Protein Slows Digestion? Nope.

By Jordan Feigenbaum MS, Starting Strength Staff, CSCS, HFS, USAW Club Coach

In response to this gem of an article. I answered this on the Starting Strength nutrition forum, but I thought I’d repost it here. The article’s claims are italicized and my responses are in bold. 

The food that we consume is absorbed and its nutrients are subsequently sent to different organs through the blood.

The food that we consume is absorbed and its nutrients are subsequently sent to different organs through the blood. Not really the case literally. Protein and carbohydrates get absorbed as amino acids and monosaccharides through the small intestine’s brush border> into the enterocyte (cell)> into the portal vein> to the liver first before going anywhere else, then they get distributed based on lots of factors.

Fats get absorbed as fatty acids directly into the enterocyte (cell) and packaged into the chylomicron (with cholesterol, phospholipids, etc.)> into the lymphatic system> into the venous circulation and then go to some tissues, but mainly those who express high levels of mitochondria for beta oxidation or peroxisomes for long chain fatty acid oxidation. Principally, these are the liver and skeletal muscle.

However, a slow or sluggish digestive system isn’t able to perform its assigned function effectively. That is why a person experiencing a bout of slow digestion is bound to feel extremely uncomfortable post lunch or dinner. Nausea, bloating and vomiting are the most common symptoms of sluggish digestive system that occur after having meals.

Notice they do not define a normal GI transit time for a mixed meal, a slow GI transit time for a “bad” meal, nor do they distinguish between a pathologically slow state like gastroparesis or ileus or obstruction and a “slow” transit time occurring due to a specific meal composition. Yes, there is a marked difference.

Constipation or common digestive problems like diarrhea and irritable bowel syndrome can make the digestive system sluggish.

Diarrhea is actually the GI contents moving too fast. IBS has physiological symptoms of a combination of diarrhea, constipation, abdominal pain, and abdominal bloating. Seems like it might not make the digestive system sluggish, right? Though if you’re constipated, sure (and fiber and/or some probiotics tend to improve symptoms by increasing motility and osmotic pressure in the intestine to propel the contents)

Although protein is good for health, excessively high amounts of protein in the diet can slow down the digestive health. This is because, the body has to really work to digest protein.

Not the case at all. Proteins are initially broken down via the acidic pH of the stomach (and further in the small intestine by pancreatic enzymes that are all part of our normal physiology) and are absorbed very rapidly into the portal circulation. Whey, for instance- spikes blood plasma levels of amino acids (digestive end products of protein) within 20 minutes of ingestion.

Mixed meals confound the “speed” component, i.e. what is the fat content (slows gastric emptying), fiber content (soluble slows, insoluble speeds), total kCal content (larger is slower), tonicity of the meal (isotonic empties faster than hypo or hyper tonic from the stomach to the small intestine), etc. In addition, the hormonal milieu at the time with respect to previous meals also influence gastric transit time. Ghrelin, for instance- increases when you’re hungry and increases the motility of the gut.

Don’t forget about existing food in the GI tract. See how this is quite complicated to talk about? Let’s not forget about drugs….

At any rate, Carbohydrate rich and protein rich foods empty at about the same rate, but normal gastric emptying following a meal is 2-6 hrs….so yea- perhaps this whole article is a bit silly, eh?

Unlike simple carbohydrates, proteins are heavy, hence are not easy to digest and so when its presence is alarmingly high in everyday meals, the consequence is a slow digestive system.

Now this is easy to see that this is wrong…

People with intestinal problems such as Crohn’s disease tend to have a sluggish digestive system besides bowel dysfunction (diarrhea or constipation), vomiting and stomach pain. In this condition the lining of the small and large intestine are inflamed. However, in most cases, the swelling infiltrates in the inner layers of the bowel tissue. This chronic inflammatory disease considerably slows down digestion as the food tends to move at a very slow pace through the intestine.

Fuark. Crohn’s is, currently, a dysregulation of inflammation in response to bacteria in the walls of the GI tract, which results in proinflammatory substances causing direct mucosal injury.

Crohn’s usually presents with diarrhea, fatigue, weight loss, and crampy abdominal pain plus oral ulcerations, perianal fissures, perirectal abscesses, and malabsorption BECAUSE THE FOOD CAN’T BE ABSORBED BECAUSE IT’S MOVING at a normal speed but the mucosa can’t absorb it.

A point to note that although food is digested in the stomach, most of the digestion occurs inside the intestine. Experts say that the intestine is the place where nutrients are observed and eventually circulated in the bloodstream to various parts of the body. However if the food stays for longer time in the stomach, this can affect the digestion process. This condition is known as gastroparesis, in which the stomach takes more time to transfer the ingested food to the intestine. This happens because the stomach muscles that are assigned the task of pushing the food to the intestine, lose their ability to work efficiently. Gastroparesis is the result of malfunctioning of the vagus nerve that regulates movement of muscles lining the stomach wall.

Most common KNOWN causes of gastroparesis:

1) diabetes mellitus
2) idiopathic
3) post-surgical (especially if vagus nerve damaged)

Other causes:

-etoh and tobacco, weed
-infection (mono, chagas, rotavirus)
-CNS injury like a tumor or cerebrovascular event
-PNS pathology (parkinson’s or guillan barre)
-other issues (cancers, hypothyroid, lupus, intestine obstruction, portal hypertension, HIV, stroke and migraines)

So…yea, protein is UNLIKELY to be the cause of “slowed” gi emptying….



When Should You Do Conditioning?

By Jordan Feigenbaum MS, CSCS, HFS, USAW Club Coach, Starting Strength Staff

If you haven’t seen this article yet give it a read, as it should set the tone for this blog post. Just as an aside to those who disagree with this blog post or Mark’s article, save the ad hominem attacks and please present your analysis within the context of both anecdotal evidence and scientific evidence. If you’re going to use the latter, please make sure you read the entire study and look at the data before you make claims, as it will save everyone a lot of time and you some future embarrassment if you, ya know, missed something.

At any rate, I recently got hit with this statement and was asked for a response:

Quick question for you-my friend goes to Gold’s and one of the trainers there said it is “better to do cardio before weights”. I would love to get your opinion on the matter.

So instead of calling into question the validity of a trainer’s opinion who works at a Gold’s gym, which would be an ad hominem attack that doesn’t really address this statement, I thought I’d do this in a blog post about conditioning in general. I’m saving the heavily annotated discussion of this topic for my book and thus, this will merely be a reflection of what I believe the current science says and my experience in working with people as a coach.

To begin, we need to talk about what the goals of a training program, in general, actually are for an individual. In other words, WHY IS A PERSON TRAINING? If there is no clear-cut goal, I’d make the semantic argument that the person is just exercising for no particular reason, which is fine too. On the other hand, if a person does have a specific goal, yet is not taking specific steps to achieve this goal then the person’s training is, by definition, suboptimal. In short, we need to clarify what is the goal of the person we’re answering this question [When should I do conditioning?] in order to provide an accurate answer. Additionally, we need to get a clearer picture of what exactly the person is doing training or exercise wise depending on their current level of commitment to their goal. As you can see, there are lots of unknowns here that we can’t possibly answer and thus, the discussion needs to shift to be more general. So what we’ll do is go over the important considerations to determine optimal conditioning timing, frequency, etc. with respect to three general goals:

  1. Health
  2. Weight Loss
  3. Performance

Here’s the first question: How much conditioning* training is optimal? (cue explosions for dramatic affect)

* conditioning can be considered analogous to cardio (low intensity steady state-LISS, High intensity interval training (HIIT), circuits, etc.)

I’d make the argument that within the context of an individual who is following an intelligent training program that’s centered around planned progressive overload of the big lifts, e.g. the squat, bench, deadlift, press, power clean, and chin/pullup, that the optimal conditioning volume (total frequency and duration of conditioning efforts) should be the smallest amount needed to produce the desired goal. Let’s look at this from the health perspective first.

We know that training increases oxygen delivery to tissues, causes adaptations at both the tissue (macro) and cellular (micro) level, and alters hemodynamic properties (hemoglobin, blood viscosity, etc.) that all result in increased capacity to do work and sustain activity. The real question we should be asking from this perspective, however, is what sort of training most optimally reduces major negative health outcomes…ya know, like death, cancer, cardiovascular incidents, etc. Well, as it turns out the literature suggests that the stronger someone is, i.e. the more force they can produce with their muscles to move an external object, the lower the morbidity and mortality rates when compared to both sedentary populations and those who were more “aerobically developed” from doing typical conditioning/cardio training and, more interestingly perhaps, the same rates of morbidity and mortality as those who were the strongest and the most aerobically developed. As it turns out, there’s more than a nugget of truth on ol’ Rip’s adage:

Stronger people are harder to kill than weaker people, and more useful in general”-Mark Rippetoe

Does this mean I’m saying people who are training/exercising for health purposes shouldn’t do any sort of conditioning? No, that’s not what I’m saying. I’m implying that you get a pretty decent stress from weight training to drive conditioning adaptations that have an observably profound effect on clinical outcomes. If you desire additional capacity for another purpose, i.e. you want to be able to run further/faster or have more “wind” when doing a particular activity (e.g. pick-up basketball), then doing some supplemental conditioning work will be useful in achieving these goals. However, let’s not be confused with what the literature is saying about how this will affect health.

This being said, if someone is not training in an intelligently implemented manner with a focus on the only incrementally loadable, systemically stressing modality there is, e.g. barbells, then he or she will need to do more conditioning work in order to supplement the lack of actual training stimulus he or she is getting from the gym. High intensity interval training (HIIT) is the obvious choice, as the adaptations and metabolic responses to this style of conditioning tend to mirror that of resistance training, whereas low intensity steady state cardio pales in comparison (though there is a purpose for this style training that we’ll discuss alter).

HIIT causes the skeletal muscles to move to relatively high velocities and contract with high forces compared to LISS. Because the demand for energy is so high during HIIT, it is appropriately referred to as anaerobic or glycolytic training, as the rate of energy production is so high that aerobic (with oxygen) energy producing pathways can’t keep up. When done appropriately, HIIT increases basal metabolic rate (BMR) significantly over many hours post exercise (more calories burned in total), increases mitochondria biogenesis (makes new energy producing and calorie burning power plants in the cell to increase BMR chronically), increases skeletal muscle’s uptake of nutrients (instead of fat), does not cause muscle catabolism (like LISS), and results in even more pronounced cardiorespiratory conditioning adaptations in the heart, lungs, and vascular tissues. HIIT works so well, clinicians are using it in COPD, MI, and Obese patient populations instead of LISS. Just sayin’…..

In sum, I don’t think there’s a good reason to do tons of conditioning work if you’re just interested in health UNLESS you need the extra conditioning work to produce other desirable changes, e.g. performance increases or fat loss.

So, how much conditioning is optimal for increasing performance? The answer (duh), is IT DEPENDS ON YOUR SPORT. If you’re a marathoner you’re obviously going to have a higher total conditioning volume than a weightlifter. Similarly, the types of conditioning are going to be different. Marathoners need steady state “tempo” work in order to develop efficiency in running, which is more strength and strength-endurance limited than it is limited by someone’s lungs/heart. In other words, you don’t stop running because you’re out of breath, you stop running because your legs are tired. This is a strength deficit, through and through, which is ameliorated by actually training to get strong AND doing longer runs to acclimate the body to become more efficient at running and therefore require less energy. If you’re a weightlifter, the only reason you’re doing conditioning is to improve your ability to lift weights, i.e. put pounds on the bar or improve recovery enough to increase training frequency (by being better conditioned) to aid in putting weight on the bar.

So the optimal amount of conditioning for a marathoner and a weightlifter are different, but the answer is still the same as what we covered in the health section, i.e the smallest amount needed to produce the desired goal. This will, of course, be different for everyone.

I bet you already know the answer to how much conditioning is optimal for weight loss (and you’d be correct): the smallest amount needed to produce the desired goal. Basically, we want to get the most out of the least so we have somewhere to go when we get stuck. Anyone who’s ever gotten really lean knows about getting stuck, which requires manipulation of conditioning efforts (usually adding more), training, and food intake (usually small reductions in carbs and fat). Unfortunately, people get greedy with results and think MORE IS BETTER, and cut out a bunch of energy (calories) and add a bunch of conditioning. Truth is, more isn’t better; BETTER IS BETTER.

By removing a bunch of calories when it’s not needed or, equivalently, adding a bunch of conditioning when it’s not needed you miss out on getting the best return on investment (ROI) possible and are, for no reason, reducing the amount of food you’re eating and increasing the amount of activity you’re doing. What do you think the body is going to do? It’s gonna say “Screw you guys I’m going home!”

Look, two things are happening here.

Thing 1: With calorie restriction, which is needed to lose weight, your metabolism slows down.

Thing 2: If your conditioning is mostly LISS, your metabolism slows down, i.e. you become more efficient at creating energy (no, this is not good). The current thinking on this mechanism has to do with reduced expression of uncoupling proteins in the mitochondria, which normally make the mitochondrial less efficient at creating energy (ATP).

So, imagine all the typical cardio bunnies starving themselves and doing hours of cardio on the elliptical; low intensity mind you because how are you supposed to read Elle magazine when you’re doing HIIT? Their metabolisms are slowing down from both ends and then boom, a big blowout weekend (or week) and what happens? Lots of fat deposition because their metabolisms are so depressed it’s the only thing that can happen. Yes Virginia, their BMR will increase transiently due to the “refeed” of a hypercaloric couple of days, but lots of adipose tissue will also get stored.

So, in short….how much conditioning should you do? The smallest amount needed to produce the desired goal.

The next question is rather obvious, what is the purpose of conditioning?

From a health perspective, there’s really not a lot of purpose for pure conditioning modalities unless it’s either facilitating another related (e.g. fat loss) or unrelated goal (e.g. more conditioning for sport) OR the person isn’t training and therefore needs something to supplement them.

From a performance standpoint, the purpose of conditioning is to drive the adaptations specific to that sport. Returning to the marathoner vs. weightlifter, the marathoner is obviously going to spend more time doing steady state stuff and their interval work will have different work to rest ratios (1:1-1:3 will be the bulk of it) versus the weightlifter not doing hardly any steady state stuff and sticking to interval work with 1:5-1:20 work to rest ratios. The only exception to the “drive the adaptations specific to that sport” mantra is if the sport is a weight class sport and thus the conditioning’s purpose may also include fat loss/weight manipulation

From a weight loss perspective, the purpose of conditioning is fat loss pure and simple. HIIT trumps LISS in this regard, as even though a longer LISS session certainly burns more calories during the activity, the HIIT burns more calories in total than the LISS by increasing resting metabolism over the course of hours-days post workout. People will say “Well you burn a higher percentage of fat doing LISS than HIIT”, which is true. On the other hand, I don’t really care about the percentage of fat I burn, I care about the total number of fat I burn, which is much greater in HIIT since the total energy expenditure is much higher. Kind of a dumb argument if you ask me.

The final question, which is the original motivation for even writing this things is: When should you optimally do conditioning?

Now, there’s really no reason to discuss the health perspective on this since the only reason to do conditioning for health is in order to increase performance or improve fat loss so we’ll stick with those.

Performance-wise, this all depends what kind of athlete you are. If you’re in a sport that’s conditioning focused then there will likely be plenty of times you’re going to be doing conditioning only during practice or programmed sessions. I could make the argument that if there are skills you need to practice that these should be incorporated first before the conditioning work, as it is highly fatiguing and might interfere with practicing optimal technique of the skill. This is the same for strength/power training, i.e. it should come first for virtually any athlete who’s going to train multiple modalities in the same day even if he or she is going to split them up into multiple training sessions in the course of the day (i.e. 2 or 3-a days). Will doing a heavy squat session first or in the AM negatively impact the ability to do a long tempo run second or in the PM? Of course, duh. However, the squat session is going to have less of an effect on the run as the run would have on the squat. Moreover, the runner is going to get a more useful stimulus from the squats than the run provided the context we’re discussing is the off season or GPP/accumulation phases. On the other hand, I could make the argument that during more specific training phases or in-season cycles, the runner should run first and then do a lighter, more attenuated squat session later to try and preserve strength during the season. Applying this same rationale to a weightlifter and the answer becomes crystal clear, conditioning comes after the weights 100% of the time with respect to developing performance.

When talking optimal conditioning timing concerning weight loss, the answer is really even clearer in my opinion. Optimally, you’d do conditioning (HIIT mostly) on your OFF days, i.e. days you’re not training with weights. See, resistance training provides a super potent stimulus to the body to increase metabolism, burn calories for hours post workout, partition nutrients favorably, and otherwise adapt to the stress imparted upon it. Adding conditioning workouts to a resistance training session, therefore, is not optimal in that you’re already getting a big time stimulus from training anyway and there’s MORE benefit to be had by doing it on your off days where you where previously receiving no stimulus (or a waning stimulus from the previous day’s training). Remember, the goal here is to signal as much possible increase in BMR, favorable nutrient partitioning, and net calorie burn as possible.

Understandably, many people do not have a flexible enough schedule to do this and so the crux of the matter becomes this: Should I do cardio before or after weights? Answer (you probably already know this): AFTER!!!!

Resistance training provides a more potent stimulus than conditioning, period. Why? Because resistance training is heavier, has longer ranges of motion, and overall imparts more stress on the human organism (or at least it should). If you did conditioning before training, you’re fatiguing motor units, depleting the muscles of energy, and overall reducing possible intensity, volume, etc. that could possible be attained in the session as a whole. Now, weight training first will certainly attenuate the amount of intensity or effort a person can put into conditioning but this is not as severe as the opposite since, ya know, conditioning is easier than burying a heavy squat.

My stock recommendation for those who have to get in and out of the gym in an hour and can’t train more than 3-4x a week is as follows: Spend 45 minutes doing progressively heavier barbell training and 15 minutes doing HIIT everytime. Period.


Booze and Barbells Part II

By Jordan Feigenbaum MS, Starting Strength Staff, CSCS, HFS, USAW CC

In case you missed part one of this three part series, click here. In today’s blog entry we’re going to talk about how alcohol affects skeletal muscle and the sex steroid, testosterone. Things can get pretty complicated in a hurry here, but what I aim to do is provide some basic science background for my readers as well as how a certain stressor, i.e. alcohol, can alter the internal milieu. I actually just used the words “internal milieu”, which describes the internal environment of the human body just so I could provide the following quote to pay homage to my previous physiology professors:

“The stability of the internal environment [the milieu intérieur] is the condition for the free and independent life”- Claude Bernard

The concept of the internal environment being important for physiological normalcy and a rationale for the human body’s homeostatic underpinnings was later expanded upon by Walter Canon’s characterization of homeostasis in 1932. He [Canon], proposed four characteristics of homeostasis as follows:

  1. Constancy in an open system, such as our bodies represent, requires mechanisms that act to maintain this constancy. Cannon based this proposition on insights into the ways by which steady states such as glucose concentrations, body temperature and acid-base balance were regulated.
  2. Steady-state conditions require that any tendency toward change automatically meets with factors that resist change. An increase in blood sugar results in thirst as the body attempts to dilute the concentration of sugar in the extracellular fluid.
  3. The regulating system that determines the homeostatic state consists of a number of cooperating mechanisms acting simultaneously or successively. Blood sugar is regulated by insulin, glucagons, and other hormones that control its release from the liver or its uptake by the tissues.
  4. Homeostasis does not occur by chance, but is the result of organized self-government.

It is important to appreciate the homeostatic mechanisms that the human body possesses in order to maintain an “even keel”, as without redundant pathways in place things can go awry in a hurry. At any rate, while the overall concept of the internal milieu and it’s influences on homeostasis are critically important, further discussion of it would preclude our look at just how alcohol/ethanol can alter skeletal muscle metabolism and testosterone levels. To begin, let’s talk a bit about skeletal muscle.

One of the most common effects of alcohol on striated muscle, i.e. skeletal and cardiac muscle, is fiber atrophy or reduction in size. Skeletal and cardiac muscle are both striated, as they have repeating sarcomeres and appear (under the microscope) to have alternating “light” and “dark” bands.

Screen shot 2013-06-12 at 6.07.19 PMSmooth muscle on the other hand, which is found in lots of places like the walls of the vascular system and the GI tract, do not appear striated under a microscope because they lack the organized, repeating structure of the sarcomere.

At any rate, striated muscle size is a result of the balance of protein synthesis and protein breakdown. In other words, the net flux of protein reflects the protein being built (synthesized) and deposited minus the protein being broken down and metabolized. If something were to either increase protein synthesis or inhibit (prevent) protein breakdown, their would be a net gain in protein levels. On the other hand, if the rate of protein breakdown is increased OR the synthesis of new protein is inhibited, there will be a net loss of protein. In general, a net gain of protein within muscle tissue results in hypertrophy (increased size) and a net loss of protein in the muscle tissue results in atrophy.

Ethanol tends to decrease striated muscle protein synthesis [1]. Interestingly, the resulting atrophy appears to be greatest in Type IIB fibers, which are a subtype of the fast-twitch muscle fibers that produce high amounts of force, contract rapidly, and are anaerobic. Some researchers actually classify type II muscle fiber atrophy as part of a diagnostic criteria of alcoholic myopathy, however this selective decrease in size also occurs in other issues like calorie malnutrition, neuropathy, etc. Additionally, only about 33% of chronic asymptomatic alcoholics show significant type II fiber atrophy without malnutrition, neuropathy, etc. although other studies report 40-60% of alcoholics presenting with significant atrophy [1]. Urbano et al. goes head to head with Preedy et al in the following quotes:

In fact, it [ethanol] is the most frequent cause of toxicity to striated skeletal and cardiac muscle in adults in dose dependent fashion [1].

“Due to the ethanol-induced reduction of muscle phosphorylase activity, decreased rates of protein synthesis and whole-body protein metabolism by 15–30%, predominantly in type II fast-twitch anaerobic fibers that utilize glycolytic metabolism.Type I fibers were not overly affected and there was no clear decrease in muscle protein breakdown [5].

As far as how this occurs on a cellular level, it appears as though ethanol consumption disrupts the translation of would-be muscle-protein RNA, but not it’s transcription. For background information, muscle protein synthesis signalers (like eating a protein-rich meal or training) increase the transcription of certain DNA to muscle protein RNA. Muscle protein RNA is then translated into muscle protein, which is shuttled to it’s target and deposited as muscle. Through increased binding of a variety of different regulatory sites on the muscle protein RNA, translation is decreased and total muscle protein synthesis decreases [2].

Measuring decreases in total muscle protein synthesis can be tricky in the laboratory settings, as most of the time a total nitrogen balance measurement is used. Remember, protein is the only macronutrient with nitrogen as a component. Therefore, it intuitively makes sense that the amount of nitrogen taken in minus the amount of nitrogen excreted can give insight into the nitrogen balance of a person or animal. Unfortunately, some people take this sort of information as definitive with regards to what is actually happening in the muscle specifically. Remember, all tissues (lungs, gut, kidney, visceral organs, etc.) are made up of protein, which are also turned over regularly and thus influence total body protein and nitrogen balance. Lang et. al. provide a nice quote describing this:

However, whole body measurements represent the sum of many vastly different organ systems (e.g., muscle and nonmuscle protein synthesis and hepatic secretory protein synthesis) and provide little information concerning individual processes or tissues.

So while total body nitrogen balance tells us what’s happening on a body wide or systemic level, it does not tell us what’s happening in just the muscle tissue. Muscle protein turnover, in sum, makes up less than 30% of total body protein turnover anyway [3]. Other studies, however, have shown that with acute alcohol intoxication muscle protein synthesis decreases in skeletal muscle, heart, intestine, bone, and skin. Additionally, chronic ethanol exposure has been demonstrated to decrease skeletal muscle protein synthesis in rats [4, 5]. It appears that ethanol exposure is potentially harmful to overall protein synthesis, as described in the following quote:

“However, experimental and clinical studies have clearly demonstrated that ethanol itself is a direct noxious agent to heart and skeletal muscle in a progressive, cumulative, and dose-dependent manner, an effect independent of nutritional, vitamin, or mineral factors.”-[Nguyen et al. (6)]

There are only a couple of things left to discuss with respect to actual skeletal muscle function and ethanol. First, muscle glycogen concentration tends to increase in chronic alcohol patients because glycogen cannot be degraded as efficiently. This is due to a partial inhibition of the biochemical pathway for glycogenolysis (glycogen breakdown) as well as glycolysis (glucose breakdown) [5]. In contrast, acute alcohol exposures tend to decrease glycogen storage, especially post workout as some of the mechanisms used to store glycogen in skeletal muscle are inhibited and instead fatty acid production is increased. These effects are independent of acetaldehyde toxicity, which was discussed in part one of this series [5].

Ethanol and acetylaldehyde also tend to increase formation of reactive oxygen species due to their effects on vitamin metabolism. Reactive oxygen species (ROS) tend to increase cellular damage and stress in the skeletal muscle, thus increasing damage to cells of the muscles which may increase atrophy.

Moving along, let’s start our discussion about alcohol and testosterone production by covering the general overview of testosterone production in vivo (in the body). This will give us some background to what is normal so we can consider the effects of ethanol on the internal milieu and homeostasis.

Gonadal-AxismennewestNormally, males produce testosterone in the Leydig cells of the testes from cholesterol via increasing leutinizing hormone (LH) activity within the testes. LH increases an enzyme called cholesterol desmolase, which is responsible for converting cholesterol to pregnenolone. Pregnenolone will go on to be converted through various enzymes to testosterone and thus, but first it needs to be formed from cholesterol. Thus, increasing the enzymatic activity of cholesterol desmolase helps to increase testosterone production.

Naturally, one would ask well what increases LH? Gonadotropin releasing hormone (GnRH) is secreted by the hypothalamus in the brain. GnRH is released into blood vessels that carry this peptide to the anterior pituitary gland (hypothalamic-hypophysial portal system). GnRH is normally secreted in a pulsatile fashion, i.e. it is not constant. It acts on certain cells in the anterior lobe of the pituitary gland (gonadotropes) to cause them to manufacture and release LH, which is also released in a pulsatile fashion. LH is released into the systemic (body-wide) circulation where it ends up traveling to the testicles and causing the Leydig cells to pump out testosterone, as described above.

As discussed at the beginning of this post, most, if not all of the body’s pathways are tightly regulated to keep it on an “even-keel”. Let’s explore this now that we know the testosterone-producing pathway. Testosterone produced by the Leydig cells provides what’s known as “negative feedback” on the hypothalamus and cells of anterior lobe of the pituitary, effectively decreasing secretion of GnRH and LH. Thus, when testosterone levels are high, GnRH and LH levels are low. Conversely, when testosterone levels are low, the frequency and amplitude of GnRH pulses are increased. A downstream effect of this is increased LH release and thus, increased signaling to the Leydig cells to produce more testosterone because the negative feedback signaling is removed.

As we’ll see in the upcoming discussion of ethanol’s effects, perturbation at any level of this pathway can result in deleterious effects. So, how does ethanol affect testosterone production and/or signaling?

As it turns out, ethanol exposure appears to lower GnRH levels, which leads to reduced LH secretion from the anterior pituitary and reduced testosterone production by the Leydig cells of the testes [7]. Mechanistically, this occurs because a hormone normally produced in the testes and hypothalamus at very low levels, β-endorphin (an endogenous opiod), normally only slightly suppresses testicular testosterone production and release. In the hypothalamus, β-endorphin results in decreased GnRH release. Adams and Cicero have shown an increase in β-endorphin after acute alcohol exposure [10]. Naltrexone, a treatment currently used in alcoholism to decrease alcohol cravings, blocks B-endorphin activity and may prevent reduced testosterone levels. Three other ways ethanol affects active GnRH levels is through acetalaldehyde, which is toxic, disturbing nerve impulses outside the hypothalamus that signal GnRH production WITHIN the hypothalamus, and finally, ethanol appears to interfere with processing of the inactive GnRH precursor to the active GnRH form according to Uddin et al.

LH levels actually decrease with alcohol exposure, which is not what we’d expect. Harkening back to our homeostatic mechanism discussion, if testosterone production falls, we’d expect GnRH and LH levels to increase to “right the ship”. However, as discussed above GnRH levels actually decrease and so do LH levels. Mechanistically, the decreased LH levels appear to be due to the toxic affect of ethanol directly on the anterior pituitary gland where LH is released by interfering with GnRH’s signaling of LH production in the cells that they act on (gonadotropes). Another effect of ethanol on LH that causes it’s decrease is that alcohol in the blood tends to result in the anterior pituitary gland’s production of less potent LH variants, thus decrease the level of LH in the blood and the quality of LH in the blood too.

A study done by Steiner and colleagues in 1996 found that when males were given a 15-percent alcohol solution that was administered every 3 hours, around the clock, together with a diet replete with protein, vitamins, folic acid, and minerals (total daily alcohol dose was 220g or 3g/kg body weight, which equals 15 drinks) that the testosterone levels in the men’s blood declined 5 days into the study and continued to fall over the entire period. This was attributed to a decrease in testosterone production in the Leydig cells of the testes and increased removal rate of testosterone from the blood via catabolic processes. On the other hand, Southren et al. found that the increased testosterone catabolism or breakdown is only present in men without liver disease, whereas the clearance is decreased in men with liver disease.

Numerous studies in human and animal models have since confirmed reduction in testosterone levels after either acute or long term alcohol exposure. Acute alcohol ingestion appears to result in a significant reduction in testosterone levels that lasted for 96 hours in a rat model [9].

Sarkola and Eriksson actually found that testosterone can increase in men exposed to a low dose of ethanol, although this is a transient effect due to the predomination of decreased liver clearance of testosterone from the blood compared to the decreased testosterone production in the testes. Unfortunately, during the latter stages of elimination of alcohol or when alcohol has been completely eliminated, testosterone production decreases even more. Similarly, in higher doses of alcohol consumption, e.g. 1.5g/kg, the decreased production of testosterone predominates over the transient decreased clearance rate of testosterone. This has been confirmed by experiemental evidence from Välimäki et al in 1990 and Ylikahri et al. in 1974 [10].

Another interesting finding is that alcohol abuse and subsequent impaired testosterone production tends to result in testicular atrophy/shrinkage, which occurs in about 75% of men with advanced cirrhosis [10]. The atrophy most likely results from the toxicity on the testes, decreased LH and FSH production, and other confounding factors causing decreased sperm cells and sperm production.

Finally, and perhaps one of the more important ways alcohol effects testosterone’s activity and blood levels is that ethanol exposure tends to increase aromatization of testosterone and testosterone precursors. Aromatase is an enzyme that converts testosterone to estrogen and thus, increased aromatization results in increased conversion of testosterone to estrogen. Additionally, the immediate precursors to testosterone, androstenedione (Mark McGwire?) can be “aromatized” to another estrogen subtype called estrone. Scientific evidence points to this “increased aromatization” as a byproduct of increased estrogen production and not a decrease in estrogen clearance [10]. Aromatization is not a good thing above physiological normal (homeostatic) levels in men, as the authors conclude:

“In addition to causing breast enlargement, estrogens appear to exert a negative feedback effect on LH and FSH production and may thereby contribute to alcohol’s suppression of those key reproductive hormones.”

While alcohol certainly has some benefits, which we’ll get to I PROMISE, it’s important to know the deleterious effects that alcohol can have on the internal milieu, especially as it pertains to training. Again, I’ll leave you with my favorite axiom related to alcohol consumption and training:

“If you’re drinking enough to get drunk, you’re drinking enough to mess with your results.”


Until next time.


1)  Urbano-Marquez, A.; Fernandez-Sola, J. Effects of alcohol on skeletal and cardiac muscle. Muscle Nerve 2004, 30, 689-707.

2) Lang, CH, Wu, DQ,  Frost, RA. Inhibition of muscle protein synthesis by alcohol is associated with modulation of eIF2B and eIF4E. American Journal of Physiology-Endocrinology and Metabolism 1999, 277, 268-276.

3) White JP, Baynes JW, Welle SL, Kostek MC, Matesic LE, et al. (2011) The Regulation of Skeletal Muscle Protein Turnover during the Progression of Cancer Cachexia in the ApcMin/+ Mouse. PLoS ONE 6(9)

4) Preedy V. R.,Peters T. J.,Patel V. B.,Miell J. P. (1994) Chronic alcoholic myopathy: transcription and translational alterations. FASEB J. 8:1146–1151

5) Preedy V. R., Peters T. J. (1990) Changes in protein, RNA, DNA and rates of protein synthesis in muscle-containing tissues of the mature rat in response to ethanol feeding: a comparative study of heart, small intestine and gastrocnemius muscle. Alcohol Alcohol. 25:489–498.

6) Nguyen VA, Le T, Tong M, Silbermann E, Gundogan F, de la Monte SM. Impaired Insulin/IGF Signaling in Experimental Alcohol-Related Myopathy. Nutrients. 2012; 4(8):1058-1075.

7) Vatsalya Vatsalya, Julnar E. Issa, Daniel W. Hommer, and Vijay A. Ramchandani. Pharmacodynamic Effects of Intravenous Alcohol on Hepatic and Gonadal Hormones: Influence of Age and Sex. Alcohol Clin Exp Res. 2012 February; 36(2): 207–213.

8) Sarkola, T. and Eriksson, C. J. P. (2003), Testosterone Increases in Men After a Low Dose of Alcohol. Alcoholism: Clinical and Experimental Research, 27: 682–685

9) Steiner, J., Halloran M.M., Jabamoni K., Emanuele, N.V., Emanuele, M.A. Sustained effects of a single injection of ethanol on the hypothalamic-pituitary-gonadal axis in the male rat. Alcoholism: Clinical and Experimental Research 20:1368–1374, 1996.

10) Emanuele, N.V., Emanuele, M.A. (1998) Alcohol’s Effects on Male Reproduction. The Alcohol and Other Drug Thesaurus. Vol. 22, No.3.

The Truth About Gluten

By Jordan Feigenbaum MS, CSCS, HFS, USAW CC, Starting Strength Staff

Unless you’ve been living under a rock or living off the grid for some time, chances are you’ve at least heard about gluten and gluten-free diets. There is good reason for this as gluten and similar nutrients have been the subject of a flurry of recent research efforts and clinical observations. To begin, let’s talk about what gluten is and why we’re even bringing it up.

Gluten is a protein that’s found in all products containing wheat, barley, rye and other foods as a binding agent and even in some prescription drugs. Gluten generally increases elasticity of the dough and improves its texture to aid in palatability. It lets bread rise and maintain its shape as well.

Gluten is made up of what we call prolamin proteins. This essentially means that gluten is made of constituents rich in proline (prol-) and glutamine (-amin) and in wheat’s case, these prolamin proteins are gliadin and glutenin [1]. The prolamin proteins in barley, rye, and corn are: hordein, secalin, and zein, respectively. Oats also contain a prolamin protein known as avenin, although this is a rather minor constituent in comparison to the others.

I will detail how these prolamin proteins interact with our bodies later on in this article, but for now we can say that these proteins resist being broken down in the small intestine by the usual proteases and peptidases [2]. Proteases and peptidases are enzymes that help the body break down proteins from food we ingest for absorption in the small intestine. We can intuit that this might possibly be a bad thing as I’ll discuss later.

As mentioned before, gluten is a hot topic these days. Using the Google search engine and typing in “gluten free” results in over 82 million hits. Originally the topic of gluten intolerance or using a gluten free diet was limited to those suffering from celiac sprue disease. However, the number of those diagnosed with celiac disease has been increasing steadily in recent times, affecting approximately 1 in 133 Americans and countless undiagnosed people. It is important to understand that this disease commonly goes undiagnosed, for almost 11 years in most cases [3]. The issue isn’t a lack of a formidable test to diagnose celiac or gluten intolerance, the test exists and it is very specific, however it is not very sensitive- or at least not as sensitive as some clinicians would prefer. At any rate we cannot deny that “gluten” and “gluten-free” are buzzwords in today’s health and fitness world.

Consider this, in 2003 there were approximately 135 “gluten-free” food products were introduced to the market and in 2008 alone there were 832 introduced. The growth in the gluten-free food sector has recently been estimated to be 15-25%. Then there’s the bevy of research coming out of the medical field.

A New England Journal of Medicine (NEJM) article catalogued 55 diseases associated with gluten intake including : osteoporosis, irritable bowel syndrome, anemia, cancer, fatigue, canker sores, rheumatoid arthritis, lupus, multiple sclerosis, numerous autoimmune diseases, anxiety, depression, schizophrenia, dementia, migraines, epilepsy, neuropathy, and autism [4]. Government agencies associated with Celiac disease also report a decrease in symptoms for patients going on a gluten free diet with the following diseases: rheumatoid arthritis, Parkinson’s disease, neuromyelitis, Down’s syndrome, peripheral neuropathy, multiple sclerosis, seizures, ataxia and late-onset Freidreich ataxia, brain fog, osteoporosis, type 2 and type 1 diabetes mellitus, and anemia [5].

There are many reasons to believe that some people have become more intolerant of gluten as the generations go by. Celiac disease prevalence is increasing and reports of increasing sensitivity to gluten have also come to light. Plausible causes of this include the genetic manipulation of wheat and other grains, increased exposure to gluten, prolamin proteins in more and more food products at higher concentrations, and increased public knowledge of gluten intolerance or celiac itself[6].

While going gluten-free hasn’t been established as a weight-loss protocol in and of itself, anecdotal evidence disputes this with many people seeing weight loss as a nice byproduct of utilizing this diet. Some experts postulate that this is because without gluten in the diet overall calorie intake is decreased, while others claim it’s because gluten drives one to consume more palatable food. I tend to agree with this sentiment.

There is little certainty whether or not gluten is directly correlated to weight loss or gain, except in celiac patients that is. celiac patients often present with nutritional deficiencies stemming from malabsorbtion of digested food in the gut. When they switch to a gluten-free diet, however, their gut lining is repaired and they absorb more nutrients. So we could imagine that if a celiac patient ate a similar amount of food before and after the switch to a gluten free diet and now they are absorbing more nutrients than before, they might potentially gain some weight.

Interestingly enough, gliadin, which is found in gluten, exhibits what’s known as an ­insulin-mimetic effect. Gliadin mimics insulin’s effect on fat cells, that is, it attaches to the same receptor that insulin does on fat cells and causes it to incorporate glucose from the bloodstream into the tissue and store it as fat, just like insulin does. Insulin normally has a negative-feedback loop that keeps it in check. So when insulin levels rise more and more blood glucose is shuttled into the fat tissue and when blood sugar has been returned to a normal level insulin levels fall as the hormone (insulin) no longer interacts with its receptor. Gliadin, however, does not exhibit this negative-feedback loop and stays attached to the receptor and continues to exert its effect [7]. Also gliadin interacts with digestive hormones such as cholecystokinin (CCK), which is involved in regulating appetite control. This gliadin exerts a negative effect essentially blocking appetite control and potentially causing storage of fat via its insulin-mimetic effect [7].

With all that out the way let’s delve in to what foods contain gluten, how gluten and prolamin proteins interact with the body, and what, if anything, we should do about it! Gluten, as mentioned before, is in all products made of wheat, processed with wheat, or anything that uses wheat, barley, rye, or modified food starch. These foods include:

-beers, breads, candies, cakes/pies, cereals, cookies, crackers, croutons, gravies, imitation meats, pastas, processed lunch meats, salad dressings, sauces (including soy sauce), self-basting poultry, soups, maybe oats during production, modified food starch, medications/vitamins may use gluten as a binding agent, play dough

Foods that don’t contain gluten include:

– corn, gluten-free flour, polenta, rice, tapioca, fresh meat, fruits, most dairy, potatoes, vegetables, wine/liquor/cider/spirits

When we take in any food it’s usually through the mouth (hopefully) and digestion, but not absorption, starts immediately. From the mouth the food is compacted into a bolus as it moves down the esophagus and to the stomach. In the stomach some digestion takes place but it and all the previous digestion pales in comparison to what is to come, digestion-wise, in the small intestine. After passing through the stomach the partially digested food enters the small intestine which is about 21 feet long and comprised of three different parts listed here from beginning to end: the duodenum, jejunum, and ileum.

Digestion primarily occurs in the duodenum, whereas absorption primarily occurs in the jejunum and ileum. We can think about the small intestine as a long tube with finger-like projections known as villi. The layer of cells covering the inside of this digestive tube are called enterocytes and these cells interact with any and all of the digested food particles including gluten and its components gliadin and glutenin. Enterocytes are sealed off between each other by what’s known as a tight junctions (zonula occludens), which is made up of three distinct proteins: cadherins, zonulins and occludins. We can generally think of the tight junctions in the gut as being impermeable or resisting the transmission of any molecule, substance, or compound between the cells. In a healthy person this would mean that absorption of nutrients happens directly across the enterocyte (transcellular) and not in between them (paracellular).

We already know that gliadin and gluttenin are not digested by the enzymes in the small intestine, via proteases and peptidases, and as such they interact with the enterocytes directly [2]. When these prolamin proteins interact with enterocytes they cause a disruption of the tight junctions of the small intestine. They do this by binding to a zonulin receptor on the enterocyte which causes a release of zonulin, which was previously bound tightly, and a subsequent remodeling of the enterocyte’s structure and a loss of occludin. So we no longer have zonulin and occludin doing their job binding tightly to one another and we get an opening in the small intestinal wall, or permeability of the digestive tube [8].

Chronic exposure to gliadin from gluten or similar substances can cause a down-regulation in production of zonulin and occludin, which further increases small intestine permeability [8]. This permeability allows molecules and substances to move freely into the body’s circulation or blood stream. Now these things are foreign and wherever these particles end up are recognized by the body’s immune system and this is bad news.

With this permeability other gliadin, glutenin, and prolamin proteins initiate an immune response, both the innate and cell-mediated immune cascade to be exact. The innate immune response causes the body’s inflammatory cells to be attracted to wherever these foreign materials end up. The innate immune response also ends up signaling inflammatory chemicals to be released to help destroy the invading foreigner. An enzyme called transglutaminase helps modify gliadin and gluttenin so that it more effectively stimulates the immune system [8]. We could envision a situation where all this inflammation in remote areas that these foreign substances have relocated could cause some serious damage and it’s not hard to see why the New England Journal of Medicine has associated 55 diseases with gluten intake and reactions.

With a permeable gut due to faulty tight junction functioning we get antigenic materials into our circulation. Some clinicians refer to this as leaky-gut syndrome, although it’s not widely recognized in Western medicine. Gut permeability has been linked to allergy induced autism, nutritional deficiency, increased absorption of toxins, liver inflammation, infection, rheumatoid arthritis, asthma, multiple sclerosis, vasculitis, Crohn’s disease, colitis, Addison’s disease, lupus, thyroiditis, chronic fatigue syndrome, and fibromyalgia [9].

So what do we make of all this? The research and anecdotal evidence seems to suggest eliminating gluten and similar prolamin protein-rich foods from the diet is probably a good idea. Eliminating wheat products, barley, rye, and other potential trouble sources like corn and oats is not very difficult to do, just don’t eat the products and use grass-fed meats, wild-caught fish, vegetables, nuts, fruits, roots, tubers, and seeds to make up your diet. By committing to 30 days of this elimination diet you will be able to accurately assess what effect, if any, these foods have on you. Do you feel better, look better, perform better at the end of this period of time?

After the elimination period you can try and revisit one of the eliminated foods to see what happens. Does it make you feel sick, gassy, or bloated? If so, you might be better off without it. Essentially you are drawing a line in the sand and setting a baseline for your own nutrition. By establishing a “normal” level of digestive health you can tweak the parameters to fit your own goals. If fat loss is the goal avoiding the wheat products might be smart due to the insulin-mimetic effect, their potential hyperpalatability, as well as avoiding processed foods in general. If you are looking to put on some size then you should also think about optimizing your ability to absorb the foods you eat so perhaps taking in potentially noxious food stuffs isn’t a good idea. Hopefully you liked this article! Please share it with friends, family, and coworkers if you did!




2) Lammers KM, Lu R, Brownley J, et al. (July 2008). “Gliadin induces an increase in intestinal permeability and zonulin release by binding to the chemokine receptor CXCR3”. Gastroenterology 135 (1): 194–204.e3. doi:10.1053/j.gastro.2008.03.023. PMC 2653457. PMID 18485912.






8)  S. Drago et. al Gliadin, zonulin and gut permeability: Effects on celiac and non-celiac  intestingal mucosa and intestinal cell lines. Scandinavian Journal of Gastroenterology, 2005; 41: 408-419


Don’t Get Mistaken For Santa Claus

By Jordan Feigenbaum MS, CSCS, HFS, USAW CC, Starting Strength Coach

If this scene seems familiar....

If this scene seems familiar….

Anyone who knows me or has read anything I’ve published in recent history knows I don’t buy into the “watch what you eat around the holidays so you don’t get fat” hype. My reasoning is quite simple, the holidays are a time to cherish your family and friends, relax, and not worry about how many calories, carbohydrates, etc. you’re taking in. If you bring your food scale to my Christmas dinner, I’m slamming the door in your face….seriously.

On the other hand, there’s this weird behavior trend that I’ve noticed here in ‘Merica, that is, the “holiday season” is not limited to the actual holidays, but rather it lasts for five weeks or so from the Thanksgiving feast to the New Years Eve part. Giving your mouth free range to consume anything you want to for this extended period of time is a good recipe for feeling like trash come January 2nd and putting on more than a few pounds. Additionally, people seem to get busier and busier every holiday season and tend to miss more training sessions. It’s an understandable plight, but there’s hope! We’ve got about 2 weeks left from now until NYE and here are five pro-tips to help you avoid having to buy a bigger size dress or pair of pants for your New Years Eve party!

1) Isolate the Excess

These days people have company holiday parties (usually multiples), family gatherings (usually multiple), and it’s really easy to find yourself in situations where the food and drink is sub-optimal over and over again. It’s really difficult to stay on track when you’re not in control of the menu, but I have found that restricting intake during the rest of the day and week seems to be fairly easy if someone doesn’t have to be hyper-vigilant in their social situations. The easiest trick in the book is to lean towards a carbohydrate-restricted diet that’s based on lean protein sources, vegetables, and no added fats besides fish oil for breakfast, lunch, and snacks. When you get to the party or event, do what you want. If you’re craving a piece of pie or a cookie go for it. Another glass of wine? You bet. While I can’t guarantee that you’ll be okay if you find a way to put down 5000 calories at each of your holiday gatherings, I can say that it’s pretty easy to restrict calories at other times like breakfast and lunch when you’re not under any social pressures to do what anyone else is doing. Furthermore, I’ve found that after following this reduced intake for a few days hunger seems to decrease a bit as the body ramps up fat burning. Finally, having one or two holiday gatherings (and subsequent “cheat” meals) per week seems to keep metabolism humming along nicely. I’ve seen people actually get leaner during the holiday season with this approach. Remember, lean protein sources like egg whites, chicken breast, turkey, lean beef or fish, protein powder, etc., green vegetables ad libitum, and no added fats except for fish oil.

2) Bump the Intensity

Hopefully you can still find some time to train during the holiday season. One of the best ways to improve the way your nutritional intake is partitioned amongst your body’s tissues is to train heavy (relatively) with barbell exercises like the squat, bench press, deadlift, press, and power clean. To bump up your metabolism and improve this nutrient partitioning even further, add in some high-intensity interval training (HIIT) at the end of your workouts. Using any type of cardio, e.g. running, rowing, elliptical-ing, kettlebell swings, etc., go as hard as you can for 20-30 seconds, rest for 60-90 seconds, and repeat 6-10 times total. You’re welcome.

3) Sleep as Much as Possible

Unless you’ve been living under a rock for the past couple of years, you’ve probably heard about how lack of sleep can effect body composition. Additionally, stressful times like the holidays seem to result in decreased sleep levels for people. If you can, try to get as much shut-eye as you can. Supplements like ZMA, melatonin, and valerian root can help if you’re struggling in this department.

4) Drink More Water

That bloated feeling after a big holiday meal is a pretty gratifying experience, well for a few minutes anyway. Afterwards, we all kind of wish it would dissipate so we can re-buckle our belts, right? Wait, am I the only one who does this?!??! Anyway, most people don’t drink enough H2O anyway, and this probably decreases a bit during the holidays. This can impair the transit of food through your GI tract, make you constipated, feel bloated, etc. Simply put, if you increase your water intake significantly, you won’t experience these effects (or at least they’ll be reduced). Aim for 2-3L (just use your Nalgene) above what you’re taking in now. Yeah, you’ll be going to the bathroom a lot, but you won’t be looking like Santa Clause (or Mrs. Clause) either.

5) Prioritize the Celebrations

While there are many holiday gatherings, all spreads are not created equal. For instance, if you go to a party and what they’re serving doesn’t look that good to you don’t gorge yourself on that stuff! Wait until you get to the party that’s full of the goods before letting your hair down. The calorie balance thing is more of a long-term thing anyway. Calories don’t have a clock, so your daily intake probably matters much less than your weekly intake. Plan accordingly! If you know you’re going to an awesome party with really good food and drink, don’t blow it at your work’s potluck with the questionable finger foods and off-label soda. Just my 0.02.

So get to it, folks! Stick with the lean proteins and veggies, add in some HIIT, drink up, and wait for the quality buffets! Hope this helped.


The Nutrition Continuum

By Jordan Feigenbaum MS, Starting Strength Coach, CSCS, HFS, USAW CC


Yea, it’s that time again Resolution Time! People will be thinking about, discussing, and ultimately arguing about the diet that they’re going to start for the new year. People have this interesting desire to be “right” when it comes to the diet or protocol they pick, so much so that they’ll argue extensively to prove their diet’s superiority (ultimately showing they are just sooooo smart). Guess what, Virginia? All diets/protocols that are worth the paper or bandwidth they occupy works via the same principle, caloric restriction. Somebody just got mad….

In recent times people have tried to argue that it is ALL about calories, while other camps have argued that calories DON’T matter. Guess who’s right? Everyone! It is true, without a shadow of a doubt, that in order to lose weight you must burn more calories than you take in, a so-called negative calorie balance. On the other hand, the idea that the amount of calories you burn, require, etc. is some sort of static variable is laughable. In this instance, calories aren’t so important because the other variables in the equation are changing at the same time. There’s some sort of middle ground that seems to be a no-man’s land, but this wasn’t the purpose of this article anyway. What I want to talk about is my proposed Nutrition Continuum, which is a fancy (read:proprietary) way of describing the diet protocols that work from the most relaxed all the way to the most restricted. I’d hazard a guess that that “lose weight” will still be the most common New Year’s resolution so invariably people will be seeking out diets that will work. What I want to do is provide a sort of “on-ramp” for anyone to a nutritional regime that is well-suited for their current level of buy-in (commitment/motivation). People with different levels of buy-in, goals, and beliefs (as they relate to diet) will need different protocols, thus we can piece together a nutrition continuum of sorts.


1) Low buy-in/accountability

Folks that fall into this group do not have the motivation (yet) to weigh, measure, and track their intake and THAT’S OKAY! Not everyone is ready to geek out on their food and break out the food scale and weigh and measure every morsel that goes into their gullet. Probably the best option for people falling into this category is utilizing a lower carb approach most of the time. This sort of nutritional protocol does not require a lot of thought other than “Is it a meat or animal product?” or “Is it a vegetable?” This allows the person to simply adjust their meals in any situation without having to be anal about the amounts of food coming in. Some easy tweaks to this template are to add some starchy carbohydrates or a post-workout shake in the meal immediately following training, using dense fat sources like nuts/nut butter/oils to increase the caloric intake, etc. While not optimal for performance and physique, this is a nice “elevator pitch” for dietary change that will help many lose body fat and eat healthier. Note the absence of any weird “rules” or “exceptions” to the diet. This helps for increased compliance.

Going low-carb helps people lose weight by both spontaneously reducing their food intake and increasing their fat-burning ability (via enzymes and cellular trafficking). Instead of people having to weight and measure calories and macros to reduce their calories, and thus lose weight, low-carb diets tend to do this automatically. Things can go awry, however, if dense fat sources are a staple of the diet as it’s quite easy to get a bunch of extra calories from oils/nuts/nut butters. Even those these fats may be healthy, you can certainly overdo it calorie-wise. Additionally, people’s metabolisms tend to slow down at various intervals (from 3 or 4 days to 2 weeks) when carbohydrates are excluded from the diet. This can be prevented with programmed “refeeds”, i.e. eating a substantial amount of calories from carbohydrates every 5-7 days. The other thing that can go wrong is people not actually eliminating carbohydrates even though they’ve eliminated a certain food product like wheat or gluten. A person may still be eating copious amounts of fruit or starchy vegetables and missing out on the many benefits of a low-carb diet.

So while it’s easy to “pitch” the low-carb approach (and it’s easy to do), there are many pitfalls in this approach as well. All in all, this is a good starting point for most when it comes to changing their diet.

2) Moderate buy-in/accontability

This style of eating or dieting requires that the person does a little bit of portion control, but it’s so simple that you’re either on-board or not. Unlike many more complex nutritional schemes (with no negative connotation), the meal components and portions are set from the get go. All the person needs to do is actually eat them. Good examples of this style of diet are the Velocity Diet (Biotest) or Rapid Fat Loss Protocol (Lyle McDonald). Basically, depending on someone’s bodyweight, the person will consume lean protein at a certain amount, essential fatty acids, some green vegetables, and nothing else. Say we have a 180lb male who strength trains 3x per week and he wants to lose as much body fat as possible in 2-4 weeks. He would take in 200-230g of protein from lean sources like chicken breast, turkey breast, egg whites (no yolks), protein powder, etc., a couple grams of fish oil, and green leafy vegetables, that’s it. The beauty in this is that there is really no “thinking” after the initial calculations of protein (1.1-1.5g/lb) and thus, no “gray zones” to get lost in and get off track. The problem with this style of eating should….rest of article here!