: coffee in the morning doesn't even occur if you're a
S1: habitual user of caffeine, right? Even if your habitual use
S1: of caffeine is pretty low, like 200mg a day, it's
S1: a moot point if you're a regular caffeine drinker. Anyways.
S1: This idea that caffeine could somehow upregulate the cortisol awakening
S1: response to the extent to where you'll experience an afternoon
S1: crash later on in the day, and in people with
S1: high chronic intakes of caffeine 300 to 600mg a day,
S1: which many people get, the cortisol response is abolished completely. Right?
S1: So so first of all, there's no issue if you're
S1: a habitual caffeine drinker of just having your coffee within 30,
S1: 60 to 60 minutes of waking up, it's going to
S1: have a barely an impact at all on your cortisol levels. Now,
S1: the idea here is that the other flaw, in my opinion,
S1: for delaying caffeine intake based on concerns with prolonging the
S1: peak secretion of cortisol is the same. Peak secretion of
S1: cortisol happens with your first exercise session of the day,
S1: or your first cold shower of the day, or anything
S1: like that. So based on that logic, you would avoid
S1: just stimulating your body in general all morning and you
S1: just do whatever yoga and breathwork and sip some non-caffeinated
S1: tea because otherwise you're going to die of a horrible
S1: afternoon crash at 2 p.m.. It's just it's not really
S1: the case. It doesn't work like that. There's not a
S1: significant enough impact on cortisol for that to be the factor.
S1: And then when you look at adenosine, well, when you wake,
S1: there's an immediate but gradual build up of adenosine, like
S1: you're sleep deprived or your sleep drive starts like basically
S1: right when you wake. So suggesting that adenosine levels as
S1: many podcasters and social media people who are saying don't
S1: have your cup of coffee within 30 60 minutes of waking.
S1: They're saying that adenosine levels are are continuing to decline
S1: upon waking. And that's just a lack of understanding of
S1: the proper sleep wake cycle. Influence on adenosine. Adenosine is
S1: actually rising as soon as you wake up. It's not declining,
S1: and you're not going to contribute to further decline by
S1: having a cup of coffee in the morning. Your adenosine
S1: levels are already going up as soon as you wake up,
S1: and you don't have to delay caffeine intake in order
S1: to to to not have a crash later on in
S1: the day. Um, and there's also no evidence to suggest
S1: that daily typical caffeine intake is associated with daytime sleepiness.
S1: If there were the hack for that would just be
S1: as soon as you start to feel sleepy later on
S1: in the day, have another cup of coffee and it
S1: would throw any any concern like that out the window. Anyways.
S1: Another cup of coffee, another serving of caffeine. So in summary, though,
S1: there may be an upside to delaying your morning caffeine
S1: intake if you are already sufficiently slept because you know why.
S1: You know why. Dump something into your body if you're
S1: already awake. Really? The the cortisol peak adenosine avoiding afternoon
S1: crash issue is a moot point. Like you are not
S1: going to throw off your body's sleep drive or circadian
S1: rhythm by having a cup of coffee right when you
S1: wake up. I suppose the only exception to that rule
S1: would be if you are trying to adjust to a
S1: new time zone and you've woken at like 4 a.m.
S1: because it's, you know, it's it's 7 a.m. back home,
S1: but it's 4 a.m., uh, you know, um, uh, on
S1: the Pacific Time zone where you're at. And so you
S1: get up at 4 a.m. and you have a cup
S1: of coffee. Well, it's going to be a lot harder
S1: for your body to adjust to your new time zone
S1: if you're doing that. In that case, it would make
S1: better sense to wait to have your cup of coffee
S1: until you actually do want to start waking up, if
S1: that makes sense. Same thing with light, where blue light
S1: blockers don't have coffee, you know, don't get a cold shower.
S1: Don't do a hard exercise session until the time of
S1: morning has actually arrived, at which point you want to
S1: send your body a wakefulness signal. So hopefully that makes sense. Um, man,
S1: I'm going to link to this full article in the
S1: show notes at bengreenfieldlife.com. Slash 476 I spent more time
S1: on that than I thought, so I'm not even going
S1: to get a chance to get into some of the
S1: questions that have come through for this week on Ozempic.
S1: You know, I'll answer the Ozempic one real quick. Uh,
S1: and we'll leave it at that. So because I got
S1: two questions on this, Dave asked, would you recommend stacking
S1: Carlisle Curb or the Pendulum Probiotic, which are two natural
S1: ozempic alternatives with, uh, tirzepatide, which is a GLP one agonist.
S1: And then another person says, uh, can you take Carlo
S1: Courbe and the pendulum GLP one supplement at the same time?
S1: I'm gonna give you my quick 32nd response to this
S1: and go listen to my podcast with Colleen Cutliffe from
S1: pendulum or my podcast from from Carlo Curb the Doctor
S1: from New Zealand. If you want to learn more about
S1: how those work is natural GLP one agonist without taking ozempic.
S1: But here's the deal Kalokairi. The active ingredient in that
S1: is MRSA, a highly bitter compound that when you swallow
S1: the capsule an hour before a meal, triggers the bitter
S1: receptors in your small intestine to significantly reduce appetite by
S1: increasing not just GLP one, but also two other appetite
S1: satiating hormones called CCK and Pai. Um, the might be
S1: pai pai or pie. It's not important anyways. Uh, the
S1: pendulum glp1 probiotic operates on the microbiome level, increasing akkermansia, butyricum,
S1: and Bifidobacterium to increase your level of satiety and fullness
S1: via the microbiome pathway, a different pathway. And then finally,
S1: my third method of controlling hunger. Exogenous ketones, like drinkable ketones,
S1: can suppress ghrelin, the hormone that can cause you to
S1: become hungry. So if you don't want to use ozempic
S1: or Tirzepatide or anything like that, or or or any
S1: GLP one injectable agonists, but you want the most amount
S1: of hunger suppression you can get naturally without the nausea
S1: and the muscle wasting, etc. even though I realize the
S1: muscle wasting that can be solved through adequate protein intake
S1: and weightlifting, you can wake up in the morning. You
S1: can take the pendulum GLP one probiotic before lunch. An
S1: hour before lunch, you can take kilo kerb. An hour.
S1: Before dinner you can take kilo kerb mid afternoon, you
S1: can drink a shot of ketones and you can literally
S1: lose weight, very effectively suppress hunger and cravings. And I
S1: want to have Cheetos or Doritos or Twinkies all day long,
S1: hitting those hunger mechanisms on multiple pathways. And it works beautifully.
S1: I have many clients who do this now. So again,
S1: the pendulum GLP one probiotic. When you first wake up,
S1: call carbonara before lunch, Carlo Carbonara before dinner, shot of
S1: ketones at some point during the day and you will
S1: not even think about food, even if you're the most
S1: foodie food person on the planet. So yes, you can
S1: combine them. And that's how I would do it if
S1: you were going to do it. I will link to
S1: those products in the show notes if you want to
S1: check them out. If you go to Bengreenfieldlife.com slash 476
S1: I mentioned one last thing about my move to Idaho. Uh,
S1: in the in the beginning of this podcast, and what
S1: I had mentioned was or what I was wanting to
S1: mention to you is I am hiring a caretaker, a
S1: live on land caretaker to be my go to right
S1: hand person for my new farm in viola. You will
S1: be a maintenance person or family, a handyman or a
S1: handy woman or a handy family. You will be working outside, inside,
S1: fixing things up, keeping biohacking equipment, uh, receiving mail, sending
S1: out packages on my behalf, sometimes grocery shopping, assisting with
S1: vehicle maintenance and tool upkeep, doing yard work, lawn mowing,
S1: weed whacking, etc. basically, you'd be my right hand person.
S1: You'd be on site hanging out about six hours a day,
S1: five days a week, occasionally, uh, pitching in on weekends, uh,
S1: watching the house, uh, when my family's gone, when we're traveling, etc.. And, uh,
S1: that's a it's a full salaried position with bonuses, with benefits. Uh,
S1: there is even an entire home on my new property
S1: that you can live in as a part of this position,
S1: a three bed, two bath home. That would be the lodging.
S1: If you're interested in being a caretaker. Uh, if you
S1: have experience with livestock care, permaculture, regenerative agriculture, farming, uh,
S1: experience as a handyman or handywoman, you're good at fixing stuff.
S1: You're good at manual labor. Uh, you preferably kind of
S1: dig health and biohacking and farm life. Also, you could
S1: be a fit for this position, and I'm, uh, wanting
S1: to fill it by September of 2024. Here's where you
S1: can apply. Go to bengreenfieldlife.com slash caretaker. That's Bengreenfieldlife.com slash caretaker.
S1: There's a form there. You can fill out the form.
S1: You can apply for the position. See, uh, see, uh, basically,
S1: if the job description appears to be a fit for you, uh,
S1: move to Idaho. Or if you're already in Idaho, great.
S1: You're already settled in. And, uh, you could be the
S1: person who's going to be my right hand man or
S1: woman or family working at the new Greenfield home as
S1: our primary home care taker and land caretaker. Let's go
S1: to Bengreenfieldlife.com slash caretaker if you're interested in that position.
S1: That's all I got, folks. Go to Bengreenfieldlife.com slash 476
S1: for all the show notes. Until next time, I'm Ben Greenfield.
S1: Wish you an incredible week. Thanks so much for listening
S1: to me. Do you want free access to comprehensive show notes?
S1: My weekly roundup newsletter, cutting edge research and articles. Top
S1: recommendations from me for everything that you need to hack
S1: your life, and a whole lot more. Check out bengreenfieldlife.com.
S1: It's all there Bengreenfieldlife.com see you over there! Most of
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