Hormonal Responses to a Fast-Food Meal – Research Review

Title and Abstract

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?


A Short History of Beverages and How our Body Treats Them – Research Review

Title and Abstract

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.


Straight Talk About High-Fructose Corn Syrup: What it is and What it Ain’t. – Research Review


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


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.


Milk The New Sports Drink? A Review


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



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.


Extremely Limited Synthesis of Long Chain Polyunsaturates in Adults: Implications for their Dietary Essentiality and use as Supplements

Plourde M, Cunnane SC. Extremely limited synthesis of long chain polyunsaturates in adults: implications for their dietary essentiality and use as supplements. Appl Physiol Nutr Metab. 2007 Aug;32(4):619-34.
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).