Answer: The above question sort of encompasses a few different potential things and I’m not 100% sure which you’re asking so I’ll just cover them all.  First realize that one fuel that the brain cannot use is fatty acids, at least not directly.  This has led to the oft-stated belief that the brain can only use glucose. But this is incorrect as the brain has an alternative fat derived fuel which are ketones (or ketone bodies, the two major of which are beta-hydroxybutyrate and acetyl-acetate). 

Ketones are produced primarily in the liver (from the breakdown of fatty acids) and exist predominantly as an alternative fuel source for the brain (they can also be used by skeletal muscle) during periods of low-carbohydrate availability.  This probably was originally important during periods of complete starvation; now very low-carbohydrate diets (defined here as any diet containing less than 100 grams per day of carbohydrates) effectively ‘exploit’ this mechanism.

Now, on a carbohydrate based diet, the brain runs essentially on 100% glucose since ketones are generally not produced in significant amounts under those conditions (there are a couple of odd exceptions, one is following very long duration endurance exercise where a post-exercise ketosis can occur due to changes in fuel metabolism).  So what happens when you remove most or all carbohydrates from the diet?  Does the brain magically switch to using ketones?  For the most part, no.  Studies done way back when show that there is an adaptation phase that may last about 3 weeks while the brain ramps up its ability to use ketones for fuel.  

Even there, after that roughly 3 week period, the brain still only derives about 75% of its total fuel requirements (about 400 calories per day or thereabouts) from ketones; the other 25% come from glucose (which the body can produce through a variety of pathways that I won’t detail here; all of this is explained in excruciating detail in my first book The Ketogenic Diet).  Mind you, this is only relevant on a very low-carbohydrate diet.  Even if the brain could still use ketones on a carb-based diet they wouldn’t be produced in large enough amounts for it to be relevant.

So I think that answers at least part of your question: when first starting a low-carbohydrate diet, it takes the brain about 3 weeks to adapt to using ketones for fuel; even then it only gets about 75% of its total fuel from them.  This scans pretty well with what many experience on the diet, they don’t feel fantastic for the first 2-3 weeks of the diet (while they are adapting). Some of that, mind you, is related more to mineral intake than anything else (early studies found that sufficient intake of sodium, potassium and magnesium eliminated all of the fatigue and lethargy that occurred on very low carbohydrate diets).

But there is a related question that often comes up which has to do with switching back and forth between fuels (this is especially relevant for some cyclical ketogenic diets such as what’s described in The Ketogenic Diet or in my Ultimate Diet 2.0).  Here I am unaware of any research on the topic and most of what I have to say is just based on empirical evidence, what people have reported over the 15+ years they’ve been giving me feedback.

Certainly early in the diet there is often a period where the alternation of high and low carbs often causes some people distress, they get the same headaches and issues going from high-carbs back to low-carbs for a couple of weeks.  Probably just a function of ‘interrupting’ the adaptation to ketone metabolism in the brain and there might be some rationale to doing 2-3 straight weeks of a ketogenic diet prior to inserting refeeds or carb-loads.

At the same time, after more extended periods on the diet (perhaps 6-8 weeks), switching back and forth from a carb-based to a ketone-based brain metabolism seems to cause most people no problems. They can sort of drop in and out of ketosis (even throughout the day under certain conditions) and not really notice anything one way or the other.  Interestingly, even after extended periods off of a low-carbohydrate diet, most people don’t report the same early adaptation phase that they went through the first time on the diet; they go back onto a ketogenic diet and don’t notice anything.

This suggests to me that there is some type of long-term and/or almost permanent change in the brain in terms of its ability to use ketones for fuel with long-term exposure to them.  Again, I have exactly zero research to back this up; it’s just an observation.  But even there you’d still expect to see the same basic 75/25 split, just with an easier switching back to ketone metabolism after that initial adaptation phase.

Hope that answers your question.

Answer: First a quick definition for anyone who isn’t familiar with the abbreviation: as discussed in the Comparing the Diets Series , a CKD refers to a cyclical ketogenic diet.  This is simply a diet that alternates between periods of very low-carbohydrate eating (typically 4-6 days) and very high-carbohydrate eating (1-3 days).  Dan Duchaine’s Bodyopus, Mauro DiPasquale’s Anabolic Diet and my own Ultimate Diet 2.0 are all examples of CKD’s.  My first book The Ketogenic Diet discusses CKD’s generally in mind-numbing detail.

Now back to the question: does ketosis negatively impact on cognitive function?  And the answer is one huge it depends.  Certainly early studies found that, in the short-term (first 1-3 weeks), low-carbohydrate diets tend to cause some problems.  For this reason short-term studies (usually a week long) tend to report decrements in a lot of things including cognitive performance.

Empirically, as well, many report fatigue, lethargy and a sort of mental ‘fog’ until they adapt to the diet (the brain adjusts to using ketones for fuel over those first 3 weeks).  I’d note that supplementing with sodium, potassium and magnesium seems to go a long way towards limiting or eliminating that feeling of fatigue.

So, for most I certainly wouldn’t recommend starting a very low-carbohydrate/ketogenic diet right before some major test or cognitive challenge.  Odds are it’s going to cause problems.

But what about someone who has adapted to being in ketosis. There there tends to be huge variance.  Some people are sort of neutral to it but I know of many who report far better brain functioning when they are in ketosis.  I couldn’t tell you the mechanism, this is just one of those self-reported things.  But it tends to be highly variable (and I can’t think of any studies that have examined cognitive performance after long-term adaptation to low-carbohydrate diets).

CKD’s add another complication, outside of some exercise research on Cyclical Ketogenic Diets and Endurance Performance that looked only at performance, I’m unaware of any work on CKD’s and cognitive performance.  I bring this up as some people do report changes switching back and forth between very low and very high carbohydrate intakes.

Quite in fact, many who find that they feel ‘great’ in ketosis feel a bit dopey or sleepy when they switch back to high carb intakes.  This is probably related to either blood glucose swings or a big increase in brain serotonin (which tends to cause lethargy and fatigue) but it does occur.

Similarly, some seem to go through at least a brief re-adaptation (in terms of fatigue, etc.) going back from high carbs to low-carbs.  Again, this is pretty variable, many people can switch back and forth from one extreme to the other and don’t seem to notice anything.  I have no idea why, just reports I’ve seen.

So back to the question, should you switch out of ketosis for your test?  It’s a hard question to answer and you’d have to think back to your previous switches from low- to high-carbs during the CKD.  If you find that you’re fully adapted to ketosis and function fine mentally, and that you get dopey going back to high-carbs, I’d probably suggest you stay on low-carbs through the test.

If you’re one of those people who don’t seem to have ever fully adapted to being in ketosis (they do exist), you might want to move back to at least moderate carbs a day or two before your test.  Unfortunately, there’s just too much variability for me to give you any advice beyond that.

Answer: Cramping is unfortunately a very complicated topic and while many simple solutions are often thrown out, they don’t always seem to work.   Usually the culprit is issues with hydration per se or electrolyte levels; electrolytes are things like potassium, calcium, sodium and magnesium they are involved in transmission of the electrical signals in the body.  Hence their name.

I’d note that hydration and electrolyte levels are intertwined as the amount of water in the body affects the relative concentrations of the electrolytes in the body. So if there is more water present, the relative concentration of each of the electrolytes will be lower because the water will dilute them.  By the same token, if you are dehydrated, the relative concentrations of the electrolytes goes up.

Most ideas about cramping tend to focus on a single electrolyte, potassium was blamed for quite some time which is the basic origin of the ‘eat a banana to stop cramping’ idea.  Bananas are an excellent source of dietary potassium.

The problem is that cramping is way more complicated than this and can be related to all of the different electrolytes, not simply the absolute amounts of each but the interactions between them.  Fixing the problem often entails trying different things to figure out what’s causing the problems for a given individual.

Now, a potential issue specific to very low-carbohydrate diets (less than 100 grams of carbohydrate per day) and cramping per se is that these diets cause water loss.  As well, the water losses can vary massively from a low of perhaps 1-2 pounds up to 10-15 pounds in larger individuals.    As well, very low-carb diets cause electrolyte losses and this can cause cramping and fatigue.

As I detailed in my first book The Ketogenic Diet, very low-carb dieters need to supplement their daily electrolyte intake with the following at a bare minimum:

• 3-5 grams extra sodium hydrochloride
• 1 gram potassium
• 300 mg magnesium

Not only should this help with cramping issues, this has also been shown to fix some of the fatigue issues that often beset people when they start ketogenic diets.  Of course, an adequate calcium intake is important under all conditions for bone health.  How much you need depends solely on how much dairy foods you’re eating so whether or not you need to supplement extra will depend on that variable.

While you generally have to supplement magnesium separately, you can cover at least some of the potassium and sodium requirements with something like LiteSalt.  This is a table salt that contains 1/2 sodium chloride (standard table salt) and 1/2 potassium chloride.  It tastes just like normal salt but gives a better balance of sodium and potassium.  I’d note that pure potassium salt tends to be a bit bitter which is why I don’t recommend it; most won’t use it regularly.

So the above would be a good first step.  I’d note that empirically high doses of the amino acid l-taurine seems to help with cramps in some people.  If your hydration is good and you’re getting the above electrolytes but are still having problems with cramping, you should consider adding l-taurine to the mix.

I should also mention that stimulants in general and the Ephedrine/caffeine stack (as well as the drug clenbuterol) can cause cramps.  This is even more true on low-carbohydrate diets.  The reason is that they both cause calcium to flow into the muscles, essentially putting them in a low-level state of contraction.  When you put heavy training on top of this, cramping often occurs.   This is likely just an interaction between the low-carbohydrate diet causing dehydration and electrolyte loss, the EC/Clen causing calcium to go into the muscle and then throwing training on top of it.  It’s not very much fun.

I’d note that even for individuals who aren’t on very low-carbohydrate diets, cramping can still occur especially if they do a lot of training in the heat; as well some of the extremist attitudes towards diet such as ‘Never eat sodium’ among bodybuilders and other trainees can cause problems.  Again, this can be related to both hydration and electrolyte imbalance.  Unfortunately, it’s nearly impossible to give more than vague guidelines on this.

Recent research has found that water and salt loss during training can vary about 10-fold between people. This makes giving a specific single guideline (e.g. drink 1 gallon water) impossible even if people try to do it to keep things simple.

At least in terms of training, the old guideline was that you should weigh yourself before and after workout and for every 1 kg (2.2 lbs) of weight lost, you needed 1 liter (32 oz, 4 cups) of fluid to replace it.  This turns out to be wrong, you actually need 1.5 liters (48 oz, 6 cups) of fluid to replace every 1kg of weight lost.

Please note that you don’t have to pound this right after training, but you need to consume that much extra over the course of the day to cover losses.  Athletes who do a lot of training in the heat who don’t replace fluid losses can get into trouble pretty quickly.

As well, note that plain water is actually the worst rehydration drink out there.  As I discussed in Milk as an Effective Post-Exercise Reydration Drink, fluids containing sodium and potassium are retained far better than those that don’t.  Milk also provides good carbohydrates and high-quality protein so it does double duty after training if you can stomach it.

I’d note that, again, weight loss during a given bout of training can vary many fold.  One athlete might lose 1-2 kg (2-4.5 lbs) and another might lose 8kg (17 lbs).  Like I said, it’s impossible to give a specific value of how much fluid to consume because of this.  Weighing before and after for a few workouts will tell you what your personal hydration requirements are.

I’d also mention that sodium losses during activity are just as variable and calculations show that one athlete might only lose a gram or two of sodium during training while another can lose upwards of 20 grams.  I am currently unaware of any non-laboratory way to determine sodium losses during training.

But I also don’t believe in heavily restricting sodium for athletes; training in the heat requires that electrolytes be replaced and liberal use of something like the LiteSalt I mentioned above is a good idea for a number of reasons.

So anyhow, that’s sort of a basic look at cramping.  It’s a place where I wish I could give more firm guidelines but they simply don’t exist.  There is just too much variability and what works for one may not work for another.  In general, it tends to be related to hydration and electrolyte intake and this tends to be more of an issue on very low-carbohydrate diets.  But it can become an issue on carb-based diets as well.

So make sure you’re getting sufficient fluids, don’t skimp on salt (and get a sodium/potassium salt) and consider supplementation if you’re still having issues.  Some people seem more prone to have issues with stimulants as well so if they are causing cramping, you may need to drop them completely.

Answer: Ok, let me take these on one at a time.

In my first book The Ketogenic Diet, I talked about something called the ketogenic ratio (KR) which is an equation/concept used in the planning of ketogenic diets for epilepsy patients. The equation basically gives you the potential ketone producing potential of a given meal depending on the relative ketogenic or anti-ketogenic effect of the different macronutrients.

So the KR of a given combination of nutrients can be estimated with the following equation:

Click to See A Bigger Version

Protein turns out to be partially ketogenic (46%) and partially anti-ketogenic (58%), reflecting the fact that some amino acids can be made into ketones, while other are made into glucose).  Carbohydrate is 100% anti-ketogenic and fat is mostly (90%) ketogenic (the 10% anti-ketogenic is due to the fact that the glycerol portion of triglycerides, explained in A Primer on Dietary Fats, can be converted to glucose in the liver).

Quoting from that section of The Ketogenic Diet:

This equation represents the relative tendency for a given macronutrient to either promote or prevent a ketogenic state (1). Recalling from the previous chapter that insulin and glucagon are the ultimate determinants of the shift to a ketotic state, this equation essentially represents the tendency for a given nutrient to raise insulin (anti-ketogenic) or glucagon (pro-ketogenic).

For the treatment of epilepsy, the ratio of K to AK must be at least 1.5 for a meal to be considered ketogenic (1). Typically, this results in a diet containing 4 grams of fat for each gram of protein and carbohydrate, called a 4:1 diet. More details on the development of ketogenic diets for epilepsy can be found in the references, as they are beyond the scope of this book.

However, invariably when people tried to apply the KR to low-carbohydrate fat loss diets, one of two things happened.  If the person set calories appropriately and used the KR, the protein intake ended up being far too low (because dietary fat had to be so damn high).   Alternately, if they set protein appropriately and tried to scale dietary fat to the proper ratio, the caloric intake ended up being too high.

The former was a poor choice from the standpoint of protein sparing; the second limited (or eliminated fat loss).

So basically I threw out the ketogenic ratio.  As noted above, it’s crucial for the development of epilepsy treatment diets (anyone wanting more information on this topic should purchase the excellent The Ketogenic Diet: A Treatment for Epilepsy by Freeman, Freeman and Kelly.

But for dieters and folks seeking body recomposition, it made setting up appropriate diets impossible.

Additionally, there isn’t convincing evidence in my opinion that ketosis is crucial for the benefits of the diet. Yes, ketones are protein sparing but only when dietary protein intake is inadequate in the first place.  When protein is set appropriately (e.g. 1-1.5 g/lb lean body mass as discussed in The Protein Book), the development of ketosis isn’t that critical to spare protein.  Simply, protein is the most protein sparing nutrient and other things (e.g. ketones vs. carbohydrates) only matter if protein is inadequate in the first place.

Even the hunger blunting effects of ketosis is up to debate and much of the recent literature on the topic suggests that it is actually the increased dietary protein intake that is causing the decreased hunger, rather than the presence of ketones per se.

Which is a long way of saying that I don’t think that the ketogenic ratio, or even the development of ketosis is important to the overall success (or failure for that matter) of low-carbohydrate diets.  In the Ultimate Diet 2.0, I addressed this rather explicitly in a section titled “What About Ketosis?”

For the most part, I simply see ketosis as a “side-effect” of fat loss (burning to be more accurate), more than something to be explicitly sought out. That is, when you accelerate fat oxidation with the methods above, you tend to enter ketosis. Ketosis in and of itself isn’t any big deal. For that reason, I won’t talk about monitoring ketone levels with Ketostix or anything like that. Frankly, using a low-carbohydrate/ketogenic diet for the fat loss phase of the UD2 has more to do with lowering insulin, raising catecholamines, and ramping up fat oxidation; ketosis is simply a tangential effect.

Which brings me to your second set of questions. For background,  low-carb dieters have often used a product called Ketostix which change color to indicate the concentration of ketones in the urine. Yes, you pee on them and they change color to indicate the presence or absence of ketones in the urine.

There are a number of problems with Ketostix not the least of which is that urinary ketone concentration is at best a very indirect indicator of what’s going on in the body.  True ketosis is defined in terms of blood concentrations (terms ketonemia), not urine (terms ketonuria).  But since you can’t easily measure ketones in the blood (no, you can’t put blood on the Ketostix, I tried it years ago and it doesn’t work), the next best thing is urinary ketones.

Now, obviously, if you have ketones in your urine, you certainly have them in your bloodstream.  However, the absence of ketones in the urine doesn’t mean that you’re not still in ketosis (as defined by blood concentrations).  You might be in ketosis as measured by blood levels but simply not be excreting any in the urine.  Or not excreting enough to change the Ketostix.

Basically, there are a variety of things that influence whether or not there are enough ketones present to be excreted in the urine in sufficient quantities to make the Ketostix change colors.  For example, you might not be making ketones in sufficient quantities (this happens in lean people, especially if they are very active), lots of water can dilute your urine and the ketone concentration, some other variables can impact on whether or not you show ketones on the Ketostix.

As you might imagine, at the end of the day, I don’t think focusing on ketosis per se (or the lack thereof) or the Ketostix is very valuable.  You can develop deep ketosis by gorging on dietary fat (especially Medium Chain Triglycerides) but your calories will be so high that you won’t be losing much, if any fat, that way.  And you can lose fat without ever showing a single ketone in the urine.  Basically, there’s just no real correlation between ketosis, what the Ketostix are showing and fat loss.

Basically, I have seen too many dieters focusing on the Ketostix instead of what’s important: relative amounts of fat and lean body mass lost. Focus on the latter, if you’re losing fat and maintaining lean body mass, your diet (low-carbohydrate or otherwise) is working, whether you are in ketosis or not.

Answer: Dieting in general tends to lower serotonin in the brain and this can cause depression in susceptible people.  Interestingly, this effect seems to be more likely to occur in women than men (women being more susceptible to depression in general).  In my experience, low carbohydrate/higher proteins diets tend to be even worse in this regards for reasons I’ll explain now.

First and foremost, nutrient intake per se affects the production of neurotransmitters with the effects being both direct and indirect.

In a very direct way, specific amino acids are the precursors for specific neurotransmitters in the brain.  Tryptophan is a precursor for serotonin in the brain and the amino acid tyrosine (as well as phenylalanine which converts into tyrosine in the body) is the precursor for dopamine (and subsequently adrenaline/noradrenaline).

As an extreme example of this, researchers will sometimes use something called acute tryptophan depletion (accomplished by providing an amino acid solution containing all of the amino acids except tryptophan) to drastically lower brain levels of serotonin.  This is used to test various things but, among other things, it tends to cause acute depression in those who are susceptible.   However, this is a pretty extreme type of intervention, decreasing blood tryptophan levels massively (by about 80%); in dieting, tryptophan levels only drop by about 10%.

As usual, it gets more complicated.  The different amino acids have different transporters in the body and some amino acids use the same transporter; this means that different amino acid can compete for transport.

Specifically relevant to this topic is the fact that both the branched chain amino acids (BCAAS), tyrosine and phenylalanine and tryptophan all use a transporter called the Large Neutral Amino Acid (LNAA) transporter.  Again, this means that they compete for transport, meaning that levels of the different amino acids can affect the transport of the other. Which means that the relative amounts of the different amino acids will impact on how much is getting into a specific tissue in the body; in this case the brain.

If there is a large amount of tryptophan relative to the other LNAA, there will be greater serotonin production in the brain; if there is less tryptophan relative to the other LNAA, there will be less tryptophan transport into the brain and impaired serotonin production.

This brings us to one potential problem with higher protein intakes per se: most dietary proteins contain a lot more LNAA than they do tryptophan.  One exception is a derivative of whey called alpha-lactalbumin which has the highest tryptophan content of any dietary protein; recent studies have found that consumption of this protein can increase the ratio of tryptophan to the LNAA in the bloodstream, increasing brain serotonin synthesis.  For comparison, while most dietary proteins may ony contain about 2 grams of tryptophan per 100 grams, alpha-lactalbumin contains nearly 5 grams of tryptophan per 100 grams.

As well, there is an interaction with the carbohydrate intake of the diet.  Diets very high in carbohydrates and low in protein are known to raise plasma tryptophan and serotonin levels (which is probably why such diets make some people sleepy and dopey).  It’s worth mentioning that unless dietary protein is taken to exceedingly low levels (below 5% of total calories), the real-world impact of high-carbohydrates and low-protein isn’t that massive in terms of its effect on serotonin levels in the brain.

However this may explain why some people who are prone to depression tend to crave low-protein/high-carbohydrate foods at certain times (stress, seasonal affective disorder), they are trying to self-medicate themselves and improve serotonin levels.

In any case, let me explain why carbohydrates can impact on all of this since this will help clear up why lowering carbohydrates can cause problems.

The reason is this, the uptake of some of the LNAA (especially the branched chain amino acids) are insulin sensitive; for example, when insulin levels go up, blood levels of the BCAA go down.  This shifts the tryptophan:LNAA ratio towards tryptophan such that more gets transported into the brain, potentially increasing serotonin production.

The corollary to that is that when carbohydrates are reduced (and high quality dietary protein is increased), there is the potential for serotonin levels to be reduced. Between the increased intake of LNAA from most high-quality proteins, decreased clearance of them due to reduced insulin levels and the overall effect of dieting in general on plasma tryptophan levels, this all adds up to problems for people at risk for depression.

Which is a long way of answering your question with a resounding yes.

Both dieting in general and low carbohydrate/higher protein diets in specific can cause issues with depression in susceptible people.  I do find it a bit surprising that what I consider fairly moderate intakes of both protein and carbohydrates are causing you to experience this but some of it may depend on the depths of depression you experienced (e.g. your genetic susceptibility).

It may also explain why it takes a good 2-3 months for your symptoms to show up, a very low carbohydrate (e.g. 100 grams per day or less) and/or higher protein diet would probably cause things to go south that much faster.

Ok, so that’s what’s going on, what are the solutions?  I wouldn’t tend to generally recommend lowering dietary protein and increasing carbohydrates (higher protein diets having a number of benefits in terms of weight and fat loss) but, depending on the specifics of your situation (e.g. training, etc.) that might be one option.

Assuming it isn’t, here are some things to consider:

1. Add the protein I mentioned above, alpha-lactalbumin to your daily protein intake.  High in tryptophan, it will help support serotonin synthesis.  Consuming some near bedtime might help with sleep, taking it at other times throughout the day may help with overall mood.  In this context, I’d note that having a relatively higher carb/lower protein meal at dinner time may help with some of the sleep issues.

2. Consider supplementing with 5-hydroxytryptophan.  5-HTP is another precursor to serotonin in the brain that many have used to deal with depression and sleep problems. Doses seem to vary significantly but 50-100 mg taken up to three times daily may be worth considering to keep serotonin levels from falling while dieting.

3. Given that your symptoms only show up after 2-3 months of dieting, I’d strongly suggest taking a full diet break (discussed in detail in A Guide to Flexible Dieting) between periods of active dieting.  Basically, perhaps every 2 months, take 2 weeks to raise calories and carbohydrates to restore brain serotonin levels back to normal. Then you can enter another phase of active dieting, stopping before the depression really sets in to take another full diet break.  I think you get the idea.

I hope that helps and good luck.

Or should I use goal weight?

Answer: First off let me address the second question, using goal weight.  With few exceptions I don’t recommend using goal weight to set anything for the simple reason that most people tend to pick a goal weight that is exceedingly unrealistic and this tends to make them set calories very strangely.  That is, unless someone sets a goal weight that is perhaps 10-20% below their current weight, using goal weight will tend to do odd things.  So I don’t recommend it.

As to the first question, as usual it depends and there are pros and cons to each method.   Let’s look at them and then I’ll explain why I tend to use total weight regardless.

Part of the complication is that total daily energy expenditure has several components to it; classically these included resting energy expenditure (REE), the thermic effect of food (TEF), and the thermic effect of activity (TEA).

Recently, interest in non-exercise activity thermogenesis (NEAT) and spontaneous physical activity (SPA) has also been generated based on the observation that people differ greatly in their ability to burn off excess calories through NEAT/SPA.  This topic is discussed in more detail in Metabolic Rate Overview.

And while a good deal of work shows that resting energy expenditure is related primarily to lean body mass.   It’s worth noting that lean body mass includes a lot more than muscle mass, something that is often forgotten.  I’m not aware of any work linking the thermic effect of food to lean body mass specifically.  The calories burned during activity tends to be related to total body weight (since you’re moving the entirety of you weight) and, depending on how active someone is, this can actually make up a fairly large portion of total energy expenditure.  So while part of daily energy expenditure is certainly related to lean body mass, not all of it is.

As an additional complication, there is the issue of getting an accurate measurement of lean body mass in the first place, a topic that I discussed recently in Problems with Measuring Body Composition.  Admittedly this is a minor issue as many body composition methods can get you within 3-5% of true body composition and any variance in lean body mass based on that inaccuracy will be fairly small.

As a final issue, there is the simple fact that no matter how you estimate your starting calorie levels, it’s never more than an estimate (this is something that is altogether too often forgotten) and it will always have to be adjusted based on real world changes in body weight and body fat.

For this reason, I tend to simply use current total body weight and go from there.  It’s faster and easier, and unless you’re dealing with extremes (e.g. of age, body composition, activity) tends to get most people within shooting distance anyhow.

So, as I discussed in How to Estimate Maintenance Caloric Intake, for someone engaging in about an hour of moderate intensity activity per day, I will tend to assume a maintenance caloric intake of between 14-16 calories per pound current body weight.  Is this a perfect value correct for everyone?  No.  Is it pretty close most of the time?  Yes.

I’d note that, in recent years, due to drastically decreasing daily activity (outside of the gym), this value is often turning out to be a bit too high and many people are ending up towards the lower end (or lower than 14 cal/lb) as often as not.  Sitting in front of the computer all day burns squat for calories, even being on one’s feet burns significantly more.

So an individual weighing 170 pounds would have an estimated maintenance caloric intake between

• 170 pounds X 14 calories per pound = 2380 calories
• 170 pounds X 16 calories per pound = 2720 calories

Just to simplify the math, let’s split the middle and assume a maintenance level of about 2500 calories for this person.

Depending on the goals, I’d make adjustments to caloric intake based on that starting point.  A fairly standard moderate deficit fat loss diet might be a 20-25% reduction from maintenance.  Or 500-625 calories per day for an intake of 1875-2000 calories per day.

Which, as it turns out is about 11-12 calories per pound total weight.  And, as I discussed in How to Estimate Maintenance Caloric Intake, a very common moderate deficit calorie level is ~10-12 calories per pound anyhow.  So we could have saved a lot of time by just using that value in the first place.

More extreme diets would use larger deficits, of course.  For example, the low-calorie phase of my Ultimate Diet 2.0 uses a full 50% reduction from maintenance which would bring our subject to 1250 calories per day.  But that’s a different kind of diet since there are only 4 low-calorie days before raising them again.

Of course for muscle gain, you’d go the opposite direction, perhaps increasing calories by that same 20-25% (depending on a host of factor).  So you might end up at 3000-3125 calories per day or 17.5-18 calories per pound.  I typically use 16-18 cal/lb as a starting point for muscle gain and, as you can see, even using a slightly more complicated method yields an identical value.  So I tend to just use the fast one (with total weight) and then make adjustments from there.

Again, let me reiterate that these are all only rough estimates; they should only be treated as such rather than as holy writ.  While I don’t have the space to go into the approach I use to adjust calories (both are discussed in the final chapters of both The Rapid Fat Loss Handbook and A Guide to Flexible Dieting), the key is that those values must be adjusted based on real world changes in body weight and/or body fat levels.

And since this is true whether or not you use lean body mass or total weight, I tend to just use faster estimates using total weight and then adjust from there.  Outside of extreme situations, this typically works well enough and since you have to adjust things anyhow, I don’t see much of a benefit to using the more complicated approaches.

I hope that answers the question.

Answer: Nuts are sort of strange nutritionally. On the one hand they are generally very nutritious, they provide a decent amount of quality protein and, although sometimes high in fat, the fats they contain are generally of the healthy kind, nuts are generally high in fiber as well. Nuts are also a good source of magnesium, Vitamin E and research indicates that they may contain important phyto-chemical compounds beneficial to human health; diets containing nuts have also been shown to improve blood lipid profiles.

On the other hand, they can be extremely nutritionally dense (that is, providing a lot of calories in a very low volume). This gives them the potential to negatively affect body weight.

However, a fairly large body of research indicates that nuts don’t seem to impact body weight negatively, at all. That is, various research studies have provided some amount of nuts in addition to the normal diet to see what happens to body weight. In general, the addition of nuts has had limited or no impact on body weight. Phrased differently, despite the addition of calories from nuts, weight doesn’t change/isn’t affected. What’s going on?

Research has identified three possible mechanisms to account for the observed results.

Satiety: Nuts appear to increase fullness and calories from nuts seem to be compensated later in the day. That is, it’s suggested that the calories from nut intake results in a spontaneous decrease in food intake later in the day such that total energy balance is unchanged.

One type of study, called a preload study has examined this, providing a fixed number of calories from nuts and then seeing what happens to spontaneous food intake at a buffet type meal later on. Invariably, nut intake (one study tested almonds, chestnuts, and peanuts) causes people to eat less at the buffet meal

However, despite the impact of nuts on fullness, this still isn’t sufficient to account for the lack of an impact on body weight from nut consumption and other mechanisms must be at work.

Increased Energy Expenditure: Some work has identified an increase in energy expenditure due to nut intake; some research has found an increase in resting energy expenditure with chronic nut intake as well. This could be due to the protein content (protein has the largest effect on TEF for example), the fatty acid profile, or both.

Increased Fecal Energy Loss: With nut consumption, there is increased energy loss in your poop, that is, some proportion (one study found a 7% increase) of ingested calories are excreted without absorption. This is likely due to the fiber content of the nuts or some other compound that limits digestive/absorption capacity for nuts.

The three factors above have been shown to account for 95% of the total energy value of the nuts so there is still a small amount unaccounted for. In any case, nuts, despite their high energy content, simply don’t seem to have the negative impact on body weight that one might expect. Which, mind you, doesn’t mean that you can eat them with no attention to portions or intake of other food, recall that a big part of the above effect is due to caloric compensation. If you’re adding a ton of calories from nuts and don’t end up reducing your intake from other sources, the potential for fat/weight gain certainly is there.

Which is basically a long way of saying to eat them, just not without paying some attention to overall intake.

Reference:

Mattes, RD. The Energetics of Nut Consumption. Asia Pac J Clin Nutr (2008) 17 (S1): 337-339.

A: A fairly standard dose of fish oil in the studies is the equivalent of 6X1 gram capsules. The average capsule has 180 mg epa and 120 dha so 6 capsules will provide 1020 mg epa and 720mg dha for a total of 1.8 grams of total fish oil. I would consider this basically the minimum daily amount that would be beneficial on any level.

Some work has identified that the body will hit a limit (in terms of plasma saturation) on DHA at 1.2 grams per day which is the equivalent of 10X1 gram fish oil capsules. That would also provide 1.8 grams EPA for a total of 3 grams per day of fish oil. Under most conditions, I think this is more than enough.

A friend who uses fish oiils to control her arthritis will often go as high as 15X1 gram capsules although I haven’t seen that supported in the literature. I’d note that higher doses are not better here (although some are currently recommending absurd amounts). Excessive fish oil can impair the body’s ability to mount a proper immune response, as well as impairing insulin release.

Carlson’s fish oil contains roughly the equivalent of 4X1 gram fish oil capsules per tsp., I don’t know the values on cod liver oil offhand.

My current generic recommendation is the middle level, 10X1 gram capsules per day for 3 grams total fish oil. This should provide maximal benefits (in terms of partitioning and health) with minimum negatives. Individuals trying to control a specific excessive inflammatory condition may wish to experiment with higher doses (15X1 grams capsules or 3-4 tsp Carlson’s fish oil per day).