Dietary proteins have been shown to be more effective at prolonging satiety and suppressing food intake than carbohydrates and fats. However, different dietary proteins appear to vary in their ability to influence satiety and reduce food intake.

This is nicely demonstrated in a new study by Sebely Pal and Vanessa Ellis from the University of Curtin, Perth, Australia, published in the British Journal of Nutrition.

Pal and Ellis studied 22 healthy male normal-weight volunteers, who were studied on four separate occasions in a randomised, single blind, cross-over design study. On each occasion the subjects were given a liquid test meal, containing either tuna, turkey, whey or egg albumin, administered as a chocolate-flavoured shake.

Whey protein resulted in a significantly lower blood glucose and significantly higher insulin response than the same amount of tuna, egg, or turkey protein. Similarly, subjects rated their level of hunger as lower after the whey protein compared to the other proteins.

Most importantly perhaps, mean energy intake at an ad libitum meal four hours after the test meal was around 100 KCal lower with the whey meal than with the tuna, egg and turkey meals.

The authors speculate that this satiating effect of whey proteins may be related to the fact that whey protein has a faster rate of digestion and absorption than other proteins, producing a rapid peak in plasma amino acids which may contribute to their effect on satiety. Whey proteins also have one of the highest concentrations of branched-chain amino acids (BCAA) compared to other protein sources, which, in turn, may affect release of enteral hormones or insulin.

Interestingly, insulin, apart from its well-known actions on glucose and lipid metabolism, is also thought to be a satiety hormone, with increased insulin levels in the brain eliciting a net catabolic response influencing food intake regulatory mechanisms

Although these findings suggest a potential for hunger suppression and weight loss in overweight or obese individuals, it would be important to show that there is no compensatory effect in caloric intake that may develop over time as subjects go into negative energy balance over time.

Such an effect would ultimately defend body weight and prevent long-term weight loss.

Nevertheless, the study supports the notion that at least in the acute setting, all proteins may not be equal in their ability to satiate and decrease hunger.

AMS
Denver, CO

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Pal S, & Ellis V (2010). The acute effects of four protein meals on insulin, glucose, appetite and energy intake in lean men. The British journal of nutrition, 1-8 PMID: 20456814

As blogged before, any medical condition that affects mobility, can potentially promote weight gain and the development of obesity with all its mental, physical and socioeconomic sequelae.

This of course also applies to patients diagnosed with multiple sclerosis (MS), a progressively disabling disease of the central nervous system currently affecting an estimated 2·5 million people worldwide. Multiple sclerosis is also the most common non-traumatic cause of disability in young adults.

In addition, patients with multiple sclerosis also often have psychiatric comorbidities ranging from depression, anxiety and social phobias to sleep disorders and chronic pain, which can all further adversely affect ingestive behaviour.

In a paper by Ruth Ann Marrie and Ralph Horowitz from the University of Manitoba, Winnipeg, Canada, just published in Lancet Neurology, the authors discuss why recognising obesity and other chronic illnesses in patients with multiples sclerosis is so important.

Apart from promoting the obvious sequelae of hypertension, diabetes and heart disease, obesity is also associated with delayed diagnosis of multiple sclerosis and obese patients tend to have higher levels of immobility and disability at the time of diagnosis.

Conversely, the diagnosis of comorbidities could be delayed by mistakenly attributing neurological symptoms such as progressive inability to walk, pain, or seizures to the pre-existing diagnosis of MS.

Corticosteroids used for relapses, may also contribute to weight gain and worsening of diabetes.

As the authors point out in the discussion:

“Further work is needed to establish whether pre-existing comorbidities affect the risk and phenotype of multiples sclerosis and, if so, how. Data from some studies indicate that comorbidities and health behaviours also affect disease progression. These findings need to be verified, and a broader range of disability outcomes, such as upper extremity and cognitive function, need to be taken into account. From a therapeutic perspective, important questions include whether comorbidities affect treatment choice, response, tolerability, and adherence, and whether we should use different treatment strategies in the presence of a comorbidity.”

As in all patients with impaired mobility and other physical or mental comorbidities, weight management can be challenging and should probably start well before weight gain sets in.

AMS
Edmonton, Alberta

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Marrie RA, & Horwitz RI (2010). Emerging effects of comorbidities on multiple sclerosis. Lancet neurology, 9 (8), 820-8 PMID: 20650403

Readers may be well aware that the use of cannabis or “hashish” can induce the “munchies”, an acute craving for highly palatable foods.

Now Garron Dodd and colleagues from the University of Manchester, UK, have identified a new brain peptide called hemopressin that acts through cannabinoid receptors to reduce food intake in rats and mice. Their findings are published in the latest edition of the Journal of Neuroscience.

Hemopressin is a short, nine amino acid peptide found in the rat brain that behaves as an inverse agonist at the cannabinoid receptor CB(1), where it inhibits agonist-induced receptor internalization.

In their studies, Dodd and colleagues found that this peptide dose-dependently decreases night-time food intake in normal male rats and mice, as well as in obese ob/ob male mice, when administered centrally or systemically, without any obvious adverse side effects.

Hemopressin specifically blocks the hyperphagic response to CB(1) receptor agonists, while having no effect on eating behaviour in CB(1) receptor null mutant male mice.

Obviously, the discovery of this peptide not only increases our understanding of the complex neurobiology of ingestive behaviour but may also lead the way to new treatments for obesity.

It should however be noted that we have already had potent inhibitors of the CB(1) receptor for the treatment of obesity (readers will recall rimonabant), which were withdrawn from the market due to increased incidence of depression.

Nevertheless, it may well be that endogenous inhibitors of the endocannabinoid system (like hemopressin) may well be better tolerated previous inhibitors of this system.

Perhaps we have not seen the last of our attempts to decrease appetite by blocking the endocannabinoid system just yet.

AMS
Edmonton, Alberta

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Dodd GT, Mancini G, Lutz B, & Luckman SM (2010). The peptide hemopressin acts through CB1 cannabinoid receptors to reduce food intake in rats and mice. The Journal of neuroscience : the official journal of the Society for Neuroscience, 30 (21), 7369-76 PMID: 20505104

In the days when fast food referred to food on four legs that you had to chase after, feeding yourself and your family was not without risk. Thus, being wiling and able to take risk, must clearly have been of an advantage, especially if you were hungry.

It turns out that hunger actually does influence people’s decision making as far as taking risks is concerned.

At least, this is the finding of a fascinating study by Mikael Symmonds and colleagues from the University College London, UK, published in the latest issue of PLoS One

Based on the hypothesis that animals’ attitudes to risk may well be influenced by metabolic state (hunger and baseline energy stores), in that animals are more likely to express a preference for risky (more variable) food sources when below a metabolic reference point (hungry), and safe (less variable) food sources when sated, they decided to expose trial participants (19 healthy young men) to a series of controlled feeding experiments during which they were asked to make risky decisions by participating in a lottery game.

Specifically, the researchers hypothesised that baseline metabolic reserves and alterations in metabolic state would systematically modulate decision-making and financial risk-taking in their study participants.

Testing was undertaken in three different feeding states: fasted, immediately post-meal and 60 minutes post-meal.

Metabolic state significantly affected choice, with a significant fall in risk-aversion immediately after eating. In addition, the immediate impact of nutrient intake on risky choice showed a dependence upon baseline indices of body mass index (BMI), percentage body fat and circulating leptin concentrations. Higher baseline leptin (a marker of energy stores) correlated with an increase in riskier choices (i.e. a greater fall in risk-aversion) immediately after eating compared to the fasted state.

Furthermore, there was a significant positive relationship between the levels of the hunger hormone ghrelin and risk-taking behaviours.

Not surprisingly, the authors suggest that these findings provide profound insights into a wide range of human behaviour from eating disorders to obesity.

Not only will hungry (and skinny?) people take more risks but they are also likely to be far more impulsive than in the sated state. In fact, the studies suggest that thinner people (lower leptin levels) may be generally more prone to risky behaviours than people with higher body fat (higher leptin levels). But weight loss (as in dieting) may also make people more prone to taking risks.

Similarly, hungry people are likely to take more risks with their food choices (i.e. go for the crap) than people who are less hungry.

If nothing else, this study has important implications for Casino owners: feel free to ply your customers with alcohol but go easy on the food.

On that note - HAPPY CANADA DAY everyone!

AMS
Forest Lake, Illinois

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Symmonds M, Emmanuel JJ, Drew ME, Batterham RL, & Dolan RJ (2010). Metabolic State Alters Economic Decision Making under Risk in Humans. PloS one, 5 (6) PMID: 20585383

I am currently in Oslo for the 20th European Meeting of the European Society of Hypertension. Some of my readers may recall that 25 years ago, I started my research career with studies on the effects of salt on blood pressure - the debate on salt reduction was not new then - the debate is still alive today.

The question is not whether or not increased salt intake can increase blood pressure in some people - indeed, it does and much of my work at the time focused on trying to understand the physiology and genetics of this phenomenon.

Proponents of sodium restriction point to the number of heart attacks and strokes that could theoretically be prevented if population-wide salt reduction did indeed translate into lower blood pressure for the population, but to this date, this has yet to be shown in a prospective randomized-controlled trial proving that eating less salt actually saves lives.

Critics of these proposals fear that reducing the salt intake of the population may have unintended consequences for some.

A new spin on this theory of unintended consequences now comes from a paper by John Hayes and colleagues from Pennsylvania State University, published in the latest edition of Physiology and Behavior.

Hayes and colleagues examined the response of so-called “bitter supertasters” to varying amounts of salt in a wide range of foods. These bitter supertasters make up about 25% of the population and are genetically hypersensitive to bitter tastes, leading them to naturally avoid some vegetables and other foods that taste naturally bitter.

The researchers assessed the liking and intake of foods with varying amount of saltiness among 87 healthy adults (45 men).

Supertasters reported greater saltiness in chips/pretzels and broth at levels comparable to regular-sodium products; greater sensory and/or liking changes to growing sodium concentration in cheeses (where sodium ions mask bitterness) and broths; and less frequently salting foods.

Increased propensity for bitter supertasting, independently explained variability in consuming high-sodium foods by impacting salt sensation and/or liking.

Bitter-supertasters reported greater changes in sensation when more salt was added to broth, which then associated with greater changes in broth liking, and with more frequent high-sodium food intake.

In contrast, greater papillae number was associated with less frequent high-sodium food intake via reduced liking for high-fat/high-sodium foods.

The researchers conclude that, variation in sensations from salt is associated with differences in hedonic responses to high-sodium foods and thus sodium intake between bitter-supertasters and non-supertasters.

Despite adding less salt, bitter supertasters consumed more sodium through food, as salt was more important to preference, both for its salty taste and masking of bitterness.

The researchers suggest that bitter-supertasters may use increased salt to mask bitterness in naturally bitter foods including vegetables and other foods that may be deemed to be healthy.

Reducing salt intake may make these foods less appealing to supertasters and may therefore adversely affect their nutrient intake.

Whether or not this is in fact true, it does appear that some people may have a natural (genetic) preference for higher salt in their diets - and may respond to population wide restrictions in salt use by simply reaching for the shaker.

AMS
Oslo, Norway

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Hayes JE, Sullivan BS, & Duffy VB (2010). Explaining variability in sodium intake through oral sensory phenotype, salt sensation and liking. Physiology & behavior, 100 (4), 369-80 PMID: 20380843