One of the proposed causes of obesity and metabolic syndrome is the excessive intake of products containing added sugars, in particular, fructose. Although the ability of excessive intake of fructose to induce metabolic syndrome is mounting, to date, no study has addressed whether a diet specifically lowering fructose but not total carbohydrates can reduce features of metabolic syndrome. A total of 131 patients were randomized to compare the short-term effects of 2 energy-restricted diets-a low-fructose diet vs a moderate natural fructose diet-on weight loss and metabolic syndrome parameters. Patients were randomized to receive 1500, 1800, or 2000 cal diets according to sex, age, and height. Because natural fructose might be differently absorbed compared with fructose from added sugars, we randomized obese subjects to either a low-fructose diet (<20 g/d) or a moderate-fructose diet with natural fruit supplements (50-70 g/d) and compared the effects of both diets on the primary outcome of weight loss in a 6-week follow-up period. Blood pressure, lipid profile, serum glucose, insulin resistance, uric acid, soluble intercellular adhesion molecule-1, and quality of life scores were included as secondary outcomes. One hundred two (78%) of the 131 participants were women, mean age was 38.8 ± 8.8 years, and the mean body mass index was 32.4 ± 4.5 kg/m(2). Each intervention diet was associated with significant weight loss compared with baseline. Weight loss was higher in the moderate natural fructose group (4.19 ± 0.30 kg) than the low-fructose group (2.83 ± 0.29 kg) (P = .0016). Compared with baseline, each intervention diet was associated with significant improvement in secondary outcomes. Reduction of energy and added fructose intake may represent an important therapeutic target to reduce the frequency of obesity and diabetes. For weight loss achievement, an energy-restricted moderate natural fructose diet was superior to a low-fructose diet.

Background

Every since John Parillo said that fruit makes you fat over 30 years ago, fruit has held an odd place in the world of dieting.  It’s quite common to see contest dieters talking about ‘dropping out fruit’ and removing fruit from the diet is not an uncommon recommendation when someone stalls on their diet.

More recently, the rabid furor and hype over refined fructose (and especially High-fructose corn syrup or HFCS) has only added to this.  If reports I’m seeing are right, the consumption of fructose and/or HFCS will make you fat, drive up blood pressure and make your muscles fall off.  HFCS is responsible for the problems with the economy (when Obama isn’t being blamed), the war in Iraq and just general human meanness and unhappiness.  Ok, I may be exaggerating slightly but it’s only slightly.

I addressed the issue of HFCS in Straight Talk About High-Fructose Corn Syrup: What it is and What it Ain’t. – Research Review, an article that drew quite the share of comments (inane and otherwise) and I’d point readers towards that article for a more detailed look at what I’m going tot talk about next.

Make no mistake, studies have clearly shown that excessive fructose intake (and this is usually due to an excessive HFCS intake and that is typically due to the consumption of non-diet soda) cause problems. But often the studies are, well, let’s just call them silly.  They almost always revolve around the chronic intake of simply non-physiological intakes of whatever is being studied (sometimes pure fructose, sometimes HFCS).

In one that people like to cite at me, rats (rarely a good model for humans) were fed a 60% fructose diet for 6 straight months and this induced leptin resistance.   I was actually going to do a research review on it (mainly to point out everything wrong with it) but couldn’t be bothered.  The short version is that a 60% fructose diet isn’t even possible in humans.  Humans don’t do well with large amounts of pure fructose intake as it causes stomach upset.

And if you’re going to argue that most fructose in the diet comes from HFCS (which is about half fructose), that means that the equivalent 60% fructose diet in a human would consist of 120% of the diet being from HFCS.   Except that that is impossible.

I’d mention, humorously, that the rats didn’t actually gain weight during the 6 months of fructose overfeeding; rather,  it was during the high-fat part of the study that the weight gain occurred.  But the anti-HFCS crusaders (who are often pro-fat) missed that point since they seem to only read abstracts on this stuff.  Not that it applies in either case because it’s freaking rats and the diet was completely impossible for a human to achieve in the first place.

In another study, humans were given 200 grams of pure fructose to see what happened.  I don’t recall the details but the results were negative.  First and foremost, that’s 800 calories of pure fructose which is just a ton.  Second, again going by the fact that HFCS is only about 1/2 fructose (the other half is glucose) that would be the equivalent of someone eating 400 grams of HFCS. 1600 calories per day just from HFCS.

That’s about 16 standard sized non-diet sodas per day (or one super duper mega insane Big Gulp).  Now, I’m not saying that’s healthy, I’m not disagreeing that that is a problem.  But have you ever seen someone drinking that much soda who didn’t have the rest of their diet look like absolute shit?   Usually the ones refilling the 128oz cup with coke are eating a ton of other junk food.   My point being that the HFCS may not be the only thing causing issues here.  Yet folks are fixated on HFCS as the source of all evil.

Which isn’t to say that smaller amounts of fructose don’t or can’t cause issues.  I wrote an article over 10 years ago looking at this issue and it was clear that beyond a certain level (about 50 grams of pure fructose per day) there was the potential for issues.  At the time, the big endpoint had to do with blood triglycerides.  Fructose is metabolized almost exclusively in the liver (quite in fact almost zero incoming fructose will ever reach the bloodstream in humans) and this is a rate limited process.  Above a certain point, fructose starts being converted to fat in the liver.

It’s worth mentioning that some studies have also found that, because it doesn’t raise insulin, fructose consumption doesn’t blunt fat oxidation after you eat it.  So while eating a ton of fructose at once (which is abnormal) can cause fat production in the liver, the body burns more fat.  Almost as if it all sort of cancels out.

But the above invariably was looking at either absurd levels of pure fructose or HFCS.  What about fruit?  To a degree, fruit has become sort of guilty by association.  One of the sugars in fruit is fructose and the hysteria over HFCS (again coming primarily from non-diet soda and refined foods) and the fructose content has caused people to lose their minds.

Basically, people have written off anything containing HFCS or fructose IN ANY AMOUNT.  If either are on the label, that food is ‘evil’. Evil I tell you.  Even consider eating it and your muscles will fall off and you’ll explode with fat.  You’ll start beating your pets and probably become a serial killer and end up with your story on Law and Order: SVU.  Fructose is serious stuff if Internet message boards are to be believed.

But it’s key to realize that fruit doesn’t even contain that much fructose in the first place, about 7% by weight.  So a 100 gram piece of fruit (a medium sized apple or banana for reference) might contain about 7 grams of fructose in addition to the other calories.  Even if you use a 50 grams per day cutoff, that’s 7 medium pieces of fruit.  Not impossible but that’s a lot of fruit.

A second issue is that fruit, as opposed to pure fructose or HFCS, contains other stuff, micronutrients, anti-oxidants, flavonols and everything else that might, just might, impact on how it’s metabolized in the body.  You can’t automatically throw out the fruit with the dishwater (yes, I’m mixing my metaphors) because studies of purified fructose/HFCS using insane amounts have found problems.

Finally is an issue that the dynamics of how nutrients are handled while dieting (that is, in a hypocaloric state) are often vastly different than when someone is weight stable or gaining weight.      So yeah, it’s pretty clear that large amounts of fructose/HFCS are a big issue for the average person who is inactive, gaining weight and for whom the entirety of their diet is pretty much crap.  But that doesn’t mean that fruit as part of an overall hypocaloric weight/fat loss diet is automatically the same problem.  And that, finally brings us to today’s paper.

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The Paper

The researchers set out to address two questions.  The first was whether a calorie restricted diet that specifically restricts fructose would improve markers of the metabolic syndrome.  They also hypothesized that a diet high in natural fructose (From fruit) would be superior to one where fruits were limited.

Towards this end, 131 patients were recruited of which 107 finished the study, all were obese (average body fat 40%) and nearly 80% of the subjects were women.  After determining basal caloric requirements, subjects were placed on meal plans of 1500, 1800 or 2000 calories.  The diet itself consisted of 55% carbs, 15% protein and 30% fat and the main difference between the two groups was the fructose content.  One group was limited to less than 10 grams of fructose per day, the other was allowed 50-70 grams of fructose per day coming almost exclusively from fruits.

Food was not provided for the subjects (arguably the biggest limitation of the study); rather they were given meal plans and had to record their food intake at least once weekly (food reports can be notoriously inaccurate and I’ll come back to this).  Adherence to the diet was defined as at least 80% attendance for scheduled clinic visits.

A variety of things were measured including weight and waist measurement along with body fat percentage.  A Tanita BIA scale was used and I’d note (as I discuss in Measuring Body Composition: Part 1 and Measuring Body Composition: Part 2) BIA is not a perfect method as it can be drastically impacted by changes in hydration state.  A vast number of metabolic variables including blood glucose, blood pressure, insulin, creatinine, uric acid cholesterol, triglycerides and others were also measured.  A measure of quality of life was also made in both groups.

The study lasted 6 weeks and these were the results.

In terms of changes in the measured health parameters there were no significant differences between groups in terms of anything.  The fructose group showed a slightly better drop in blood glucose (no surprise there) and the low-fructose group showed a slightly better drop in blood pressure; neither of these reached statistical significance.

I’d comment here that this isn’t uncommon: in a dieting situation, most things change/improve as a function of the weight/fat loss and diet composition tends not to matter.  This is a point lost on many who look at dieting situations (such as a recent study where a high fat intake caused no problems when weight was being lost) and extrapolate it to situations where someone is weight stable or gaining weight.    Basically, weight/fat loss tends to trump just about everything else but that doesn’t meant that the same results will be seen if the person is gaining weight.

But what about the weight/fat loss?  The two groups’ weight losses were 4.19+-0.30 kg and 2.83 +-0.29kg after six weeks.  And perhaps to the surprise of many, the high-fructose group was the one that lost the greater amount of weight.  Body Fat percentage also dropped 2.09+-6.32% in the low-fructose group compared to 2.89+-6.33% in the high-fructose group but this wasn’t statistically significant. The BMI drop was also higher in the high-fructose group but the change in waist to hip ratio was not.

I’d note that there was massive overlap in total weight loss and I’ve reproduced the actual results below.

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Weight Loss for High vs. Low Fructose Diets

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Like I said, a huge amount of overlap even if the weight drop was larger in the high-fructose group.  There was an improvement in quality of life in both groups with no difference between them.

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My Comments

Ok, so what does this paper say?  I think the first point I’d make is that this current idea that carbs make you fat or prevent weight/fat loss is clearly incorrect.  I wish someone would send this paper to Gary Taubes to help him try to remove his head from his ass.  Both groups lost a significant amount of weight and fat and did it eating 55% carbohydrate.

And clearly, at least in the population tested (obese subjects, mostly women), fructose in the form of fruit caused no problems.  At worst, the high-fructose diet was no worse than the low-fructose diet (in terms of all health parameters measured).

And, at least looking at weight loss, it may have been slightly superior.   The researchers had no real explanation for the differential given that the caloric intakes were supposed to be identical.    They suggest that perhaps the higher intake of anti-oxidants, etc. from the fruit might have played a role.  They also point out that the low-fructose diet had a higher glycemic load (since natural fruits had to be replaced by higher glycemic index carbs, I doubt this given the Glycaemic Index Effects on Fuel Partitioning in Humans – Research Review.

Rather, I suspect that the difference in weight loss is just a weird artifact of the study especially given that there was no significant difference in changes in body fat percentage or waist/hip ratio.  While higher insulin doesn’t really impact on fuel utilization, it does impact on water retention, causing the kidney to resorb water.  Lowering insulin (as would occur in the fructose group) might have caused greater water loss.

There is also the issue of the diet not being perfectly controlled since only meal plans were given.  Fructose tends to blunt hunger in many people (this occurs through a vagally mediated mechanism in the liver which sends a fullness signal); perhaps the high-fructose group ate a bit less.  Again, this isn’t really supported by the lack of body fat or waist/hip ratio changes.

Regardless, clearly the idea that the data on massive intakes of either fructose or HFCS doesn’t seem to apply to fructose coming from fruit.  At least not in the population tested.  As I mentioned above, the fruit group did at least as well on all measured markers and was slightly superior in terms of weight loss.  The idea that fruit needs to be eliminated because it contains fructose would seem to be flawed, at least in this group.

Of course, readers of this site are wondering if this applies to leaner individuals and this study can’t answer that question. I’d note that for every anecdotal report of someone removing fruit and getting lean, there are just as many (and many coaches) who keep fruit in the diet and their guys get plenty lean.  One is Borge Fagerli (aka Blade) who has found, in many clients, that the re-addition of fruit to the diet helps people get lean.  But that’s not research, just his observation.

PURPOSE OF REVIEW: Update recent advancements regarding the effect of high-animal protein intakes on calcium utilization and bone health.

RECENT FINDINGS: Increased potential renal acid load resulting from a high protein (intake above the current Recommended Dietary Allowance of 0.8 g protein/kg body weight) intake has been closely associated with increased urinary calcium excretion. However, recent findings do not support the assumption that bone is lost to provide the extra calcium found in urine. Neither whole body calcium balance nor bone status indicators, negatively affected by the increased acid load. Contrary to the supposed detrimental effect of protein, the majority of epidemiological studies have shown that long-term high-protein intake increases bone mineral density and reduces bone fracture incidence. The beneficial effects of protein such as increasing intestinal calcium absorption and circulating IGF-I whereas lowering serum parathyroid hormone sufficiently offset any negative effects of the acid load of protein on bone health.

SUMMARY: On the basis of recent findings, consuming protein (including that from meat) higher than current Recommended Dietary Allowance for protein is beneficial to calcium utilization and bone health, especially in the elderly. A high-protein diet with adequate calcium and fruits and vegetables is important for bone health and osteoporosis prevention.

Background

For decades now, it’s often been thought, felt or claimed that a high dietary protein intake had a detrimental effect on calcium metabolism and bone health; certainly many groups promoting low-protein dietary approaches tend to echo/parrot this idea.

This idea came around in the mid-20th century but was based on some, shall we say, questionable research.  In it, totally purified proteins were given (that is, no other nutrients were present) and a loss of calcium in the body (in the urine) was documented.  It was simply assumed that this had a negative impact on bone health.

Despite later research showing that it was much more complicated than this (i.e. that proteins containing other nutrients had different effects and that other parts of the diet played a major role in the overall effect), this idea is simply repeated as if it were still unquestionably true.  I dealt with this issue to some degree in The Protein Book, in a chapter called Protein Controversies, which is reproduced here on the main site.

As well, there has long been a secondary data set (seemingly ignored by anti-protein folks) showing that higher protein diets actually IMPROVE bone healing following things such as breaks or fractures.  Clearly the idea that ‘protein is bad for bone’ is a bit more complicated than just a soundbite.  The review paper I want to look at today examines the topic in some detail.

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The Paper

The paper begins by pointing out that bone is over 50% protein to begin with and that there has long been concern that the modern Western diet is detrimental to bone health due to the production of acids within the body.  This is something I imagine readers have at least seen mentioned in recent years (I get the occasional question about it) with some going so far as to claim that the body’s pH is THE KEY to all health (some even claim that a drop in cellular pH is the cause of cancer).

While it’s not quite that cut and dry, clearly the modern Western diet tends to promote the production of metabolic acids and at least some degree of metabolic acidosis.  This is due to a number of factors including a high protein intake (proteins are acid promoting), insufficient fruit and vegetable intake (both of which are net base producing for the most part), along with other factors such as sodium and potassium balance (excessive sodium intake relative to potassium can increase the acid load of the body).  You can find long lists of foods online in terms of their net acid or base producing potential.

And certainly, as discussed briefly in Protein Controversies, acidosis can cause problems in the body.  It’s relevant to today’s paper in that the body appears to buffer this acid load by releasing calcium, presumably from bone.  In that current research is suggesting that the RDA for protein is actually too low for some populations (notably older individuals) and with the current interest in high-protein diets for weight/fat loss and maintenance, it’s important to know whether or not these dietary approaches are having negative impacts on bone health.

The paper looks in some detail at the issue of acid/base balance and calcium metabolism. As noted above, the generation of metabolic acids causes a number of effects in the body, all of which could potentially impact negatively on calcium metabolism and bone health.  As well, studies clearly show both that:

1. The generation of metabolic acids causes increased calcium loss in the urine
2. Counteracting acidosis with base-forming minerals (e.g. potassium bicarbonate) decreases calcium excretion

While the above is clear, the direct impact of dietary protein on bone health is a bit less clear with the results of more direct epidemiological data showing mixed results in terms of the actual impact on bone health.  As well, citing a review by Fenton, the paper points out that:

…neither calcium balance nor the bone resorption marker, N-telopeptides, was affected by diet-induced changes in net renal acid excretion despite a significant linear relationship between an increase in renal net acid excretion and urinary calcium.

That is, while it’s clear that increased dietary acid load causes increased urinary calcium excretion, it’s less clear if this has any real direct impact on the body’s net calcium balance or overall bone health.

Moving on to more direct effects, the paper looks at the very old data (using primarily purified proteins) showing that for every increase in dietary protein by 1 gram, there was a 1 mg increase in urinary calcium loss (raising the question of why not simply scale calcium intake to protein intake to offset this); this led to the assumption that bone health was being compromised.

However, in direct contrast to this, the majority of epidemiological studies find that a higher protein intake is associated with increased bone mineral density with only a few finding a negative impact.  As well, while weight loss per se tends to cause a decline in bone health, some research has found that high-protein weight loss diets reduce the loss of bone mineral content; that is, high-protein intakes on a diet are beneficial.

The primary acid formation from protein comes from the sulfur containing amino acids (cysteine and methionine) and these are found in higher amounts in animal vs. vegetable proteins; it’s often been assumed that a higher vegetable protein intake would therefore have less of an impact on bone health.

However, this also turns out to be incorrect; the paper points out that studies of high-meat protein intakes either show no overall effect on net calcium balance and a higher animal protein intake is actually associated with increased bone mineral density; as well studies show a negative association between vegetable protein and bone mineral density.

It’s worth noting that strength/power athletes, who have traditionally consumed a high-protein diet are typically found to have higher bone densities compared to sedentary individuals.  As the paper points out:

Changes in bone mass, muscle mass and strength track together; thus maintenance or an increase in muscle mass and function maintains or enhances bone strength and mineral density.

And while the increase in urinary calcium excretion with increasing protein cannot be simply ignored, current data suggest that this isn’t actually due to a loss of bone mass.  Rather, increased protein intake leads to increased calcium absorption from the gut; the loss in the urine is simply due to more calcium being absorbed.   The increased loss is simply due to more being absorbed from the diet; interestingly, this effect is more pronounced when calcium intake is low to begin with.

In terms of mechanism, higher protein intakes raise levels of the hormone IGF-1, which stimulates bone formation; this probably explains the benefits of a high-protein intake on bone healing.  As well, high protein intakes have been shown to decrease levels of parathyroid hormone (PTH), a hormone that is involved in the loss of bone mass.  Low protein intakes are associated with increased PTH and lowered bone mineral density.

Finally, as I mentioned in the introduction, you can’t simply look at protein intake outside of the rest of the diet and there are clear interactions with other nutrients.  I mentioned above that protein intake interacts with calcium intake, increased absorption.  As well, a high protein intake has been shown to increase bone health in older individuals when calcium and Vitamin D are supplemented.  Finally, ensuring a sufficient intake of fruits and vegetables (which neutralize the acid load of protein) should help to ensure the impact of dietary protein on bone health is positive rather than negative.

Summing up, the researchers conclude thus:

Although a high meat or protein intake increases renal acid load and urinary calcium excretion, recent findings do not support the claim that bone is the source of the extra calcium lost in the urine.  In addition, evidence is lacking that shows high-protein intakes, including that from animal sources, affect whole body calcium balance or contribute to osteoporosis development and fracture risk.

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Summing Up

I don’t have a whole lot to add to the above conclusion.  Clearly the negative impact of dietary protein on bone health would appear to be overstated to some degree. Under certain circumstances (low calcium/Vitamin D intake, insufficient intake of fruits and vegetables), it’s certainly possible that a high-protein intake could have negative impacts.  But again this comes down to an issue of context.   And in the context of sufficient net acid neutralizing foods (fruits, vegetables, sufficient potassium intake) along with sufficient calcium/Vitamin D intake, the impact of protein on bone health would appear to be positive overall.

There is substantial evidence that static stretching may inhibit performance in strength and power activities. However, most of this research has involved stretching routines dissimilar to those practiced by athletes. The purpose of this study was to evaluate whether the decline in performance normally associated with static stretching pervades when the static stretching is conducted prior to a sport specific warm-up. Thirteen netball players completed two experimental warm-up conditions. Day 1 warm-up involved a submaximal run followed by 15 min of static stretching and a netball specific skill warm-up. Day 2 followed the same design; however, the static stretching was replaced with a 15 min dynamic warm-up routine to allow for a direct comparison between the static stretching and dynamic warm-up effects. Participants performed a countermovement vertical jump and 20m sprint after the first warm-up intervention (static or dynamic) and also after the netball specific skill warm-up. The static stretching condition resulted in significantly worse performance than the dynamic warm-up in vertical jump height (-4.2%, 0.40 ES) and 20m sprint time (1.4%, 0.34 ES) (p<0.05). However, no significant differences in either performance variable were evident when the skill-based warm-up was preceded by static stretching or a dynamic warm-up routine. This suggests that the practice of a subsequent high-intensity skill based warm-up restored the differences between the two warm-up interventions. Hence, if static stretching is to be included in the warm-up period, it is recommended that a period of high-intensity sport-specific skills based activity is included prior to the on-court/field performance.

My Comments: As I discussed recently in The Importance of Context, people these days seem to love them some absolutes and there tends to be no shortage of them to go around, especially when it comes to training.  Always do this, never do that, you get the idea.   The situational context is irrelevant, there are simply black and white absolutes that apply across the board.

And a recent never is that you should never ever static stretch before high-intensity training of any sort with endless coaches and gurus repeating that idea.  And certainly this seems to be based on quite a body of research.  A number of studies have shown that extensive static stretching done immediately prior to various types of exercise performance such as vertical jumping, sprinting and weightlifting impair strength and/or power output.

Now, as I mentioned in Warming Up for the Weight Room Part 1, even if static stretching does decrease strength and power outputs, there may still be times to do it before training.  Usually this is in the case of a severe muscular tightness that impairs either technique or safety.  In that context, proper technique and not hurting the person is far outweighed by any decrease in performance.

However, I made another point in that article which was this: many of the studies don’t really reflect how athletes typically go about their training.  That is, anyone who has trained as an athlete or actually coached athletes in the real world knows that it’s fairly rare (especially among strength/power type athletes, endurance guys are often years behind the curve) to go straight from static stretching immediately into high-performance work.  At the very least some type of drills are generally done between the two, usually more than that (e.g. multiple progressive intensity sports specific warm-ups) is done.

There is also an issue of the extent of stretching: many of the negative performance studies have used levels of static stretching that far exceed what most athletes would ever do in practice (again, something anyone who’s actually worked with athletes would know).  That is, it would be rare to hold a stretch for 2-4 minutes in the real world, static stretching of perhaps 30 seconds per muscle group would be far more realistic.  Yet it is generally that type of extremely prolonged static stretching that has been tested and found to impair performance (some studies have shown shorter stretching periods to have a similar negative impact).

Which brings us to today’s study which set to test the above in a more real-world type of situation.

The study examined 13 netball players from the Australian Institute of Sport.  Both groups first performed a sub-maximal run as a general warm-up.  Then one group performed static stretching (9 stretches held for 30 second each) and the other performed a dynamic warm-up consisting of 16 rather common dynamic movements.  Both the static and dynamic warm-ups lasted 15 minutes. After a short-rest, both groups were tested on 20m sprint and vertical jump.  Then both groups performed a netball specific skill warm-up consisting of various short sprints, shuffling, accelerations, direction changes and jumping.  Then the performance tests were performed a second time to see if anything had changed.

And the results?  Well, in keeping with previous work, the static stretching routine did in fact hurt performance on the 20 m sprint and vertical jumping compared to the dynamic warm-up.  However, after performing the specific skills warm-ups described above, results were no different on the second set of performance tests.  That is, any loss of performance due to static stretching was eliminated simply by performing a variety of sport specific skills prior to the maximal effort testing.

Basically, by testing the athletes in a situation that more accurately reflects how athletes actually train, they found that much of the concern over static stretching is unfounded.  As they state in the discussion:

The results suggest that if an inhibitory effect was present after static stretching, that the SKILL component of the warm-up routine was able to dissipate the negative effect.  This supports the suggestion by Young and Behm that practice attempts of the required tests may offset potential negative effects of static stretching.

The also note that their results are in contrast to another study examining both a dynamic performance warm-up and a static-stretching warm-up but in that study, the static stretching was done after the performance warm-up and immediately prior to the testing.  Basically, order of warm-up matters which I also discussed in Warming Up for the Weight Room Part 1.  And so long as it’s followed by some sort of dynamic, skill specific, progressive warm-up (e.g. progressively heavier warm-up sets in the weight room, increasingly faster pickups in sprinting, etc), static stretching appears to not be quite the absolute no-no that many have made it out to be.

Quoting from the researchers conclusions:

The most important findings from this study were that a dynamic warm-up routine is superior to static stretching when preparing for powerful performance; however, these differences can be eliminated if followed by a moderate to high intensity sport specific skill warm-up.

Summing Up: Basically, static stretching is only a problem if it’s done too extensively (e.g. stretches held for very extended periods) and is not followed by appropriate sport-specific warm-ups between the end of static stretching and maximal performance (testing or training).  Which isn’t how real athletes generally train anyhow.  Which is something any performance coach who has actually worked with athletes should know anyhow.

Mercader J. Mozambican grass seed consumption during the middle stone age. Science. (2009) 326(5960):1680-3.

The role of starchy plants in early hominin diets and when the culinary processing of starches began have been difficult to track archaeologically. Seed collecting is conventionally perceived to have been an irrelevant activity among the Pleistocene foragers of southern Africa, on the grounds of both technological difficulty in the processing of grains and the belief that roots, fruits, and nuts, not cereals, were the basis for subsistence for the past 100,000 years and further back in time. A large assemblage of starch granules has been retrieved from the surfaces of Middle Stone Age stone tools from Mozambique, showing that early Homo sapiens relied on grass seeds starting at least 105,000 years ago, including those of sorghum grasses.

My Comments: In recent years, there has been quite an explosion in interest in the supposed diet of our paleolithic ancestors, essentially in an attempt to explain part of why humans are having so much trouble with the modern diet.  So far as I can tell the first paper was written in the Mid-80′s or so but even more recently it’s become quite the fad/cult/area of interest for a lot of people.

Now, while an entire article could be written about this, it’s important to note that nobody knows for sure what we ate during our evolution.  Even researchers in the field (Cordain and Eaton are two of the major ones) have arrived at rather drastically different conclusions about what our diets contained based on their assumptions because it’s all basically a lot of guesswork.  We end up with estimations based on a bunch of assumptions and not much more.

Much of it comes from an analysis of a book called the Ethnographic Atlas, a work done years ago by non-scientists who wrote down (sort-of) what extant non-modernized people were eating.  From that, various researchers, making various assumptions about the relative proportions of animal and vegetable foods in the diet have thrown out some ideas about what our evolutionary diet contained.  Those researchers have often reached utterly differing ideas based on which built-in assumptions they started with.  Other suggestions about our ancestral diet have been made by examining the current intake of extant hunter-gatherer tribes with the implicit assumption that their food intake is representative of our intake during our evolution.

I’d note that it’s unlikely that there was any singular evolutionary diet in the first place.  Humans have shown the ability to adjust to all but the most extreme environments and show an amazing ability to adapt to drastically differing diets as well.  Human ancestors evolving in say Alaska would have had far different foods available than someone living in the arid plains in Africa.  Even examining the extant hunter-gatherer tribes demonstrates this in spades: the diet of an Alaskan Inuit is radically different from say an African Bushman simply due to the difference in environment and what is available to them.  So there is no single ancestral diet in terms of the quantities, proportions or types of food that would have been eaten in the first place.

At best we can probably say with some degree of certainty that our ancestors didn’t have many of the foods available to us today.  That is, Cap’n Crunch, Ben and Jerry’s Ice Cream and Bud Light weren’t part of our evolutionary diet because they didn’t exist (much to the loss of our ancestors).  Beyond that, we can’t say with much certainty what they did eat; it’s mostly guessing because folks weren’t alive to say for sure.  And while it may be safe to assume that extant hunter-gatherer tribes are representative, it’s still an assumption.

Now, while there are many different interpretations to the ‘paleo-diet’ craze, at least one thing that most seem to agree on was that refined grains were absolutely not part of the evolutionary diet.   Bloggers, apparently unclear on the concept of irony, go on constantly about how ‘Paleo man didn’t have grains, so you shouldn’t eat them.’  Apparently that same logic doesn’t apply to the computers they use to blog with, the Internet that they blog on, their Blackberries that they use to Twitter about their blog updates, modern cars that they use to get to work or the houses they live in.  Paleo man didn’t have those either but I don’t see these folks giving those up.  Guess they only want to give up the easy stuff when it’s convenient.  But I digress.

That is, it’s generally assumed that refined grains (being currently blamed for much of modern health problems) weren’t a major part of our diet until the agricultural revolution, about 10,000 years ago.  It’s also assumed that that span of time is insufficient for man to have evolved to deal with them.  I’ll only address this second assumption by pointing readers to a new book called The 10,000 Year Explosion: How Civilization Accelerated Human Evolution wherein the authors make a rather good argument that, contrary to common belief, not only did human evolution continue once humans became civilized, that it accelerated.

Rather, in looking at today’s second paper, I want to address that first assumption: that our evolutionary diet was devoid of any type of refined cereal grain.  I imagine that, if you’ve read this far, you can guess what I’m going to say about it and what the second study concluded.

The researchers were examining cave artifacts in a cave site in Mozambique which have been dated to somewhere between 42000 and 105,000 years ago.   They mention that excavation in 2007 retrieved 555 artifacts.  Of those, 70 stone tools were analyzed and were chosen to represent the broadest range of potential plant uses.  This includes scrapers, grinders, points, flakes and miscellaneous tools.  These were analyzed and while 20% contained no starch residue, the other 80% were found to contain starch granules with the number on each tool ranging from 1 to 650.  It’s worth noting that the quantity of granules found on the scrapers was massively larger than what is found naturally in the cave, that is, they were brought into the cave.

The majority of starch granules (89%) were identified as sorghum, a grass showing a large complex of cultivated, wild and weedy types.  The researchers note that the starch granules found on the tools analyzed are structurally identical to modern sorghum plants.  As the researchers state:

The Mozambican data show that Middle Stone Age groups routinely brought starchy plants to their cave sites and that starch granules go attached to and preserved on stone tools.  I cannot prove that starch from all stone tools represents direct tool function…These early grinders are simply modified cobbles and core tools, with a suspected use that conforms to the technological action of “diffuse resting percussion” and “pounding”, which allows the grinding of plant materials.

Put differently, while more research will certainly be needed to verify or refute this claim, data that is a bit more direct than “Assumptions based on a book some guys wrote years and years ago” suggest that as far back as 100,000 years ago, humans had found a way to refine and consume at least some grains for their diet.  Or as the researchers state more directly in the abstract above:

A large assembly of starch granules has been retrieved from the surfaces of Middle Stone Age tools from Mozambique, showing that early Homo Sapiens relied on grass seeds starting at least 105,000 years ago, including those of sorghum grasses.

And even if you don’t buy the argument of the book I referenced above, that 10,000 years is more than sufficient to allow adaptation to changes in diet, it would be hard to argue that 105,000 years isn’t time enough to adapt to some degree.

Diaz EO et. al. Glycaemic index effects on fuel partitioning in humans. Obes Rev. (2006) 7:219-26.

The purpose of this review was to examine the role of glycaemic index in fuel partitioning and body composition with emphasis on fat oxidation/storage in humans. This relationship is based on the hypothesis postulating that a higher serum glucose and insulin response induced by high-glycaemic carbohydrates promotes lower fat oxidation and higher fat storage in comparison with low-glycaemic carbohydrates. Thus, high-glycaemic index meals could contribute to the maintenance of excess weight in obese individuals and/or predispose obesity-prone subjects to weight gain. Several studies comparing the effects of meals with contrasting glycaemic carbohydrates for hours, days or weeks have failed to demonstrate any differential effect on fuel partitioning when either substrate oxidation or body composition measurements were performed. Apparently, the glycaemic index-induced serum insulin differences are not sufficient in magnitude and/or duration to modify fuel oxidation.

Background

The glycemic index (GI) of foods is yet another place where endless argument and debate exists in the world of nutrition, especially as it applies to body composition.

In the early days of nutrition, as many may recall, carbohydrates were rather simplistically divided into simple and complex sources with the even simpler belief that ‘simple = bad’ and ‘complex = good’.  While this was applied to general health and such, one of the major applications and concerns over carbohydrate intake had to do with diabetic meal planning.

When it became clear that simple vs. complex was insufficient, researchers went looking for more accurate methods of measuring the differences between carbohydrates.  Sometime in the 80′s, the GI was born.

Conceptually, the GI refers to the blood glucose response to a given carbohydrate food.  A little more technically, the GI of a food relates to the area under the curve (AUC for nerdy types) of blood glucose versus time after the ingestion of a fixed amount of a test food.

Researchers would first test a fixed amount (currently 50 grams digestible carbohydrate) of some standard food, they originally used pure glucose but switched to white bread years later.  The blood glucose response to that standard food was defined as having a GI value of 100.  I want to make it clear that this value has no inherent meaning, it was simply a defined value.

Then other foods were tested, again 50 grams of digestible carbohydrate (perhaps baked potato or cereal) were given by itself after an overnight fast and the blood glucose response was measured. The GI of that food was then defined relative to the 100 value of the test standard.  So a GI of 80 meant that the test food had 80% of the blood glucose response of the test food; a GI of 120 means that it had 120% the blood glucose response of the test food.  Again, keep in mind that these values don’t really ‘mean’ anything, they are just relative value.

In any case, from the standpoint of diabetic meal planning, the GI seemed important as it would let diabetics decide which foods would have the best effect on blood glucose levels without causing problems.  Of course, for a variety of reasons, the GI concept was also adopted by athletes and the physique obsessed.

I’d note that there is much more to the GI than I have space to go into here, I’ll be writing a full article on it soon enough.  Sufficed to say that GI becomes much more complicated when you start mixing foods together, or the person isn’t fasted (e.g. you’ve eaten a meal).  Even the aerobic training status of a person modifies the GI as I detail in the research review The Influence of the Subject’s Training State on the Glycemic Index.

In any event, the big argument over the GI of foods at least with regards to body composition usually involves the insulin response and potential impact on things like fat mass and fuel utilization.  It was usually inferred that a higher GI value (remember, larger and/or longer blood glucose response) meant a bigger insulin response and for the physique obsesses, insulin equals badness.

I’d note that things aren’t this simple and at least one study suggests that foods with a lower GI may have a lower GI because of a LARGER initial insulin response as detailed in Different Glycemic Indexes of Breakfast Cereals Are Not Due to Glucose Entry into Blood but to Glucose Removal by Tissue.

The Paper

But I’m getting off topic.  What today’s paper looks at is the idea of whether differences in the insulin response (from foods differing in GI) actually have meaningful differences in terms of their effect  on insulin, fuel utilization or body composition.

Because that’s the real issue: there’s no debate that foods differing in GI generate different blood glucose responses, there is indication that this impacts on the insulin response.  But the bottom line question is whether those differences in hormonal response actually meaningfully affect anything.

In looking at the topic, the researchers examined a variety of different data sets including more acute studies along with those looking at actual changes in body composition.

The short-, mid- and long-term studies typically examined things like blood glucose, insulin, blood fatty acid levels, carb and fat oxidation and/or energy expenditure over periods ranging from 6-24 hours (or longer) after the ingestion of foods or meals differing in GI.  I’m not going to detail each and every one but, with one or two exceptions, the majority simply found no significant difference in things like fatty acid suppression or fuel oxidation despite significant differences in blood glucose and insulin response.  Even longer term intervention studies of 30 days to 10 weeks found no significant impact on weight or body composition for diets designed with different GI levels.

So in terms of data directly examining the topic, the researchers comment that:

High fasting serum insulin concentration or high first-phase serum insulin response to intravenous glucose has been proposed as a risk factor for weight gain.This may have led Ludwig to state that ‘functional hyperinsulinemia associated with high-GI diets ma promote weight gain by preferentially directing nutrients away from oxidation in muscle and towards storage in fat’.  Evidence for this hypothesis is still lacking since no effects of GI on fuel partitioning have been demonstrated to date.

Of course, there are studies suggesting that lower GI diets generate more weight loss than higher GI but there are often subtle confounds including the fact that typically GI is not the only difference between diets.  Often, with changes in the GI come differences in fiber intake, energy density of the diet, at least one study I can think of changed protein intake between groups.  So concluding that the GI per se is having an impact is incorrect.

It’s worth mentioning that low GI foods are often claimed to better control appetite than higher GI foods.  And about half of the studies examining this do find this effect, with the other half finding no real effect.  As I discuss in Is a Calorie a Calorie, this is another confound, if eating lower GI foods causes someone to eat less total food, they will tend to lose weight but it’s not due to the GI of the foods per se.  As well, if high GI foods make people eat more, they will tend to gain fat, as a function of eating more.

But this is far different than claiming that high GI foods will make someone gain fat (and/or lose muscle) at an identical caloric intake, an argument that does not seem to be supported by the above studies looking at fuel utilization directly.

I should note that there is at least some indication of an interaction between high and low GI diets and insulin sensitivity, as I discuss in Insulin Sensitivity and Fat Loss, at least one study has shown that people with insulin resistance lose more weight with lower GI diets while those with higher insulin sensitivity actually do better with higher GI diets.

Wrapping up the paper, the researchers examine the impact of insulin on fuel utilization in general terms mentioning that both the magnitude and duration of insulin response has the potential to affect fuel and fat utilization.  Without detailing all of the information, they conclude

Taking into account all of the above arguments, we speculate that under postprandial conditions, GI-induced serum insulin differences are not sufficient in magnitude and/or duration to modify fat oxidation.

Given that even tiny increases in insulin pretty much shut off fat oxidation, this actually isn’t surprising.  As I discussed in The Stubborn Fat Solution, even fasting levels of insulin inhibit fat cell lipolysis by 50% from maximal rates and almost any increase in insulin is sufficient to shut off lipolysis completely.

As this research review points out, it simply doesn’t appear that some vs. more insulin has any major impact on this.  I’d note, mind you, that fat cell metabolism can also be impacted by eating even if insulin doesn’t increase; oral ingestion of pure dietary fat also shuts down lipolysis but that’s beyond the scope of this article.

Summing Up

Ok, what does this all mean and what am I saying?  First let me clarify what I am not saying.  I don’t want folks to read this as a suggestion to go scarf down as much high GI, refined stuff as they can put down their gullets.  That would be asinine although I’m sure someone will manage to read this article as advocating exactly that.

Even if there is no significant impact on acute fuel utilization, fat oxidation or storage in the short-term for higher GI vs. lower GI foods, that doesn’t suggest that eating nothing but high GI foods is the way to automatically go.

As I noted above, for many people lower GI foods tend to control hunger better and, in general, lower GI foods are typically less refined, contain more fiber and nutrients, etc.  Even if there are no significant differences in how they impact on fuel utilization, health should always be a consideration.  There are other issues such as the glycemic load (a topic I’ll discuss in some detail later) and overall health as well.

But from the standpoint of fuel utilization, fat oxidation and the rest, there appears to be no meaningful differences in the impact of higher vs. lower GI foods in humans (the study also examined animal data where things, as usual, are different but simply don’t apply to non-rats).

I find that many people become nearly clinically insane over the issue of GI, it becomes a level of absolute dietary extremism that is simply not necessary.   For these folks, anything without a super low GI is a devil food and will cause one’s muscles to instantly fall off and be replaced by body fat.

And as with so many other topics, that’s just not the case.  Small differences in GI, especially within the context of mixed meals and lean individuals who are training regularly appear to have no significant impact on overall fuel utilization, fat oxidation, or anything else.

Messina M, Redmond G. Effects of soy protein and soybean isoflavones on thyroid function in healthy adults and hypothyroid patients: a review of the relevant literature. Thyroid. (2006) 16:249-58.

Soy foods are a traditional staple of Asian diets but because of their purported health benefits they have become popular in recent years among non-Asians, especially postmenopausal women. There are many bioactive soybean components that may contribute to the hypothesized health benefits of soy but most attention has focused on the isoflavones, which have both hormonal and nonhormonal properties. However, despite the possible benefits concerns have been expressed that soy may be contraindicated for some subsets of the population. One concern is that soy may adversely affect thyroid function and interfere with the absorption of synthetic thyroid hormone. Thus, the purpose of this review is to evaluate the relevant literature and provide the clinician guidance for advising their patients about the effects of soy on thyroid function. In total, 14 trials (thyroid function was not the primary health outcome in any trial) were identified in which the effects of soy foods or isoflavones on at least one measure of thyroid function was assessed in presumably healthy subjects; eight involved women only, four involved men, and two both men and women. With only one exception, either no effects or only very modest changes were noted in these trials. Thus, collectively the findings provide little evidence that in euthyroid, iodine-replete individuals, soy foods, or isoflavones adversely affect thyroid function. In contrast, some evidence suggests that soy foods, by inhibiting absorption, may increase the dose of thyroid hormone required by hypothyroid patients. However, hypothyroid adults need not avoid soy foods. In addition, there remains a theoretical concern based on in vitro and animal data that in individuals with compromised thyroid function and/or whose iodine intake is marginal soy foods may increase risk of developing clinical hypothyroidism. Therefore, it is important for soy food consumers to make sure their intake of iodine is adequate.

Introduction

Soy protein is one of those topics that seems to be a perennial topic of debate and argument with staunch pro- and anti-soy people out there making all kinds of seemingly good arguments for either the benefits or dangers of soy protein.  As is usually the case with extremist positions, I find that the reality lies somewhere in the middle.

Now, I think that part of the problem, as I explained in a seminar a few weeks ago, is how people, at least those in the United States (I can’t speak to the rest of the world) tend to approach things.  Folks are prone to extremes in the first place and nowhere is this more prevalent than in the health field.

Whenever some nutrient is discovered to be ‘healthy’, invariably people figure that more must be better and start mega-dosing it.  This invariably leads to some sort of backlash as people learn (often the hard way) that more is, in fact, not better.  Then they invariably go on a crusade against that nutrient not realizing that their own extreme behavior (rather than the nutrient itself) was the actual cause of the problem.

One of my favorite examples is that of oat bran back in the 80′s.  Discovered to improve blood lipid levels, people starting eating mountains of the stuff, 50+ grams per day.  People were putting down horse-doses of the stuff because, you know, more is better.  Until it was found that such massive fiber intakes, especially from isolated sources, had the potential to cause vitamin and mineral deficiencies by binding them up before they could be absorbed.

Which brings me in a roundabout way to the issue of today’s research review on soy protein and thyroid function.  As per usual, there are camps on both sides of the debate for soy protein having either a beneficial or negative effect on thyroid hormones.  And also as per usual, the truth of the matter, in terms of how soy protein affects thyroid hormones lies somewhere in the middle and depends on other factors.  Today’s review looks at them.

Background

To give readers a brief background on the topic, the thyroid gland releases two primary hormones T4 and T3 (thyroxine and trio-iodothyronine respectively) in a ratio of roughly 80:20 in response to the signal sent by TSH (thyroid stimulating hormone).  That is to say, most of the thyroid released from the thyroid gland itself is the relatively inactive T4.  Most T3 is actually made in other tissues (especially the liver but also in many other cells) from the metabolism of T4 via an enzyme called 5′-deiodinase.

Now, I imagine most readers think of T3 in terms of its effects on body weight or body fat and it’s certainly true that T3, along with the catecholamines (adrenaline/noradrenaline or epinephrine/norepinephrine depending on which side of the pond you’re on) are two of the primary regulators of human metabolic rate.  Of course, thyroid controls about a billion other things in the body too and, as one example, low T3 status can cause depression.

I should mention that iodine intake plays a crucial role in thyroid metabolism with inadequate intake of iodine causing thyroid problems.  There are many other micronutrients that are involved in this conversion process as well; these include selenium and iron (iron deficiency can impair thyroid conversion, yet another reason to eat red meat while dieting).

Now soy proteins are known to contain hormonal mimics called phytoestrogens. This include genistien, daidzein and others.  A great deal of controversy exists over the impact of these types of compounds in the human diet; while phytoestrogens may have some beneficial effects (especially in post-menopausal women for whom low estrogen can predispose towards heart disease and bone loss) other research shows negative impacts.  A lot of whether positive or negative impacts are seen depends on what’s being looked at and, of course, the dose studied.

The effect of phytoestrogens in men is far less studied and understood.  While many are concerned that the phytoestrogens present in soy may negatively impact on testosterone levels the reality is that the studies done to date, using moderate doses of soy/phytoestrogens, have found little to no impact (higher doses are often seen to cause issues).

There is likely to be a sex and population specific response to these compounds and whether or not soy has an impact on anything at all depends heavily on the amount being consumed.  Small amounts of soy protein tend to have minimal or no effects on most things studied (such as testosterone levels) while large daily amounts are often seen to have an effect.

There’s an old saw in medicine that the dose makes the poison and this is certainly one of those situations.

And, as I noted in the introduction, I think part of the backlash against soy has more to do with the human nature of people thinking more is better than with the nutrient itself.  As I mention below, the actual soy intake among Asian cultures doesn’t appear to be that high in the first place (and anyone who is worried about the impact on testosterone levels might consider that Asians, as a whole, don’t seem to be having many problems with fertility or making babies).

Again, I’m not going to focus on all of the potential effects of soy (e.g. on hormones such as testosterone) here; I only want to look at the impact, or potential impact of soy protein on thyroid hormone metabolism.

The Paper

So with that background out of the way, on to today’s research review, a review paper on the impact of soy protein on thyroid hormone status and metabolism.  As I noted above, there are two primary thyroid hormones, T4 and T3 and it appears that soy may have an impact on both.

Early work, in animals, had supported the idea that soy proteins could actually increase thyroid (mainly T4) output and this is likely where a lot of the pro-soy claims come from in terms of thyroid status (e.g. some will claim that soy will help fat loss by raising thyroid hormones).

However, as the paper points out,  studies suggests a very different effect in humans with soy protein having little to no direct impact on thyroid hormone output.  This is yet another place where extrapolating from animal research just doesn’t pan out.  Of course, there is also animal research suggesting a negative impact of soy protein, primarily the phytoestrogens, on animal thyroid status, something the pro-soy folks seem to ignore when they claim that soy will increase thyroid output.

Beyond that, at least in individuals with normal thyroid function, soy protein appears to have little to no impact on overall thyroid status.  The review examined 14 different studies (as noted above, 8 in women, 4 in men and 2 in both) and, with one exception, found little to no impact of soy intake on any measure of thyroid hormone status.  I’ll spare you all of the details, only the punchline is of any real importance.  Again, that’s in individuals with otherwise normal thyroid function.

However, in individuals with pre-existing low-thyroid (hypothyroid) symptoms, soy proteins can cause problems. Research has shown that soy protein intake may increase the dose of thyroid medication needed (the soy appears to impair uptake of thyroid medication) and individuals who are on thyroid hormones may need to avoid soy protein immediately around the intake of their medication.

Another review (Doerge DR. Goitrogenic and estrogenic activity of soy isoflavones. Environ Health Perspect. (2002) 110 Suppl 3:349-53.2002) has shown, using mainly animal work, that the phytoestrogens in soy can impair the enzyme (thyroid peroxidase) responsible for proper thyroid hormone production. That same review found that while soy protein itself could not induce a hypothyroid state, a high phytoestrogen intake coupled with a low iodine intake could.

I bring up this last point because one of the main providers of iodine in the modern diet is iodized salt and even there, diet surveys have shown a downward trend in overall iodine intake (due to a reliance on processed food and less iodinization of salt).  It’s worth noting that seaweed (another stable in Asian culture) is another good source of iodine. Even if Asian cuisine did contain a tremendous amount of soy, it would seem that the intake of seaweed, by providing iodine, would help to prevent problems from occurring.

Basically, I could see how a high intake of soy products (which are being used to fortify many foods such as cereals and protein bars, in addition to the use of soy protein powders) coupled with a misguided attempt to reduce salt intakes excessively (as is often seen in many ‘health-conscious’ individuals) could potentially cause proteins with overall thyroid metabolism.

But, and this goes to my comments earlier in the article, this is only an issue with people insistent on taking aspects of their diet to extremes.  People who are really consuming a massive amount of soy protein on a daily basis (that intake level not being seen in the Asian cultures in the first place) who also are trying to minimize sodium intake could be putting themselves at potential risk. And this is moreso the case if there is a pre-existing problem.

Summing Up

So we have several different issues at stake here in terms of how soy protein might impact on thyroid hormone status.

Clearly individuals with no pre-existing thyroid problems don’t need to worry much about soy.  And, no, I’m not saying that folks should therefore eat as much of it as possible.  Just that they needn’t go out of their way to avoid any and all source of soy in their diet.

But what about people who do have a pre-existing thyroid problem?

First and foremost, anybody who is on thyroid medication should avoid consuming soy immediately before or after taking their medication as soy protein appears to impair absorption of thyroid medication.  Individuals insistent (for whatever reason) on consuming soy near to the intake of their thyroid medication will need to increase their dose to compensate.  This, of course, should be dealt with through your medical provider/health professional.

As well, individuals with pre-existing thyroid problems (and it’s worth mentioning that females, which tend to be the primary target for soy foods, are more likely to have thyroid problems than men) may need to limit their soy intake on a day to day basis.  This is especially the case for individuals intent on reducing their sodium intake.

So…recommendations.

Trying to avoid every last bit of soy intake (for example, a typical soy protein fortified cereal may contain a few grams at most of soy) seems misguided to me, most studies examining a variety of endpoints find that it’s only when soy protein intake is excessive that any sorts of problems start. Even in the case of hypothyroid individuals, soy only appears to be a problem when iodine intake is insufficient in the first place.

Clearly, living on nothing but soy foods and soy fortified products is misguided as well.  As I mentioned above, the soy intake among most Asian cultures isn’t actually that massive in the first place and I suspect that much of the backlash against soy is primarily to do with people taking a little of a good thing, assuming a lot was better, and causing themselves problems because of it.

To me a happy medium seems the best; assuming no pre-existing thyroid problems, soy products are probably safe in moderation.  What’s moderation?  In The Protein Book, I suggested a daily maximum of perhaps 20-25 grams of soy protein on a daily basis.  Based on the average phytoestrogen content of most soy proteins (generally 2-3 mg phytoestrogen per gram of soy protein), that will keep most people below the threshold where any sorts of issues start to crop up.

I should mention that many foods are currently being fortified with soy protein (check the labels) and people may already be consuming soy protein in some amounts without knowing it.  Adding more (e.g. through a soy protein powder) may very well take people above the level I suggested above.

Frankly, unless someone is a fairly strict vegetarian or vegan, there are enough other high quality protein sources (such as meat, dairy products, whey, etc.) that I don’t see the need to consume massive amounts of soy in the first place.  But neither do I think it’s a horrible protein that no-one should ever eat because it will make their testosterone drop and give men boobs.

Soy, like all proteins has a variety of pros and cons and, in moderation, can make up part of a healthy or sports oriented diet.  Thinking that it is evil and must be eliminated is as silly as thinking it’s the best protein ever and people should consume tons of it.

Bray GA et. al. Hormonal Responses to a Fast-Food Meal Compared with Nutritionally Comparable Meals of Different Composition. Ann Nutr Metab. 2007 May 29;51(2):163-171 [Epub ahead of print]

Background: Fast food is consumed in large quantities each day. Whether there are differences in the acute metabolic response to these meals as compared to ‘healthy’ meals with similar composition is unknown. Design: Three-way crossover. Methods: Six overweight men were given a standard breakfast at 8:00 a.m. on each of 3 occasions, followed by 1 of 3 lunches at noon. The 3 lunches included: (1) a fast-food meal consisting of a burger, French fries and root beer sweetened with high fructose corn syrup; (2) an organic beef meal prepared with organic foods and a root beer containing sucrose, and (3) a turkey meal consisting of a turkey sandwich and granola made with organic foods and an organic orange juice. Glucose, insulin, free fatty acids, ghrelin, leptin, triglycerides, LDL-cholesterol and HDL-cholesterol were measured at 30-min intervals over 6 h. Salivary cortisol was measured after lunch. Results: Total fat, protein and energy content were similar in the 3 meals, but the fatty acid content differed. The fast-food meal had more myristic (C14:0), palmitic (C16:0), stearic (C18:0) and trans fatty acids (C18:1) than the other 2 meals. The pattern of nutrient and hormonal response was similar for a given subject to each of the 3 meals. The only statistically significant acute difference observed was a decrease in the AUC of LDL cholesterol after the organic beef meal relative to that for the other two meals. Other metabolic responses were not different. Conclusion: LDL-cholesterol decreased more with the organic beef meal which had lesser amounts of saturated and trans fatty acids than in the fast-food beef meal.

My Comments

For a couple of decades, there has been an ongoing argument regarding the issue of ‘is a calorie a calorie’ in terms of changes on body composition and other parameters.    I discuss this topic in Is a Calorie a Calorie?

Fundamentally, my belief is that, given identical macro-nutrient intakes (in terms of protein, carbs, and fats) that there is going to be little difference in terms of bodily response to a given meal.  There may be small differences mind you (and of course research supports that) but, overall, they are not large. And certainly not of the magnitude that many make it sound like.

It’s worth nothing that there are a couple of built-in assumptions to my argument, all of which are detailed in the article I linked to above but I want to briefly reiterate them here.

A tediously typical argument of the ‘a calorie isn’t a calorie’ types is usually something along the lines of “Clearly eating 3000 calories of jelly beans isn’t the same as eating 3000 calories of chicken breast and vegetables.”  Well…no shit.

But at that point, the argument is about more than food quality, it’s also about the macro-nutrient content.   And of course the diet containing zero protein will be bad.  But, again that has zip to do with it being clean and everything to do with there being no protein.

My basic assumptions in this argument are that both protein and essential fatty acid requirements are being met.  Beyond that, I find most of the obsession over food quality to be pretty pointless.  Again, this is discussed in more detail in the article linked above so I won’t get into it here.

Now it’s worth noting that a great deal of the difference seen between ‘eating clean’ and ‘eating unclean’ has to do with caloric intakes.  I’ve pointed out repeatedly that, and this is especially true when people are not counting their calories, certain eating patterns tend to make people eat more than others.  It’s easier to overeat donuts than broccoli.

Clearly, someone eating a 2000 calorie fast food meal will obviously get a different response than someone eating a 500 or even 1000 calorie clean meal.  But as with the argument above, at this point there is more than one variable changing; it’s not just about clean vs. unclean, you’re comparing meals of drastically different caloric value.

A far more logical comparison would be to look at ‘unclean’ vs ‘clean’ meals containing the same caloric value and the same macro-nutrient content; by controlling those two variables, the only thing being examined will be the quality of the food (rather than the total quantity or the macro-nutrient profile).

Especially when you’re talking about bodybuilders and athletes who are typically controlling their caloric content.  Under those conditions, I argue that there will be no significant difference between the two; given identical macros and calories, there is simply no real-world difference in a clean vs. unclean meal in terms of its effects on body composition (health and other effects such as hunger control are separate, albeit important, issues).

However, even there the clean freaks will make the counter-argument: they contend that even if the macros and calories are identical, the unclean meal will still be worse.  This is usually based on an assumed difference in hormonal response (usually insulin).

So who’s right?

Unfortunately, very little research has actually examined this topic in any sort of controlled way (there are at least two studies showing that high sucrose diets generate identical weight and fat losses as lower sucrose diets).  At least until this paper came along

The study’s explicit goal was to see if the metabolic response to a fast-food meal would differ to a ‘healthy’ meal of similar macro-nutrient and caloric value.

Towards this end six overweight men and two women were recruited to take part in the study although the data in the women was excluded due to the low number and possible gender effects.

Each subject consumed each of the three test meals on different days with one week in between trials. A standard breakfast was provided at 8am and the test meal was given at exactly 12pm and blood samples were taken every 30 minutes for the first 4 hours and every 60 minutes for the next two hours. Blood glucose, blood lipids, insulin, leptin, ghrelin and free fatty acids were measured.

The test meals consisted of the following:.

• Fast food meal: A Big Mac, french fries and root beer sweetened with high fructose corn syrup purchased at the restaurant itself.
• Organic beef meal: this meal used certified organic rangefed ground beef; cheddar cheese; hamburger bun made with unbleached all purpose naturally white flour, non-iodized salt, non-fat powdered milk, natural yeast, canola oil, and granulated sugar; sauce made from canola mayonnaise and organic ketchup; organic lettuce, onion and dill pickles; French fries made from organic potatoes and fried in pure pressed canola oil; and root beer made with cane sugar.
• Organic turkey meal: this consisted of a turkey sandwich made from sliced, roasted free-range turkey breast with no antibiotics or artificial growth stimulants; cheddar cheese; 60% whole wheat bread made with whole wheat and unbleached all-purpose naturally white flours, non-iodized salt, non-fat powdered milk, yeast, vital wheat gluten, canola oil, and granulated sugar; pure pressed canola oil and canola mayonnaise, stone ground mustard; organic lettuce; accompanied by a granola made with Blue Diamond whole natural almonds, Nature’s path organic multigrain oatbrain flakes, wholesome sweeteners evaporated cane juice, Spectrum Naturals pure pressed canola oil, clover honey, Sonoma organically grown raisins and dried apples. The beverage was an organic orange juice.

So the study was comparing a commercial fast food meal to two carefully designed organic meals (one beef, one turkey) from the above list of ingredients.

The composition of each meal was as follows:

It’s important to note that while the meals were similar, they were not identical in composition; it would have been better if the meals had been completely identical.

The biggest difference between meals had to do with the fatty acid composition: the fast food meal contained twice as much saturated and nearly 8 times as much trans-fatty acids with half of the oleic acid compared to the organic beef meal (which is no surprise).  Interestingly, the fast food meal actually contained more linoleic acid than the organic beef meal. The turkey meal had less saturated fat but similar amounts of linoleic and linolenic acid to the fast food meal, with the lowest amount of trans fats.

So what happened?

In terms of the blood glucose and insulin response, no difference was seen between any of the meals and this is true whether the data was presented in terms of percentage or absolute change from baseline. The same held true for the ratio of insulin/glucose, no change was seen between any of the meals.  Please read those sentences again: the blood glucose and insulin response were identical for all three meals despite one being a fast food ‘unclean’ meal and the other two being organic ‘clean’ meals.

Fatty acid levels showed slight differences, dropping rapidly and then returning to baseline by 5 hours in the beef meals but 6 hours in the turkey meal.  Blood triglyceride levels reached a slightly higher peak in the organic beef and turkey meals compared to the fast food meal but this wasn’t significant.

Changes in leptin were not significant between groups; ghrelin was suppressed equally after all three meals but rose above baseline 5 hours after the fast-food lunch but returned only to baseline in the other two meals.

The only significant difference found in the study was that LDL cholesterol decreased more after both of the organic meals compared to the fast food meal, HDL and total cholesterol showed no change after any of the meals. This was thought to be due to differences in the fatty acid content of the meals (saturated fat typically having a greater negative impact on blood lipid levels than other types of fat).

However, beyond that, there were no differences seen in the response of blood glucose, insulin, blood fatty acids or anything else measured.

Now, the study does have a few limitations that I want to mention explicitly.

1. The study only looked at a single meal.   It’s entirely possible that a diet based completely around fast food would show different effects.
2. The sample size was small: 6 overweight men and two women. It’s possible that differences would have shown up with more subjects. A related question is whether lean individuals would respond differently.  Perhaps but I doubt it.  As I discussed in The Influence of the Subjects’ Training State on the Glycemic Index, GI and insulin response are even less relevant in trained individuals.

However, with that said (along with the fact that the meals weren’t exactly identical), the basic fact is this: the metabolic response between the three meals was essentially identical.  There were no differences in either insulin or blood glucose, the fatty acid profile makes perfect sense given the composition of the meals and blood lipids showed basically no change.

Application

This study basically backs up what I’ve been saying for years:  a single fast food meal, within the context of a calorie controlled diet, is not death on a plate.  It won’t destroy your diet and it won’t make you immediately turn into a big fat pile of blubber.  And, frankly, this can be predicted on basic physiology (in terms of nutrient digestion) alone.  It’s just nice to see it verified in a controlled setting.

It’s not uncommon for the physique obsessed to literally become social pariahs, afraid to eat out because eating out is somehow defined as ‘unclean’ (never mind that a grilled chicken breast eaten out is fundamentally no different than a grilled chicken breast cooked at home) and fast food is, of course, the death of any diet.  This is in addition to the fact that apparently eating fast food makes you morally inferior as well.  Well, that’s what bodybuilders and other orthorexics will tell you anyhow.

Except that it’s clearly not. Given caloric control, the body’s response to a given set of nutrients, with the exception of blood lipids would appear to be more determined by the total caloric and macro content of that meal more than the source of the food.

In terms of the hormonal response, clean vs. unclean just doesn’t matter, it’s all about calories and macros.

Which is what I’ve been saying all along.

Wolf A, Bray GA, Popkin BM. A short history of beverages and how our body treats them. Obes Rev. 2008 Mar;9(2):151-64.

Numerous studies have demonstrated that beverages containing sugar, high fructose corn syrup (HFCS) or alcohol are handled differently by the body than when sugar or HFCS are incorporated in solid foods and as a result the overall caloric intake from solid food does not adjust to account for the calories in these beverages. A consideration of our evolutionary history may help to explain our poor compensatory response to calories from fluids. This paper reviews the history of eight important beverages: milk, beer, wine, tea, coffee, distilled alcoholic beverages, juice and soft drinks. We arrive at two hypotheses. First, humans may lack a physiological basis for processing carbohydrate or alcoholic calories in beverage because only breast milk and water were available for the vast majority of our evolutionary history. Alternatives to those two beverages appeared in the human diet no more than 11 000 years ago, but Homo sapiens evolved between 100 000 and 200 000 years ago. Second, carbohydrate and alcohol-containing beverages may produce an incomplete satiation sequence which prevents us from becoming satiated on these beverages.

My Comments

This is sort of a departure from the typical paper I talk about but I think it’s very interesting and, as you’ll see towards the end, does have some practical implication for dieters and folks looking to alter body composition.

I think it’s especially relevant after the research review I posted on Straight Talk About High Fructose Corn Syrup – What it is and What it Ain’t; for the simple fact that people are confounding what the real issue actually is in terms of causal effects on obesity.  As you’ll see as you read this, the issue isn’t with HFCS per se, but rather with the foods in which they are most commonly consumed: sweetened soft drinks.  But I’m getting ahead of myself.

After the necessary introduction, the paper first looks at changes in the patterns of beverage consumption within the US. They point out that by 2004, Americans were consuming over 135 gallons of fluids other than water or about 1.5 liter per day. Basically, Americans are drinking a lot but it isn’t water; by definition it must be something else.

The early part of the paper also trots out something called the Beverage Guidance Panel; an attempt to give fluid consumption guidelines to consumers.  In my opinion, this graphic is about as useless as the current food pyramid. It’s complicated and pointless, simply confusing people more about the issue. I’m not going to bother talking about it.

Quoting the paper, they state that “While consumption of healthful beverages is falling, consumption of the most unhealthy beverages is strong.” While milk and coffee consumption are at roughly one half of their historical maximum, with tea basically unchanged, regular soft drinks are the most popular beverage; beverages sweetened with high-fructose corn syrup are consumed at a rate of over 35 gallons per year on average. The second most popular drink is beer which at least has some nutrients.

I want folks to pay attention to that bolded bit since I’ll come back to it later on.

Positively, low-fat milk makes up two thirds of milk consumption with soft drink consumption trending downwards. However, this may be a false artifact due to how drinks are classified, energy drinks aren’t being counted as soft drinks which is making it look like folks are drinking less soda.  They aren’t, they are just drinking energy drinks instead.  And most of these are filled with sugar and calories along with the stimulant nutrients.

Looking globally, drink patterns have shown massive growth with soda products being consumed at a rate in excess of one billion drinks per day (makes you wish you’d bought stock, huh?).  Beer consumption has shown the greatest increase with tea showing a slight increase. Wine and milk consumption have fallen globally, presumably due to the introduction of all the drinks that have made America rich, proud and very fat (my comment, not theirs).

The next section of the paper got into what is arguably the most important issue of the paper: the simple fact that for all but the last 11,000 years, the predominant fluids consumed by humans were water and breast milk and nothing else. Now, they go out of their way to point out that milk is a complete beverage containing protein, carbohydrate, fat and water. Water is, of course water which provides no calories. This is important because numerous studies have shown that humans show poor compensation for fluid calories.

Let me explain that a bit. Compensation means that the body will adjust caloric intake at other times of the day (or days later) for a given caloric load. So say you eat a bunch of candy earlier in the day and it provides 450 calories. What you might see is that, later in the day, folks eat a few hundred calories less than they’d normally eat. The body ‘compensates’ for the food you ate earlier. The problem is that most liquid calories aren’t compensated for well and figuring out why is of some interest to researchers.

This is also a big part of why all of the furor over HFCS is mis-placed in my opinion: the problem isn’t with the HFCS per se, it’s the form that people are getting it which is liquid calories.  Which the body doesn’t compensate for well.  But the body wouldn’t compensate any better for a sucrose containing drink, a glucose containing drink or any other caloric drink.  Get it?

It’s got nothing to do with the HFCS content, it’s got to do with how the human body handles non-milk caloric fluids.  Which is poorly.

The paper suggests that one of two possible mechanisms may be at stake here. First, we may simply lack a physiological mechanism by which to compensate for liquid calories; we didn’t evolve consuming them and it would make no logical sense for our bodies to handle them like it handles food.

Second, it may be that liquids are treated essentially like water, being digested/absorbed too quickly to have any subsequent impact on food intake (normally eating food does things hormonally that tends to make you eat less later).

With that out of the way, the paper examines the majority of fluids consumed by humans from a historical perspective. I’m not going into deep detail for each or this would take pages. While interesting, this really isn’t that relevant to the rest of the paper or how it impacts on things like weight, fat or body composition.

The main take home point of this paper has to do with how the body responds to different beverages. Various lines of research indicate that the intake of calorically sweetened beverages do NOT reduce the intake of solid food (the compensation issue I mentioned above). Reviewing the literature, they basically point out what I wrote above.

Of some interest (especially to me since I like jelly beans) one study compared the intake of 450 kcal or jelly beans to 450 kcal of a soft drink. The jelly bean consumers actually reduced their food intake by slightly more than the 450 calories in the jelly beans (Coming soon: the Jelly Bean Diet) later in the day.

The carb containing soft drink group not only failed to compensate for the drink but also increased their intake of other foods slightly. That is, not only did they get the added calories from the soft-drink, they ate more food as well; a double whammy in terms of weight gain.

Continuing on, the paper addresses the issue of why the body shows weaker compensation to some fluids; the exact reason is unknown. The propose that one mechanism is in the way that the GI tract responds to the form of the food; solutions can stimulate stronger sensory responses than solid food (e.g. sweet drinks taste sweeter than sweet foods sometimes). As well, the components which make up the beverage or food may play a role.

Obviously the sight and smell of beverages are important, we may react badly to a repugnant or bitter smelling drink and well to a good smelling drink. How drinks affect the taste buds comes next; humans can taste sweet, sour, bitter, salty and something called umami. There is also a taste bud for fatty acids.

A sickness response to a drink can cause an aversion to foods down the road. Remember when you drank something and you threw up afterwards, and how the smell of that drink would make you gag subsequently? That’s what I’m talking about.

The sight and smell of foods also affects hormonal response, there is something called the cephalic insulin response for example, insulin can go up when people smell or taste sweet foods, long before it hits the bloodstream.  Someone in the comments of one of my articles asked about sugar free drinks and it’s relevant here as they can stimulate insulin response in some folks; I’ll have to do a full feature on this at a later date.

Then comes digestion where mixing with the other components of the stomach affects many things, including digestion rate. Average digestion rate of fluids is 1 cal/minute with water digesting the most quickly (no calories).  Other drinks digest at relatively slower speeds depending on the composition with fat containing beverages emptying slowest.

Moving into the intestine, more stuff happens including the release of a number of different hormones many of which are involved in appetite. I don’t want to detail this as there are a ton that may play a role here.  I’ve detailed some of them (ghrelin, CCK, PYY) in other articles on the site. The pattern of release of these chemicals depends on the composition of the drink and this is where we can start to see the problem.

Carbohydrates alone stimulate the least number of appetite blunting factors, protein and fat stimulate the release of more. So you’d expect much less of a compensatory response to a drink containing protein and fat (think lowfat milk) as compared to one containing only carbohydrate (think fruit juice or a high sugar soda). Which is exactly what the studies have shown.  Milk shows a nice normal compensation to intake; it’s effectively a liquid ‘food’.  Sugar sweetened soft drinks show no compensation.

So folks living on sugary drinks are causing themselves major problems. Not only do the drinks themselves have scads of calories, the body doesn’t compensate for their intake. So all of those calories essentially end up being ‘added’ to the normal food intake (which is just as often awful in folks who drink lots of soda).  In some people, the sweet taste seems to drive intake of other sugary foods so it’s a double whammy.

Alcohol is weird as it’s treated strangely in the body.  It also shows a very weird relationship with body weight. Weight often goes up with alcohol intake in men but either stays the same or goes down in women. What few direct studies exist suggest that alcohol intake does not cause compensation of food intake later on. So what explains the gender difference? Most likely, men drink in addition to eating (beer and wings) while women drink instead of eating (glass of wine for dinner). Oddly, at least one piece of research suggests that regular drinkers may be more active. It may also be that drinkers under-report their true food intake.  At least some work suggests that alcohol may improve insulin sensitivity.  More research is needed to explain this.

The paper then concludes but basically just reiterates what I wrote above so I won’t go into it any further.

Practical Application

The bottom line of the paper is this: humans didn’t evolve on anything but water and mother’s milk with other drinks such as alcohol and soft drinks coming into common usage at a much later date. Because of this, we don’t appear to have evolved good mechanisms for dealing with most types of fluid calories.

Liquids tend to digest quickly (although fluids with protein and fat, such as milk, digest much more like food) and carbohydrate only drinks such as soda don’t release as many of the appetite blunting peptides during digestion as whole food (or milk which is a liquid whole food).

This makes the consumption of sugary drinks (fruit juice or soda) a major problem. People don’t compensate for intake and end up simply adding the massive amount of calories to their diet, which is often bad to begin with.

And, repeating it again, I feel that this is the real problem with the whole high-fructose corn syrup hysteria.  As I noted in the article Straight Talk About High Fructose Corn Syrup – What it is and What it Ain’t there is nothing inherently special to HFCS that makes it particularly obesogenic outside of being a source of calories.

Rather, the issue is in the form that HFCS is being so commonly consumed which is in sugar sweetened beverages.  But sweetening those drinks with sucrose or glucose would be just as bad; the sweetener is irrelevant, the problem is that liquid calories are not compensated for.

Ultimately, I don’t think people should be drinking sugar sweetened drinks period.  Whether they are sweetened with HFCS, sucrose or glucose is irrelevant.  Drink diet soda (now the aspartame maniacs will be after me), or water, or sugar free crystal light.

I don’t usually talk in absolutes about nutrition but this is one time I will:

Don’t drink sugar sweetened soda of any form regardless of the sweetener;   They offer nothing to the diet that can’t be had elsewhere and I see no reason for their consumption at all, regardless of what sugar is present.

As a final take-home comment, I’m reminded of a client I had years ago. He wanted to lose weight and one of the habits I identified in him early was the intake of multiple cans of full-sugar soda. Simply switching him to diet soda saved him something like 800-1000 calories/day, he started losing at a nice 1-2 pounds per week with no other change to his diet.

White JS. Straight talk about high-fructose corn syrup: what it is and what it ain’t.   Am J Clin Nutr. 2008 Dec;88(6):1716S-1721S.Click here to read Links

Abstract

High-fructose corn syrup (HFCS) is a fructose-glucose liquid sweetener alternative to sucrose (common table sugar) first introduced to the food and beverage industry in the 1970s. It is not meaningfully different in composition or metabolism from other fructose-glucose sweeteners like sucrose, honey, and fruit juice concentrates. HFCS was widely embraced by food formulators, and its use grew between the mid-1970s and mid-1990s, principally as a replacement for sucrose. This was primarily because of its sweetness comparable with that of sucrose, improved stability and functionality, and ease of use. Although HFCS use today is nearly equivalent to sucrose use in the United States, we live in a decidedly sucrose-sweetened world: >90% of the nutritive sweetener used worldwide is sucrose. Here I review the history, composition, availability, and characteristics of HFCS in a factual manner to clarify common misunderstandings that have been a source of confusion to health professionals and the general public alike. In particular, I evaluate the strength of the popular hypothesis that HFCS is uniquely responsible for obesity. Although examples of pure fructose causing metabolic upset at high concentrations abound, especially when fed as the sole carbohydrate source, there is no evidence that the common fructose-glucose sweeteners do the same. Thus, studies using extreme carbohydrate diets may be useful for probing biochemical pathways, but they have no relevance to the human diet or to current consumption. I conclude that the HFCS-obesity hypothesis is supported neither in the United States nor worldwide.

My Comments

I think it’s just human nature, people seem to have a need to find a single enemy that is the cause of all woes under the sun.  The one that causes obesity, diabetes, and all manners of health problems.  Nutritionally, I’ve watched the enemy change over the years.  In the 80′s it was dietary fat, which was blamed for all the problems of humanity.  During the 90′s, things started to shift and carbohydrates became the enemy. About the same time, trans-fatty acids became the one thing that people MUST NOT EAT or they would seemingly drop dead nearly instantly.

And now, as we enter 2009, if there is a single nutrient that is blamed for everything that is wrong in the world, it is high-fructose corn syrup (HFCS).   Much of this started with a 2004 paper by Bray where he correlated changes in HFCS intake with changes in obesity, suggesting that it was the increase in HFCS intake that was driving obesity.  This was taken, as usual, far out of context into the popular realm of magazines, newspapers and tv soundbites.

Nowhere is this more prevalent than in the athletic/bodybuilding and fat loss arena where people are simply losing their ever-loving minds over anything with HFCS.  Any food that dare list high-fructose corn syrup on its label (even if the total quantity is obviously miniscule) is immediately deemed to be evil, a destroyer of not only one’s physique but a corrupter of children, a direct line to Satan himself.  Ok, maybe I’m exaggerating but not by much.

This paper addresses this idea, by looking at the hypothesis that somehow HFCS is uniquely obesity or health-problem causing beyond simply being a source of calories.  The author states that several assumptions must be found to be true to accept this idea as fact.  They are:

• HFCS and sucrose are significantly different
• HFCS must be uniquely obesity-promoting
• HFCS must be predictive of US obesity
• HFCS must be predictive of global obesity
• Eliminating HFCS from the food supply must significantly reduce obesity

I won’t detail in full every one of his arguments; the punch line of course is that none of these actually turn out to be true.  Yes, HFCS and foods containing them often contribute a large number of calories to the diet and clearly that alone causes problems; but there is nothing special about HFCS to warrant the fear about it that many seem to have developed.

What is HFCS and Is it Really Different than Sucrose?

Historically, HFCS was developed back in the 50′s as an alternative to cane sugar for food preparations.  The reasons why HFCS is superior for foods than cane sugar isn’t really that relevant; sufficed to say that HFCS is more stable and has replaced your basic cane sugar/sucrose in a lot of foods.

Now, a lot of the silliness, especially in the fitness world about HFCS probably comes out of two things.  The first is a generally anti-fructose, anti-fruit idea that started about 30 years ago with John Parillo.  Fruit is considered forbidden on a diet; nevermind that it helps a LOT of people with hunger (liver glycogen status is one of many signals to the brain) and seems to do something good for thyroid status for many people.

The second is a general confusion about what HFCS actually is, the problem is with the name, the ‘high-fructose’ part of it suggests to people that HFCS is much higher in fructose content that it actually is.  However this is not the case as the chart below shows.  The percentage of either fructose or glucose is shown for each of the types of sugars (HFCS-42, HFCS-55, Corn Syrup, Pure Fructose, Pure Sucrose, Invert Sugar, Honey).

As the chart clearly shows, HFCS-42 is only 42% fructose, lower than sucrose, invert sugar or honey (which is often considered a ‘healthy’ sugar, at least in the hippie subculture).  HFCS-55 is 55% fructose which is only slightly more fructose than the other sugars.  It’s worth noting that there are products such as HFCS-80 and 90 which contain 80 and 90% fructose but they aren’t used widely commercially.

The point being that despite it’s name, HFCS is actually no higher in fructose than many other sugars such as sucrose (table sugar), invert sugar or honey.  The ‘high-fructose moniker’ is simply a poor choice of names but HFCS will not provide any greater amount of fructose to the diet than those other sugars.

Additionally, despite Bray’s assertion that increases in HFCS corrleates with increases in obesity, the paper points out that he looked at the relationship in isolation.  During the time that HFCS intake was going up, daily food intake was also increasing, by about 500 calories per day from 1980 to the year 2000.

Additionally, intake data shows that total sugar intake did not increase over that time frame, and as HFCS intake was going up, sucrose intake was going down; leading to no change in overall sugar intake.  Rather, what people were eating more of was grains and dietary fat.  There is simply no basis to conclude that increasing HFCS intake has any correlation with rising rates of obesity.

Additionally, while it is often claimed that HFCS is sweeter than sucrose (with that being argued that HFCS will increase intake of itself), this is also untrue.  While pure crystalline fructose IS sweeter than sucrose, HFCS is identical in sweetness.  Increasing use of HFCS in the US food supply did not increase the relative sweetness of those foods.

Of course, the caloric value for HFCS and sucrose is identical at 4 calories/gram.  In that sucrose appears to have been swapped out for HFCS in a more or less 1:1 ratio, there is no reason to believe that HFCS intake is increasing caloric intake outside of simply being a source of calories.

Finally, the paper looks at the issue of absorption and metabolism of sucrose vs. HFCS. While fructose is metabolized differently than glucose (in terms of the transporters used and how it is handled in the liver), keep in mind that HFCS is only about half-fructose, just like sucrose.  Fructose malabsorption is a problem, mind you, but only when large amounts of fructose by-itself is consumed, this does not apply to HFCS.

Quoting from the paper:

Sucrose, HFCS, invert sugar, honey an many fruits and juices deliver the same sugars in the same ratios to the same tissues within the same time frame to the same metabolic pathways.  Thus…it makes essentially no metabolic difference which one is used.

So, again, while HFCS is certainly a source of calories (and many HFCS containing foods are easily overconsumed), there is nothing special about HFCS that makes it uniquely problematic.  Fruit juice or a sucrose containing soda would function identically in the body.

Is HFCS Uniquely Obesity Promoting?

Much of the concern over HFCS has to do with the fructose content as stated above; and a lot of very silly studies have come out recently showing that massive intakes of fructose by itself are problematic in terms of health or obesity.

One that is making the rounds now showed that feeding rats a 60% fructose diet for 6 months caused leptin resistance.  But let’s be realistic.  For someone on a 3000 calorie/day diet that would be the equivalent of 450 grams of pure fructose per day.  Every day.  For six straight months.  This simply has no relevance to any real human diet.

As the paper states:

A pure fructose diet is surely a poor model for HFCS, because HFCS has equivalent amounts of glucose.  Because no one would eat a pure fructose diet, such experimentation must be recognized as highly artificial and highly prejudicial and not at all appropriate to HFCS.

Rather, diets examining sucrose intake make a much more appropriate model for HFCS.  Not much has been done comparing HFCS to sucrose but what has been shows no metabolic difference between the two; exactly what would be expected due the fact that they have nearly identical composition.

Does HFCS predict either US or Global Obesity?

In a word, no.  While Bray’s original analysis suggested a correlation between increasing HFCS intake and US obesity, that relationship no longer holds.  Despite reduced HFCS intake in the last few years, obesity continues to increase.  Simply, HFCS cannot explain the continuous rise in US obesity.

Moving to the global arena, there is simply no relationship between HFCS intake and obesity rates with the two countries showing the highest rates of obesity showing the lowest intake of HFCS.

Will Eliminating HFCS from the Food Supply Affect Obesity?

You can probably guess the answer which is no.  Given that HFCS and sucrose are nearly identical in composition, given that HFCS has replaced sucrose intake in the human diet over the past 30 years, given that they are handled metabolically identically, given that they have the identical caloric value, replacing HFCS with sucrose will simply have no effect on anything.  Except perhaps to raise prices since sucrose is higher than HFCS.

Conclusion

The paper concludes, as you might imagine, by reiterating the points I’ve made above.  HFCS is in no way unique amount sugars, with a composition identical to sucrose as well as the supposedly ‘healthy’ honey.  Increased caloric intake since the 1970′s is the driver for increased obesity, with no relationship with HFCS intake per se.

In that all fructose-glucose solutions (whether HFCS, sucrose or honey) are metabolized in exactly the same fashion in the body, there is simply no reason to think that HFCS per se is particularly obesity promoting outside of being a caloric source.

Application

Now, since I know some people will mis-interpret this piece, I want to be clear: the paper is not saying that people can or should be consuming HFCS in massive amounts.  Many HFCS containing foods contain massive numbers of calories.

This is especially true of sweetened sodas and it’s interesting to note that a good bit of data suggests that such drinks can be consumed in massive amounts without signalling the body about their caloric content; but this has more ot do with their fluid nature than their composition.

What I’m getting at with this research review is that the near insane over-reaction and concern to any food containing any amount of HFCS among certain groups.  Folks on forums are throwing out the baby with the bathwater under the gross misunderstanding that HFCS per se is a unique evil which it clearly isn’t.  Within the context of a calorically controlled diet, there is no reson to believe it will have any differential impact beyond every other sugar that has ever been used.

So stop freaking out.

Roy BD. Milk: the new sports drink? A Review. J Int Soc Sports Nutr. 2008 Oct 2;5:15

ABSTRACT

There has been growing interest in the potential use of bovine milk as an exercise beverage, especially during recovery from resistance training and endurance sports. Based on the limited research, milk appears to be an effective post-resistance exercise beverage that results in favourable acute alterations in protein metabolism. Milk consumption acutely increases muscle protein synthesis, leading to an improved net muscle protein balance. Furthermore, when post-exercise milk consumption is combined with resistance training (12 weeks minimum), greater increases in muscle hypertrophy and lean mass have been observed. Although research with milk is limited, there is some evidence to suggest that milk may be an effective post-exercise beverage for endurance activities. Low-fat milk has been shown to be as effective, if not more effective, than commercially available sports drinks as a rehydration beverage. Milk represents a more nutrient dense beverage choice for individuals who partake in strength and endurance activities, compared to traditional sports drinks. Bovine low-fat fluid milk is a safe and effective post exercise beverage for most individuals, except for those who are lactose intolerant. Further research is warranted to better delineate the possible applications and efficacy of bovine milk in the field of sports nutrition.

My Comments

Milk, like all aspects of nutrition is often surrounded by controversy. From the nutjob tinfoil on the head anti-milk zealots to bodybuilders who say that milk makes you smooth, milk is often thought of as a terrible food for adult humans to eat.

Yet, objectively milk is an excellent source of high quality protein (a mix of casein and whey), carbohydrates (lactose, which admittedly some people have problems digesting) along with providing fluids, highly bio-available calcium, and electrolytes. Old time lifters often built large amounts of muscle mass with a program of squats and a gallon of milk per day; the idea is still around in various incarnations. In contrast to the anti-milk zealots, milk has been shown to have a number of potential health benefits beyond any sporting applications that may exist.

I’m not going to address the controversy regarding milk here, sufficed to say I’m on the side of milk (and dairy foods in general) being excellent for athletes and folks trying to improve body recomposition. The combination of both fast whey and slow casein is excellent for a lot of sporting and athletic applications, dairy calcium improves body composition, etc. And while dairy does contain quite a bit of sodium (which is what I suspect causes the issues with ‘smoothness’ for contest bodybuilders), this is only an issue on the day of the contest. Dropping milk out 16 weeks out can only hurt fat loss, not help it.

You can read more about that in Contest Dieting Part 1. As well I discuss dairy proteins (both supplemental and whole food) in detail in The Protein book.

Which brings me in a roundabout way to today’s article which examines recent research examining the potential of milk as a sports drink.

The paper first examines much of what I talked about above, the overall macronutrient profile of milk. In that the recent area of research for sports nutrition revolves around carbohydrate, protein/amino acid intake, along with fluids and electrolytes, milk ends up covering all of those nutritional bases.

As noted above, milk contains a combination of both casein (a slow digesting protein) and whey (fast acting), along with a large proportion of the branched chain amino acids (BCAA). It also contains carbohydrates (lactose, see my note at the end of this piece), along with minerals, both sodium and potassium. Of course, milk automatically contains fluid and hydration/fluid balance is also important for optimal performance and recovery.

Moving on the paper first examines research on milk and resistance training adaptations. A number of studies have been performed from acute (single drink) studies to longer work looking at lean body mass gain. In one acute study, both fat free and whole milk were shown to improve protein synthesis following training; the whole milk worked better although the researchers weren’t sure why.

Of more interest, milk was shown to be superior to a soy based drink (both drinks contained identical protein, carbs and calories) in terms of lean body mass gains over 3-8 weeks. In addition, not only did the milk group gain more lean body mass, they lost a bit of fat. Of some interest, it was thought that the superiority of the milk was due to its slower digestion compared to the soy (a fast protein). As I detail in The Protein Book, in contrast to recurring beliefs that whey is superior post-workout, research shows that a slow or combination slow and fast protein following training appears to be superior in terms of lean body mass gains.

Quoting from the paper’s conclusion:

“Consumption of low-fat milk appears to create an anabolic environment following resistance training and over the long term with training, it appears that greater gains in lean mass and muscle hypertrophy can be obtained. Furthermore, milk may also lead to greater losses of body fat when it is consumed following resistance training.”

Now, moving onto endurance training, it’s first important to note that endurance athletes have a couple of issues to deal with (in terms of both performance and recovery) that strength trainers don’t necessarily have to deal with. This includes hydration and performance during training/competition as well as glycogen re-synthesis and re-hydration following training. While those certainly can be an issue following very voluminous strength training, they tend to be a bigger issue for endurance type training.

Now, about a zillion studies (give or take a couple hundred thousand) have looked at the impact of carb intake on endurance performance. The research is mixed and whether or not carbs help depends on the duration and intensity of training. Of more relevance here, some research has examined whether adding small amounts of protein during endurance competition can help performance. Some of it finds a benefit, some of it doesn’t; there is still some controversy over this issue.

In this vein, some work has examine the impact of milk during endurance training. While some potential benefits (such as increased blood amino acid levels) were seen, no performance benefits were seen and the subjects reported a fuller stomach due to the milk; this was likely due to the milk more slowly emptying from the stomach. This isn’t a good thing and what research has found a benefit of protein during endurance training invariably used faster proteins (whey or casein hydrolysate). I would not recommend milk during training.

However, as a post-workout drink, milk appears to be a good choice for endurance athletes. Some work has found that the combination of protein and carbs leads to better glycogen re-synthesis, however no research has directly examined milk in this context. One study compared chocolate milk to a commercial carbohydrate drink and found that the chocolate milk was at least as good at promoting performance as the carb drink.

With regards to hydration, a previous research review I did examined Milk as an Effective Post-Exercise Rehydration Drink, finding that milk was superior to water or commercial carbohydrate drinks for re-hydration following endurance exercise, presumably due to the sodium and potassium content.

Quoting again from the paper itself, the researchers conclude that

“The limited literature that does exist suggests that milk is as effective as commercially available sports drinks at facilitating recovery for additional performance…Furthermore, milk is also a very effective beverage at promoting fluid recovery following dehydrating exercise in the heat.”

The bottom link is that milk can be an effective post-workout drink for both resistance trainers and endurance athletes.

Practical Application

Clearly the research to date suggests that milk may be a superior post-workout drink following resistance training (at least compared to a fast protein like soy) and may have benefits for endurance athletes as well in terms of promoting glycogen synthesis, recovery and re-hydration following training.

Anyone who has read The Protein Book (or my other books for that matter) knows that I’m big on milk and milk proteins, they have massive advantages in terms of their protein content, dairy calcium, and other effects. Milk is readily available, tasty and relatively inexpensive.

However, there are a couple of caveats. For large athletes who need a large amount of carbohydrates or protein following training, milk may not be an ideal way of getting it. A typical 8-oz serving of milk contains roughly 12 grams of carbohydrates and 8 grams of protein. A large resistance training athlete might need 4-5X that many nutrients following training and drinking that much milk may not be feasible.

A compromise solution might be to use milk as a base and add extra nutrients (such as maltodextrin or dextrose powder for carbs and protein powder for protein) to achieve a higher nutrient density than milk itself can provide. So 16 oz. (2 cups) of milk with extra carbs/protein would get the benefits of milk along with sufficient nutrients for larger athletes to recovery. Similar comments would apply to endurance athletes who often need very large amounts of carbs following exhaustive training; drinking 4+ cups of milk following training may not be feasible.

As a final comment, if there is one major problem with milk for many people, it’s the presence of lactose (milk-sugar). Lactose, like all digestible carbohydrates requires a specific enzyme to be broken down called lactase. However, some people lose the ability to produce lactase/digest lactose; this can occur either completely or relatively (in the latter case, folks can handle small amounts of dairy).

Lactose intolerance, which should not be confused with a true milk allergy, can cause stomach upset, gas, and diarrhea in predisposed people; it’s racially based and some ethnicities are more or less likely to have problems. For those with lactose intolerance, but who wish to use milk following training there are several options.

The first is to find a source of lactose free milk. Brands such as Lactaid add lactase to milk to digest the lactose into glucose and galactose; this typically results in sweeter milk but without the offending lactase. Lactase pills are also available which can be taken with milk to help with digestion. Finally, there are products which claim to increase lactase levels in the gut and some people find that milk consumed with other food is tolerable; additionally, regular yogurt consumption can improve the ability to digest lactose.

There is considerable interest in the potential impact of several polyunsaturated fatty acids (PUFAs) in mitigating the significant morbidity and mortality caused by degenerative diseases of the cardiovascular system and brain. Despite this interest, confusion surrounds the extent of conversion in humans of the parent PUFA, linoleic acid or alpha-linolenic acid (ALA), to their respective long-chain PUFA products. As a result, there is uncertainty about the potential benefits of ALA versus eicosapentaenoic acid (EPA) or docosahexaenoic acid (DHA). Some of the confusion arises because although mammals have the necessary enzymes to make the long-chain PUFA from the parent PUFA, in vivo studies in humans show that asymptotically equal to 5% of ALA is converted to EPA and <0.5% of ALA is converted to DHA. Because the capacity of this pathway is very low in healthy, nonvegetarian humans, even large amounts of dietary ALA have a negligible effect on plasma DHA, an effect paralleled in the omega6 PUFA by a negligible effect of dietary linoleic acid on plasma arachidonic acid. Despite this inefficient conversion, there are potential roles in human health for ALA and EPA that could be independent of their metabolism to DHA through the desaturation – chain elongation pathway.

My comments: By way of introduction, early nutrition research was very concerned with determining what were the essential nutrients for human health and survival. By definition, an essential nutrient is one that is

• Required by the body for survival
  Can’t be made by the body

It’s a bit more complicated than that and there are some nutrients which are defined as conditionally essential (glutamine is one) but this covers the basics.

Vitamins and minerals are essential, about half of the amino acids are essential and, as early research fought to determine, it turns out that some fatty acids are essential. These are called, generally, the EFAs and, as we now know there are two of them.

Due to methodological issues that I won’t detail, determining what fatty acids were actually essential was actually a fairly difficult problem in the early part of the 20th century. In early research, it was thought that there were three EFAs, alpha-linoleic acid (ALA, not to be confused with alpha-lipoic acid, an insulin sensitizer), linolenic acid (LA), and arachidonic acid (AA). When it was found that rats could make AA out of LA, it was dropped, leaving two EFAs. I’d note that, at one point, it was thought that LA was the only EFA but, as we now know, both ALA and LA are essential fatty acids.

These two fatty acids are also often referred to by their chemical names (which have to do with their structure) which are omega-3 (n-3,w-3) for ALA and omega-6 (n-6, w-6) for LA.

Now, both LA and ALA are metabolized in the body (this includes a variety of processes including oxidation in the liver) to other compounds, I’ll spare everyone the biochemical details.

LA is metabolized to gamma-linoleic acid and then eventually to arachidonic acid. As mentioned above, this is why AA was removed from the list of EFAs, since the body can synthesize it from LA, it’s not essential.

ALA is metabolized to EPA (you don’t want to know the full name) which is further metabolized to DHA (same comment). EPA and DHA are more commonly referred to as the fish oils since they are found in high amounts in fatty fish.

Now, for the most part, I’m not going to talk much about the LA->AA pathway. The reason is that excess LA/AA is actually detrimental to the body. AA has inflammatory characteristics and excess LA (esp. in relation to ALA) is thought to be a harmful to the body. I’d note that studies show that the current ratio of LA:ALA is around 25:1. It’s thought that a ratio of 4:1 or lower would be better.

Bottom line, most of us get way too much LA in the first place, unless you eat essentially a zero fat diet you get most of what you need, there’s no real need to make lots of AA from a health or survival standpoint.

Of more concern is the EPA/DHA issue which is what I want to discuss in more detail. Both are critical for things like optimal health, fat burning, etc. It looks like DHA may be even more important. Babies accumulate DHA in their brains and babies who either don’t receive sufficient DHA (from the diet) or have a rare genetic syndrome can end up with brain damage. DHA is present in large amounts in cellular membranes. Basically, sufficient DHA intake is critical.

Which brings us to the real topic of this week’s paper: Can the body convert ALA to EPA/DHA in sufficient amounts? Because, if it can, then using a source of ALA such as flaxseed oil is sufficient. If it can’t, then intake of preformed EPA/DHA via fish oils is going to be required.

Now it’s clear that the human body possesses the enzymatic machinery to convert ALA to EPA/DHA. But there is an issue of whether the conversion process can occur in sufficient amounts.

Without going into the ridiculous detail of this week’s paper, the short-answer is basically “No, it can’t.” Now, there are some methodological issues with the studies having to do with the amount (giving large amounts of ALA can cause an underestimation of true conversion) given and some other stuff but the bulk of the data points to the simple conclusion that the human body is simply terrible at converting ALA to EPA/DHA. In fact, studies using flax oil supplementation show no change in DHA levels. None. It will raise EPA a bit but the conversion to DHA is essentially zero.

There are two odd exceptions to the above that I want to mention. The first is in vegans. Due to zero intake of animal foods, they have zero intake of DHA. But while they show lower levels of DHA, they don’t show deficiency symptoms. While more research needs to be done, presumably pathways of conversion/production of DHA are up-regulated under this situation.

The other is in extreme w-3 deficiency, where plasma DHA levels typically rise after ALA supplementation. This is just a classic feedback loop, and occurs for other nutrients as well (for example, absorption of certain minerals will increase the more deficient someone is).

But beyond that, the overall impact of ALA supplementation plasma levels of EPA is small, for DHA essentially nil. And given the critical importance of both EPA/DHA on human health, fat loss and performance, the bottom line is that this makes ALA (via flaxseed oil or what have you) an insufficient replacement for preformed fish oils.

As a couple of final comments, I’d also note that supplementation of EPA doesn’t raise DHA levels either. Since all commercial fish oils I’ve ever seen contain both EPA/DHA, this is a fairly non-issue. But it is yet another reason why ALA by itself is insufficient. Not only is the conversion of ALA to EPA small, the conversion of EPA to DHA is simply nil, hence ALA won’t impact on the body’s DHA levels.

Having established that ALA intake is ineffective at increasing EPA/DHA levels, a final and related question to address is whether ALA has any effects above and beyond what EPA/DHA are doing. This week’s paper mentions one possibility which is a mild impact of ALA supplementation on cardiovascular disease. It also notes that EPA/DHA supplementation has a greater effect. Other researchers (not all agree) feel that the true EFAs are EPA/DHA, and that ALA is simply a parent compound that is not essential in its own right. Currently I tend to agree with this stance.

Summing up: the body requires EPA/DHA for optimal function. This includes fat loss, prevention of a lot of diseases, controlling inflammation, etc. While the body has the machinery to convert alpha-linolenic acid (ALA, found in high quantities in flaxseed oil), the amount of that conversion is small for conversion to EPA and negligible for DHA. Hence I don’t feel that ALA/flax oil is an appropriate EFA source. You need to be taking preformed EPA/DHA (in either capsule or liquid form). This was one of the changes I made to the second edition of the Rapid Fat Loss Handbook (the first edition allowed for flax to substitute for fish oil).