You think “roid rage” is bad? Try taking away a habitual coffee drinker’s morning java, then see what happens! Trust me, I’ve seen it and it ain’t pretty. It’s estimated that 80% of the world’s adult population consumes caffeine in one form or another, the most common source being coffee. It’s also estimated that the average daily intake of caffeine in North America is 300mg/day. There’s no disputing the human love affair with caffeine, especially in the form of coffee and soft drinks.
So what is it about this magic elixir that makes people go so crazy? Well, the stimulant properties of a strong cup of coffee can’t be denied, especially when the alarm clock buzzes at 5:00 AM. and your brain’s screaming “just ten more minutes, mom!” As the coffee giant says, “The best part of waking up is Folgers in your cup.” In addition, a stiff cup of coffee before a big meeting, a big workout, or a big night out, is enough to clear out any cerebral cobwebs, stimulate thought processes, and produce a pretty nice feel-good high.
But let’s not romanticize this topic any more than the coffee manufacturers already do. Regardless of its social acceptance, the caffeine in coffee is still a drug, an extremely addictive one with potent pharmaceutical actions. Therefore, just like I’ve done at T-mag in the past with protein and fat, I’ve assembled a roundtable of smart guys to discuss whether this chemical is a friend or a foe.
Why a whole roundtable article about caffeine? Well, in a recent Appetite For Construction column, I placed a little unassuming discussion of the latest data on caffeine and insulin sensitivity. Much to my surprise, the response to this article was overwhelming! Hate mail filed in, the T-mag forum was blowin’ up with arguments for and against caffeine and coffee, and the article even started rumbles over at several dietetics newsgroups! There’s no doubt about it, people love their coffee and will use anything in their power to justify their habits (positive or negative).
So, with all of this hubbub, Dr. Lonnie Lowery, Doug Kalman, and myself decided to have a royal rumble over this stimulating topic.
John Berardi: To start off with I’d like to throw out a bit of information about caffeine so that everyone is up to speed. Here’s a quick crash course.
First of all, caffeine, in our circles, is known as 1,3,7 trimethylxanthine and belongs to a group known as the methylxanthines. Some other methylxanthines with similar effects are theobromine (3,7 dimethylxanthine) and theophylline (1,3 dimethylxanthine). While you can continue to call it caffeine, I want to point out that the tri- and di-methylxanthines are potent chemicals that operate through several distinct physiological mechanisms, as you’ll see below.
Mechanism number one: caffeine, by virtue of inhibiting an enzyme called phosphodiesterase, increases cellular concentrations of a compound known as cyclic AMP. Cyclic AMP is the substrate for phosphodiesterase, so if you inhibit the enzyme, you get more of the substrate. More cyclic AMP means increased neural excitation (cAMP is a second messenger for neurotransmitter receptor systems, meaning that when a neurotransmitter binds its receptor, cAMP increases in the cell. So the more cAMP you have to start with, the less neurotransmitter needed to initiate a cellular event/change). In this regard, caffeine increases the sensitivity of neurons to stimuli. Therefore, when taking caffeine, internal and external stimuli are amplified as is the response to these stimuli.
Mechanism number two: Caffeine also inhibits chloride channel action. Chloride channels inhibit neuronal transmission. When caffeine comes in, it disinhibits neuronal transmission, making the nerves more likely to fire.
Mechanism number three: Caffeine antagonizes adenosine receptors. Adenosine itself can act by binding to presynaptic terminals to inhibit neurotransmitter release. In addition, it can bind postsynaptic receptors to prevent neurotransmitters from doing their job. Since caffeine can block these actions of adenosine, it can promote elevated neurotransmitter functionality.
Okay, I hope it’s clear that caffeine is a pretty potent pharmacological agent with several mechanisms of action. Just because people drink it every day and nobody’s dropping over dead immediately thereafter, it’s certainly not acceptable to take its use lightly. At this point, I’d like to get right into the debate. Let’s talk caffeine, the good, the bad, and the ugly.
First, the bad and the ugly. In reviewing the correlational or experimental data, do you guys think that there are any negative effects of habitual caffeine or coffee consumption? In other words, are there any grounds (pun intended) for avoiding this stuff?
Doug Kalman: Yes and no. Here are the major concerns:
First, we know that approximately ten grams of caffeine in one day can be lethal. That, of course, is an acute problem! Since caffeine’s half-life is pretty short, chronic, sub-lethal use doesn’t seem to present any toxic effects.
Another concern within the nutrition community is that caffeine might cause the leaching of calcium from bones, thus possibly leading to or contributing towards osteoporosis. However, the data are mixed. One line of investigation from 1994 showed that the average female’s daily intake of caffeine (300 mg) does correlate with bone loss; however, subsequent studies demonstrated that just one glass a day of milk (8 ounces) mitigated this problem.
Also, in pregnant and lactating women there’s some data that caffeine may cause malformations of the fetus, though the studies have only been in rats and at a dose equal to 70 servings of caffeine daily. An association between caffeine intake and sudden infant death syndrome (SIDS) has also been found, though it’s not well proven. Most doctors tell their pregnant patients it’s okay to have one or two cups of coffee daily.
A few more concerns: In males, habitual caffeine intake may lower sperm motility, though since Seattle doesn’t have any population problems, I doubt this to be a cause of real concern.
Also, cardiologists still debate if there’s a risk for cardiac patients to have a cup of coffee daily, but they do agree that more than that is unadvised. In terms of the diuretic effects of caffeine, one recent study found that advising people to disregard caffeinated beverages as part of their daily fluid intake is not substantiated. So, caffeine might not be the strong diuretic we once thought.
JB: That was certainly thorough, Doug. I’d agree with your synopsis. I’d like to add in the fact that recent research by Vlachopoulos and colleagues has demonstrated that 250mg of caffeine (two 6oz cups) can acutely induce arterial stiffness and short term hypertension. This work has been duplicated in other studies so it’s not just a one-time effect, although it may be only an acute effect. After all, the data correlating caffeine intake and hypertension are mixed. Lonnie, anything to add?
Dr. Lonnie Lowery: Well guys, I’m neither pregnant nor lactating to my knowledge, so I’m not too concerned about side effects. I do know that a study just hit the news regarding caffeine causing an aberration of melatonin function. This compounds the adrenergic effects, leading to insomnia. The suggestions were to avoid caffeine in the late afternoon, but isn’t this a no-brainer?
And regarding the benevolence of caffeine’s short half-life, I partly disagree; drink enough java and you can saturate your body’s ability to metabolize the caffeine. You’ll end up with chronically elevated blood concentrations. This can be good or bad, depending upon your point of view. Beyond these issues, attempts to link (food source) caffeine to diseases (heart disease, cancer, osteoporosis, etc.) have generally failed.
JB: So what I’m hearing is that caffeine use should probably be avoided in cardiac patients, in pregnant women, perhaps in women who are prone to osteoporosis and perhaps in men trying to “free the tadpoles.” If that’s what you’re saying, I’m in full agreement.
However, and you knew it was coming, this roundtable was spawned by my concerns about the effects of caffeine on insulin sensitivity and glucose disposal. How can you ignore the potential negative effects of caffeine in this regard? Are you guys trying to rile up ol’ JB or what?
Look, there have been at least eleven human studies conducted using different methodologies demonstrating that caffeine intake has a negative effect on glucose disposal and acute insulin sensitivity. Let me give you a quick review of them (‘scuze me while I pull out my notes):
– In Diabetes (2002), Thong et al gave a group of healthy, habitual caffeine drinking 20-somethings a big whack of caffeine (5mg/kg or about 350mg for a 70kg individual) after two days of caffeine withdrawal. In this study they wanted to determine the effects of caffeine on glucose uptake in an exercised leg vs. an unexercised leg. For you science types, the euglycemic, hyperinsulinemic clamp technique was used and glucose uptake was measured for 100 minutes. This measurement period occurred three hours after the exercise and one hour after the caffeine administration. Check out the results: width=”100%” border=”0″ align=”center” cellpadding=”5″ cellspacing=”0″>
As you can see, although exercise increased glucose uptake/disposal in both groups, caffeine still blunts this effect. Talking percents, caffeine reduced glucose uptake by 55% in the rested and 51% in the exercised leg. In addition, whole body glucose disposal was 30% lower. Muscle glycogen synthase (the enzyme that promotes the storage of carbs) activity is also reduced.
– In Diabetes Care (2002), Keijzers et al administered caffeine to twelve healthy people and found that caffeine decreased insulin sensitivity by 15%. The authors of this study mentioned that the epinephrine increase seen with caffeine administration was probably responsible for the effect. In addition, the authors hypothesized that, just like with many of the other effects of caffeine, habitual caffeine use may not ameliorate this phenomenon.
To corroborate the conjecture that epinephrine release is responsible for the effect of caffeine on insulin sensitivity, several studies have been done:
In JAP (1996), Van Soeren et al showed that in humans with impaired
epinephrine release, caffeine doesn’t affect glucose disposal or insulin
In JAP (2002), Thong et al showed that when 5mg/kg caffeine was administered
and epinephrine release was promoted, the insulin area under the curve was
42% greater and whole body insulin sensitivity decreased by 25% when compared
with placebo. The researchers then used a beta-blocker, propanolol, to reduce
the effect of epinephrine on the body. When this was accomplished, the insulin
resistance was abolished, completely indicating that epinephrine caused
the insulin resistance. In this study, a simple 75 gram oral glucose tolerance
test was used in conjunction with insulin and glucose measures.
– In The Journal of Clinical Investigation (1980), Deibert et al showed that epinephrine did in fact reduce tissue sensitivity to insulin by 50%. When epinephrine was high in the blood, insulin didn’t stimulate glucose disposal or prevent hepatic glucose production.
Therefore, it’s clear that it isn’t necessarily the adenosine antagonism that’s causing the effect but the epinephrine release.
In Diabetes (2001), Greer et al administered 5mg/kg of caffeine to
healthy and lean but sedentary people and saw a 25% reduction in glucose
disposal and a 35% reduction in carbohydrate storage.
DK (interrupting): Okay, I’ve heard enough! I think there are several issues here to consider. First, there are rat studies that indicate caffeine does inhibit glucose uptake. But this occurs in adipose (fat) tissue but not muscle. If you grant me that the majority of the readership here is more muscle than they are fat, then I certainly say that caffeine’s effects on metabolically inactive adipose doesn’t matter since beta-oxidation (fat burning), glycolysis (the breakdown of carbohydrate), and other cycles that produce energy take place in muscle cells (cytoplasm and mitochondria depending upon the cycle).
JB: That’s rat research. What about the human stuff? Since skeletal muscle tissue is the largest glucose disposal site in the whole body it must be contributing to the resistance. After all, epinephrine, which is released with caffeine use, is well known to reduce glucose disposal (and cause insulin resistance) in human skeletal muscle tissue!
DK: With the human stuff I have some methodological problems. One methodological issue I have a problem with is the amount of caffeine given to the subjects. In the Keijzers study, subjects received a loading dose of 3 mg/kg (~204 mg for a 150 pound person) over a fifteen minute period followed by another 0.6 mg (~40 mg) per hour for another two hours (totaling approximately 280 mg in a two hour period).
If you recall, the average caffeine intake via foods (not straight caffeine) is 300 mg per 24 hours. Without going through the whole study, the authors calculated a 15% difference in insulin sensitivity based upon the glucose infusion rate divided by the plasma insulin only during the last thirty minutes of the study. Thus, in my opinion, their calculated finding may not be representative of the truth.
A better way to determine if a typical daily caffeine dose affects insulin and glucose disposal would have been to do the study in a model of an oral glucose tolerance test, whereas at the predetermined time points (0, 15, 30, 45, 60, 90, 120, 180, 240 minutes) you measure the serum glucose and insulin. You do two studies, one with the OGTT drink alone and the second with the OGTT drink plus caffeine and compare the results in non-diabetic people. If there were a significant change or difference in the values, it would have real world implications. As of right now, I wouldn’t worry about drinking a cup of coffee and if it’s going to affect insulin levels or body fat stores for that matter.
JB: You want OGTT data? Here you go:
In The Canadian Journal of Physiological Pharmacology (2001), Graham
et al showed that when 5mg/kg of caffeine was administered to 18 young fit
males, the area under the curve for insulin was 60% greater and the area
under the curve for glucose was 24% greater in the caffeine group. These
data were collected using, you guessed it, an OGTT.
In the European Journal of Clinical Nutrition (1998), Pizziol et
al showed that 200mg of caffeine given to 30 healthy subjects in the 20
to 30-something age range increased glucose responses to an OGTT for the
second, third, and fourth hours of the test. Interestingly, there was no
impact on insulin.
In the Thong study mentioned earlier (the beta blocker one), they used an
OGTT to demonstrate that 42% greater insulin area under the curve and 25%
reduction in whole body insulin sensitivity with 5mg/kg caffeine.
In the Canadian Journal of Applied Physiology (1999), Battram et
al showed increased insulin secretion but no increase in glucose area under
the curve with caffeine administration and an OGTT.
Finally, in a yet to be published study (the work that I mentioned in my
column), four groups of normal, healthy subjects were used to evaluate the
effect of caffeine and glycemic index on insulin sensitivity (using OGTT).
The first group got decaf and a low GI breakfast. They saw a normal blood
glucose and insulin response. The second group got decaf and a high GI breakfast.
They saw a bigger insulin and glucose response in the blood.
However, when the low GI group got regular coffee with breakfast, their blood profile was worse than that of those who got the high glycemic breakfast and decaf. Therefore coffee/caffeine can turn a low glycemic meal into a high glycemic meal! Finally, the group that drank coffee and had the high glycemic meal ended up looking like diabetics.
I’ll admit that most of the studies use relatively high doses of caffeine (3-5mg/kg). But remember, it wouldn’t be so hard to accumulate these types of doses with the typical coffee and cola drinking habits of many North Americans (especially the Canadians I see every day). One 8 oz cup of coffee can contain up to 175mg of caffeine. With a five hour half-life, two large morning coffee runs can lead to the types of blood levels of methylxanthines indicated in the studies.
LL: Uh, I’d like to add a few things here before JB continues his tirade. To be fair, let me first admit that I dig my morning java. A lot. My pre-workout ritual also includes it. I think readers should know my personal feelings on this before they read my “smarty pants” banter. It’s worth it for me to brush with whitening toothpaste and deal with the rare withdrawal headache so I can go ballistic in the gym. You’ll get no apologies from me.
Getting back to the question at hand, there are a few methodological issues I’d like to address here. Honestly, a quick look at the literature reveals that pretty much everything affects glucose tolerance one way or another. I’m inclined to say “insulin insensitivity? So what?” There’s a serious difference between statistical and biological significance. I suggest that athletes don’t get too concerned about screwing-up their insulin sensitivity or glucose tolerance with caffeine.
Regardless of recent findings and “buzz” (pun intended), I’ve done enough oral glucose tolerance testing to see how variable individuals are from day to day. It’s huge, like 20%, according to other researchers. And I’ve yet to see a caffeine-using bodybuilder with glycosylated hemoglobin over 5.0% (desirable being less than 7.0%; normal is often about 6.0%).
If the daily “noise” from dozens (hundreds?) of confounding variables is so high and bodybuilders have low glycosylated Hb (i.e. healthy long-term blood sugar levels) anyway I doubt caffeine will greatly contribute to their health or physique problems.
JB: I agree with your comments about the daily variation in glucose measures, but with the consistent findings I’ve presented above, something has to be going on here. You simply can’t deny the statistically significant findings that demonstrate increased glucose and insulin as well as decreased glucose disposal all of this in healthy, young subjects.
DK: Again, what about the rat data? I think what’s happening is an inhibition of glucose uptake in fat tissue but not in muscle.
LL: I’m mostly with you on that one, Doug. I’m sure many T-mag readers have heard of “nutrient partitioning.” What if something like adenosine inhibition (from caffeine) affected tissues differently? Wait, wait? here’s a nifty quote:
studies have reported adenosine to increase insulin-mediated
glucose metabolism in adipose tissue and to decrease it in skeletal muscle.” Keijzers, 2002
Sounds like blocking that stuff (via caffeine) isn’t so bad. But overall, the research looks pretty mixed regarding “differential sensitivity.” And to be totally fair, I think that the interplay between ingested carbohydrate and hepatic production of blood sugar and muscle-versus-fat uptake requires techniques far beyond a blood sugar measurement or OGTT.
JB: First, the effect I’m describing is more of an epinephrine thing than an adenosine thing. Therefore, let’s be clear. Research has established that epinephrine causes insulin resistance, some of which occurs in the skeletal muscle. Since caffeine releases epinephrine, there’ll be some insulin resistance.
Now, if caffeine also can (and the data are equivocal) block adenosine’s effects, it might actually prevent some muscle glucose intolerance and also prevent some glucose uptake in the fat cells. Therefore the epinephrine effects of caffeine aren’t so good with respect to insulin sensitivity and glucose disposal. The adenosine antagonism seems to be good. In the end, the balance of the two still leads to less skeletal muscle glucose disposal and higher blood glucose and insulin responses to an OGTT.
LL: Well, no one’s going to disagree that EPI opposes the effects of insulin in general. (Unless perhaps they’ve been denied their morning joe and are disagreeing with everything!) But there’s something else to discuss here. Getting back to Doug’s point, I have yet to see the “caffeine controversy” pursued in bodybuilders. The large muscle mass they exhibit relative to their fat mass makes them an anomaly compared to everyone else. Since fat and muscle tissues have different insulin sensitivities, as John points out, we’re left with an utterly different research population.
I think we need some repeated trials and chronic glucose intolerance data in caffeine-using athletes. Otherwise, how can we conclude that caffeine affects them? We’re not even sure it plays a big role in the glucose intolerance that’s present in about 10% of “average” American men. And that’s to say nothing of bodybuilders, per se. We’re a different population with vastly different physiologic characteristics!
DK: In the studies I’ve been involved with (all published in some peer-reviewed format), we’ve never observed any significant changes in blood sugar values (most of these studies have employed herbal ephedrine, caffeine and/or other thermogenic substances). Thus, in regard to weight loss agents that include caffeine, I doubt there’s a negative impact on the insulin function.
In the general population, we surely do know that the overweight status and obesity lead to peripheral insulin resistance which further contribute to the obesity and yet even further contribute to Type II diabetes, heart disease and hypertension (a.k.a Syndrome X). Thus, with respect to the overweight population, insulin resistance is something that’s well worthwhile to test for. Not all overweight people are insulin resistant. We know that insulin resistant people respond very well to a controlled carbohydrate diet (such as 40% carbohydrate). We also know that diets higher in the healthy fats help increase insulin sensitivity in these individuals. The father of Syndrome X, Gerald Reaven M.D. of Stanford University, has proven that time and time again.
In those overweight/obese people who aren’t insulin resistant, the carb issue becomes one more of quality (low glycemic, high fiber) as compared to quantity. In the mildly active adult, exercise quite often ameliorates the insulin resistance problem. If it’s still an issue, a coupled effect of diet control and exercise is employed. Mainstream medicine isn’t yet aware of “glucose disposal agents” or “insulin sensitizing compounds” on a broad enough scale where these can be worked into the traditional healthcare model.
JB: Good points, Doug. Before we move on I want everyone to be clear on something. I am in no way suggesting that caffeine use or coffee drinking will cause “clinical diabetes” or clinical insulin resistance. What I’m suggesting is that there are dozens of factors that affect insulin sensitivity (both acute and chronic) including exercise timing and mode, total caloric intake, macronutrient breakdown of the diet, food selection, drugs and medications, and time of day.
While some factors may be more powerful than others, I think it’s important to recognize which factors increase insulin sensitivity and which factors decrease it. Once we know these factors we can strive toward making good lifestyle, exercise, and dietary decisions in favor of optimizing insulin sensitivity and glucose disposal in the muscle. Since I think the data are relatively clear on the fact that high dose caffeine decreases insulin sensitivity in healthy young people, we all need to be aware that coffee could present a problem for some individuals, especially those prone to diabetes, those without a regular exercise program, or those with poor dietary habits.
Now, I’ll agree with the gist of what you’re both driving at, namely that different populations respond differently to various treatments and manipulations. That’s what I was referring to before. Indeed, the study subjects I listed in my literature assault above weren’t bodybuilders or elite athletes. In fact, some studies included sedentary subjects, others included recreationally active individuals, and others didn’t list the exercise habits of the subjects. But all subjects were young and healthy. Since all three of us regularly extrapolate data from “young healthies” and apply it to bodybuilders, I hope you’re not getting self-righteous on me now just to support your love of coffee!
LL: The million-dollar question is whether these data actually matter in bodybuilders who, by all accounts, are truly unique beasts. John, you probably already know that I’ve got to point out that eccentric exercise alone is enough to reduce glucose tolerance in bodybuilders. My students and I reported on this twice last year (ASEP National Conference, 2001, Ohio Academy of Science, 2001). But don’t just take my word for it; even Holloszy’s group and Sherman, et al. (read “research studs”) reported on this back in the early nineties.
Although the intolerance is transient, the rotating body part schedule of most strength athletes makes it a chronic situation. Despite this, they are leaner than the average population and obviously have much greater muscle mass. I guess what I’m saying is that exercise is such a huge modifier of physiologic function that all the data surrounding glucose tolerance may be secondary at least regarding the body composition of athletes. But as to the severity of any one factor (i.e. caffeine), who knows?
JB: Okay, now you’re making some sense. Listen, since I’m the moderator and I get ornery if people don’t see things my way, if both of you are willing to admit that caffeine does in fact increase glucose and insulin responses to a meal (as evidenced by the studies I’ve listed above) and may reduce insulin sensitivity, I’m willing to change the focus and discuss whether or not this phenomenon actually matters or if we understand enough about insulin sensitivity to make any definitive statements about it.
LL: Before we move on ? After being involved in three recent studies related to caffeine and blood sugar, I feel like I should point out that we saw no significant changes with either fed, fasting, resting or exercise glucose concentrations. So at least nothing horrific seems to be happening. Of course, we’re not just talking about caffeine in these cases, so extrapolation is difficult.
And there’s something even more relevant. It has to do with the methods that are often employed. Let’s not forget that the destination (first floor: fat cells, muscle cells, and liver cells) of circulating glucose could change and we’d never see it with simple measurements like blood glucose or insulin levels. A finger prick or venous blood sample is akin to sitting on the curb and counting cars drive past you on a freeway. Sure, you can get “a number” but you’ll still know nada about where they’re going. This is a bummer because ultimately the site of glucose deposition is what a bodybuilder is interested in.
JB: Yes, and the studies I mentioned didn’t even focus on fasting values. They’ve looked at post OGTT (i.e. meal) values. This is a very specific situation but the most applicable one. After all, people usually have coffee with meals or with snacks. As I’ve said, I’m fairly certain that fasted values will remain intact in cases where caffeine is out of the blood by the morning. However, as I said in my last discussion of this, if the first few meals of the day jack blood caffeine levels sky high, then the person will be “diabetic” for some portion of the day while being seemingly “okay” in the morning. Therefore it looks like timing is a huge issue.
The other big issue is dose. Many of the studies I’ve brought up used pretty high doses, more than might be available in a thermogenic supplement or a daily cup of joe. It may very well be that low dose caffeine intake can offer a nice stimulant effect without the insulin resistance. That remains to be seen. So, there are certainly dose and timing issues to consider.
Either way, I agree with both of your comments about how caffeine doesn’t chronically impair insulin sensitivity. But caffeine does increase epinephrine and free fatty acids acutely, which causes poor glucose tolerance. Do you agree that if half of your daily meals (the meals after your 16 oz of morning coffee) caused aberrant increases in glucose and insulin, this would be bad for body composition, especially if those meals are higher in carbs?
DK: Sir John, since I just finished my morning coffee and I’m feeling like I’ll have Lonnie’s back up, I have a question for you. Are you stating that in an exercising or active individual, acutely increasing free fatty acids (circulating) is bad?
JB: No, Sir Doug. And I’m glad you bring this up since it relates back to my individual differences and timing comments listed above. Here are some scenarios that we have to recognize.
With sedentary individuals, especially those with a traditional Western diet high in sugar and saturated fats, elevated concentrations of circulating epinephrine and free fatty acids, in my opinion, aren’t so good since they’ll negatively affect glucose tolerance and drive insulin and glucose concentrations up after meals. And while the epinephrine may cause free fatty acids to be lost from adipose tissue, in the absence of exercise, those free fatty acids will probably just be taken back up and stored again, along with all the glucose that’s being driven into the fat cells. No one loses fat using caffeine supplements alone.
With exercising individuals, elevating circulating epinephrine and free fatty acids before exercise are exactly what we’re looking for since those fatty acids, which were once part of your love handles, will be escorted into the muscle and burned up. That’s why coffee/caffeine before exercise is probably a good thing. Not only does it jack you up for the workout but it also helps you burn up some fat.
However, there may be a negative side to pre-workout caffeine intake if it does reduce glucose disposal. Since exercise powerfully increases insulin sensitivity, the effects of caffeine may not put a dent in the already huge glucose uptake. However, the data above do indicate that high dose caffeine can substantially reduce glucose uptake after exercise. Another few studies are needed before we know what’s going on here.
Now, exercising individuals may not suffer from the effects of caffeine induced insulin resistance like their sedentary counterparts; however, I can’t imagine that increased post prandial (post meal) insulin and glucose concentrations are desirable if one wants to get leaner or minimize fat gain while trying to gain muscle.
This last comment may be macronutrient specific, though. The effects of caffeine may be negative when on high carbohydrate diets, causing poor glucose disposal, insulin resistance, and fat gain. However, caffeine may be quite positive when on low carbohydrate, high protein and fat diets.
DK: I’d postulate that there’s a huge difference between we T-Men and the Al Bundy or Fat Albert types. We certainly know that caffeine can be an ergogenic aid for very short-term exercise and endurance events, so no negative there. Now, in the terms that you put it (post-prandial aberrations), in the studies that we’ve conducted where we’re giving thermogenics (caffeine containing supplements) that are taken with meals or small snacks, we haven’t found negative changes per se in body fat levels.
In the studies where caffeine was given alone (as within coffee or in capsular form) at worst the researchers found no change in body weight or body composition, but not a negative change. So, the population where your theory might apply is in the sedentary or already overweight individual.
LL: If there’s one thing I’ve learned in umpteen years of geeking-out, it’s that the human body is incredibly adaptable. Guys who are adjusted to a high fat diet (a couple of weeks) are going to have far fewer problems, I would think, with caffeine/coffee. They already exhibit elevated catecholamine and fatty acid levels in their blood. It’s simply a shift toward using a different fuel.
Now, high-carb individuals may very well be different. They have chronically higher insulin concentrations and are generally more dependent on the whole glucose-insulin thing. There could be real problems in this case, so I guess I’m agreeing with big John in this regard. But whether the high-carb/caffeine scenario plays a big role in the ridiculous prevalence of obesity in this country is still speculative. It certainly seems contributory, though.
And I may have said this, but increased fatty acids and epinephrine are “good” or “bad” depending upon timing relative to cardio as well. I purposely drink two cups of java 60 to 90 minutes before hitting the treadmill most mornings. It not only helps me drag my sorry keester out of bed, it serves a purpose metabolically. I want to mobilize and oxidize body fat. By the time I’m done, 45 minutes later, I’ve got to believe that my “post-exercise carb window” is still largely in effect. Then I go for the instant oatmeal. I figure that catachols and fatty acids are going to be elevated from the cardio anyway, and I can’t believe that my morning treadmill session is inducing significant glucose intolerance.
JB: Okay, so I think we’ve all agreed that timing and dose of caffeine intake are crucial factors in this debate. In addition, it’s important to note that we all agree that sedentary individuals and those prone to diabetes are most at risk for caffeine induced insulin resistance. While we can’t say conclusively whether or not caffeine intake will present body composition problems for exercising individuals, there’s no doubt that metabolism will be altered by caffeine intake in this population.
Okay, we’ve focused most of this roundtable on the bad and the ugly; what about the good?
LL: That’s right, caffeine nazi, let’s not forget the good stuff. Caffeine has been repeatedly shown to preserve muscle glycogen during exercise, to improve mental focus independent of and during exercise, to improve exercise performance, to combat fatigue, to raise metabolic rate, to possess antioxidant properties, and it might even help prevent Parkinson’s disease and certain cancers.
JB: Agreed. While we can get metabolic increases from exercise and antioxidant effects from scores of other vitamins and nutrients, it’s probably a good idea to use caffeine before exercise or to stay awake if you’re the night watchman at Osgood Corporation. Remember, though, the mental alertness benefits of caffeine often fade with habituation so use it only when necessary if you desire its feel good/mental sharpness effects.
To be quite honest, in the past I was quite a coffee “pot head” as Lonnie likes to call it, especially before training. I’d brew up a strong pot of coffee and drink 20 oz of the bitter blend from my Superman mug. After about thirty minutes I’d head off to the gym and I can assure you, my workouts were intense. I gave up this practice because I believe it was causing regular headaches. However, I do miss it. Therefore even the supposed “anti-caffeine” guy believes that there’s a time and a place for coffee use (as long as it doesn’t cause you to feel like you’re getting kicked in the teeth after the effects wear off).
DK: Hey guys, don’t forget that it tastes good, too! From a medical standpoint, caffeine is also used in migraine medications and certain headache treatment formulas, so coupled with the noted benefits, it sounds like a winner to me. Too much of anything can have a negative effect, but if you understand moderation, caffeine is a good friend.
JB: How about some concluding remarks, guys.
DK: I’d like to point out that if a reader is concerned with “insulin resistance” that he should go have a fasting blood test done where insulin and glucose is tested. If your fasting insulin is above 17 micro IU/ml and the glucose is normal (<126 mg/ml), you have peripheral insulin resistance. If both the insulin and glucose are high, medication might be indicated as well as a formal test for diabetes. As far as for us, I think that this whole caffeine issue is really being overblown.
LL: I think “caffeine consequences” depend upon a myriad other lifestyle factors. I know this conclusion sounds like a copout, but think about it. Exercise is an enormous factor, so is the amount of muscle mass one carries, so is time of day (glucose tolerance sucks in the evening anyway), and I’ll bet the macronutrient profile of one’s diet matters too. Overall, I’ll admit that if caffeine contributes to adiposity or retards muscle growth even to a small degree I wouldn’t want to abuse it.
Guys with a family history of diabetes or who feel they don’t metabolize carbs well should be especially wary. And John’s lit review is enough to make me avoid caffeine during creatine and carb-loading (when insulin function is important). Keeping an open mind as data emerges is part of the game and this whole roundtable has left me a bit more cautious. Thanks Big John, you omniscient (but slightly paranoid) stud, you.
JB: While I’m getting sick and tired of agreeing with Lonnie during these roundtables, I’ll have to do so again. I am indeed an omniscient stud! Besides that, I tend to take the data a bit more seriously than Doug does. While caffeine may not be the new “silent killer,” the knowledge of its effects has to take its rightful place in the planning of any nutritional scheme.
While caffeine intake certainly won’t make you fat or diabetic, regardless of who you are, it may increase your glucose and insulin responses to meals and therefore thwart the effects of some of your low glycemic eating. But remember, dose is important. Small doses of caffeine may not be harmful. Timing is important, too. Taken immediately before exercise, caffeine may do some good things. As usual, more data is needed to clarify all the specifics, but in the meantime we’ll keep you on the cutting edge of nutritional science.