Inulin & Beta Glucan Reduce Body Fat Gain By -50% & -33%! Both Have Similar Effects on the Gut Microbiome, But Only Inulin Appears to Be More Than An Appetite Suppressant

What do these Jerusalem artichokes, agave, bananas, burdock, camas, chicory, coneflower, costus, dandelion, elecampane, garlic,jicama, Leopard's-bane, mugwort, onion, wild yams, yacon and a whole host of other foods have in common? Right! They contain inulin. Whether you will be able to get a whopping amount of 10% inulin in your diet w/out the use of supplements or "enriched" foods, is yet as questionable as how beneficial this actually is for friends of physical culture.

The gut microbiome is not just one of the hottest topics in the (health-)blogosphere, it is also a subject of ongoing research. Research, however, that is, if we are honest, still very much in its infancy. As impressive as the results from the latest studies into the metabolic downstream effects of the administration of fermentable fiber to rodents may be and as obvious as their relation to certain changes in the gut microbiome of the animals may appear - in the end, our understanding of the underlying mechanisms does not allow any reliable prognoses like "double the amount of lactobacilli and you will eventually be able to lose that pouch of body fat you've been carrying around for years now". And yet, if the results from the latest rodent experiments at the Imperial College in London, could be reproduced in humans, I can already foresee that both, the consumption and use of the foods I listed in the caption of the image to the right, as well as related products, extracts and supplements, which contain more or less significant amounts of the naturally occurring polysaccharides, we usually refer to as inulin, will increase in the months and years to come.

Fermentable fiber and the gut-brain-axes: The key to lifelong leanness?

If this is not your first visit to the SuppVersity, you will certainly be aware that the idea of a magic pill (or fiber) that will allow you to eat whatever, whenever and in whichever amounts without having to cope with the metabolic consequences is illusive. When the addition of 10% inulin (or beta glucan) to the diets of 36 male C57BL/6 mice had an "anti-obesogenic" effect, this does not mean that the poor critters who were kept on a hypercaloric high fat (41.8%) diet for 8 weeks did not get obese. What it does mean, though, is that the addition of 10% fermentable (=being food for certain gut bacteria) fiber in the form of

*the producers of these products did not fund or support the study (at least the scientists don't mention that in the respective disclosure ;-)

• inulin from Synergy(TM)*, a fructan based preparation containing both long and short chain
  fructooligosaccharides, or
• beta-glucan from Glucagel(TM)* a highly rich (,80%) barley derived b-glucan preparation

to their otherwise iso-caloric diet (the HFD control contained cellulose) was not without helped to mitigate the negative effects of this diet - a fact the majority of you, of whom I would expect that they are not on a fast-food diet should keep in mind, before they head over to their favorite online supplement vendor and type "Synergy inulin" into the search box.

Figure 1: Effect of addition of 10% fermentable fiber as inulin or beta glucan to the high fat diet of male mice on cumulative weight gain (left), body composition and fatness (middle) and food intake (right) over the course of 8 weeks (data adapted from Arora. 2013)

In spite of that, the results are simply too impressive not to think about their implications in otherwise healthy and even more so previously obese individuals. This is particularly true, because the same microbial changes about which the authors write in a previously published paper from May 2013 that the ...

"[...] increases in both Bifidobacteria and Lactobacillius and a significant increase in short chain fatty acids (SCFA) [went hand in hand with] increase in neuronal activation within the arcuate nucleus (ARC) of animals that received In [inulin] supplementation" (Anastasovska. 2013)

do not (and this is a result of the researchers very latest experiments) simply blunt the rodents appetite. If that was the case, the rodents that received the beta glucan supplemented chow and consumed 12% less energy should have had the most favorable body composition. A cursory glance at figure 1 will yet tell you that this was not the case, though.

Inulin beats beta glucan when it comes to body fat reduction / repression

If we take a closer look a the differential effects of inulin and beta glucan, there yet only one figure that really sticks out and that's the accumulation of fat within the musculature of the animals. The "beautiful marbling" people are looking for in their steaks, however, usually is a harbinger of impeding or even existing skeletal muscle insulin resistance. A muscle fat content above the high fat control (it's certainly a weakness that we don't have a "real" control group on standard rodent chow, here) as Arora et al. observed it in the tissue samples of the beta glucan group, does thus tell you something about its potential usefulness, or rather uselessness of this specific type of fermentable fiber.

Figure 2: Effects of the different types of fermentable fiber on cecal microflora groups (figures are in scientific notation, this means "1E+6" equals 1mio, "1E+9" would be 1 billion etc.; data based on Arora. 2013)

In conjunction with the information about the corresponding changes in the gut microbiome (see figure 2), which appear virtually identical in both groups (specifically the extreme increasesin in both Bifidobacteria (BIF) and Lactobacillius (LAB) really stick out), this does however suggest that the modulatory effect on the composition of the gut flora, or at least the part of it the scientists evaluated in the study at hand, cannot be the only driving force behind the beneficial metabolic effects of inulin.

Inulin or beta glucan? This is not a question... 

While the latter, i.e. inulin, which has by the way been found to directly suppress lipogenesis in a 2011 study by Belgian scientists in a similar HFD rodent model (Dewulf. 2011), appears to be promising for everyone, regardless of whether he or she is poisoning him- or herself with the standard American diet (which is, with its high fat and high carbohydrate content de facto an identical twin of the so-called "high fat diet" in rodent studies), the ingestion of larger amounts of the former, i.e. beta glucan, does at least appear questionable.

If you want to use inulin to your metabolic advantage, you better make sure you get your self a more comfortable place to answer the call of nature - it could call thrice as often! Moreover, large amounts of inulin and other fermentable fiber can induce gastrointestinal distress-

The question is therefore not so much whether it's worth supplementing (it's certainly worth to incorporate some of the initially mentioned foods into your diet, as most of them contain a whole list of other advantageous micronutrients) with inulin or beta glucan - the answer would obviously be inulin - but rather whether it's worth adding larger amounts of inulin to an already healthy diet. And while we cannot answer this question based on the results of the previously cited rodent studies, we could argue that Marwa Zenhom and her colleagues from the Christian Albrecht University in Kiel have already supplied relevant evidence that this would be the case (Zenhom. 2011). After all, the German researchers have been able to show that the PPAR-gamma related anti-inflammatory effects (significant reductions IL-12 secretion in Caco-2 cells and gene expression of IL-12p35, IL-8, and TNFa as well as NF-kB) of oligosaccharides are not (exclusively) brought about by their effects on the gut microbiome, because bacteria simply were not present in their in-vitro study with human Caco-2 cells (cells from the gut lining). Bassaganya-Riera et al. even argue that this effect could be beneficial for IBS patients (Bassaganya-Riera. 2011).

Whether having 10% of your diet in form of inulin, or to make this more conceivable, having 1 tablespoon of plain inulin for every 9 tablespoons of whatever else you eat is either feasible or reasonable, is a whole different story (to put that into perspective: The average inulin intake of Westerners is 1-10g per day (van Loo. 1995). Even 10g would yet only be enough if you ate only 100g of food within 24h!)... and I must forewarn you, if you go by the fecal volume of the mice in the Arora study, it is possible that you will spend >3x more time on the toilette than usual ;-)

References:

• Arora T, Loo RL, Anastasovska J, Gibson GR, Tuohy KM, Sharma RK, Swann JR, Deaville ER, Sleeth ML, Thomas EL, Holmes E, Bell JD, Frost G. Differential effects of two fermentable carbohydrates on central appetite regulation and body composition. PLoS One. 2013;7(8):e43263.
• Anastasovska J, Arora T, Sanchez Canon GJ, Parkinson JR, Touhy K, Gibson GR, Nadkarni NA, So PW, Goldstone AP, Thomas EL, Hankir MK, Van Loo J, Modi N, Bell JD, Frost G. Fermentable carbohydrate alters hypothalamic neuronal activity and protects against the obesogenic environment. Obesity (Silver Spring). 2013 May;20(5):1016-23.
• Astegiano M, Pellicano R, Terzi E, Simondi D, Rizzetto M. Treatment of irritable bowel syndrome. A case control experience. Minerva Gastroenterol Dietol. 2006 Dec;52(4):359-63.
• Bassaganya-Riera J, DiGuardo M, Viladomiu M, de Horna A, Sanchez S, Einerhand AW, Sanders L, Hontecillas R. Soluble fibers and resistant starch ameliorate disease activity in interleukin-10-deficient mice with inflammatory bowel disease. J Nutr. 2011 Jul;141(7):1318-25.
• Dewulf EM, Cani PD, Neyrinck AM, Possemiers S, Van Holle A, Muccioli GG, Deldicque L, Bindels LB, Pachikian BD, Sohet FM, Mignolet E, Francaux M, Larondelle Y, Delzenne NM. Inulin-type fructans with prebiotic properties counteract GPR43 overexpression and PPARγ-related adipogenesis in the white adipose tissue of high-fat diet-fed mice. J Nutr Biochem. 2011 Aug;22(8):712-22.  
• van Loo J, Coussement P, de Leenheer L, Hoebregs H, Smits G. On the presence of inulin and oligofructose as natural ingredients in the western diet. Crit Rev Food Sci Nutr. 1995 Nov;35(6):525-52.
• Zenhom M, Hyder A, de Vrese M, Heller KJ, Roeder T, Schrezenmeir J. Prebiotic oligosaccharides reduce proinflammatory cytokines in intestinal Caco-2 cells via activation of PPARγ and peptidoglycan recognition protein 3. J Nutr. 2011 May;141(5):971-7.

Y3K Fat Burners: Bile Acid Suppositories! Plus: How This Relates to Taurine, Cholesterol, Statins and Diabesity

Image 1: Is the US starving for sulfur amino acids and cholesterol?

You've learned in yesterday's post (cf. "Sodium-Alginate for 30-40% More Weight Loss and Body Fat Reduction on Mild Caloric Deficit") on the surprising fat-loss effects of seaweed extract, or sodium alginate, already that the "fat burner" of the future isn't going to be a stim, ... well, at least not necessarily or exclusively, but rather a compound that acts onto the GBA, the gut-brain axis by modulating your bodies response to food and fasting. Now, as gross as this may seem, a recently published study from the United Arab Emirates University does suggest that this fat burners may not even come in pill, but rather as a suppository!

A fat burning suppository? Wtf....

I see you are shocked, well so was I, but the alternative would be that you take a syringe and... ah, let's just assume they came out with a suppository which could deliver the same 0.66, 2.0, 6.66 and 20.0 mmol (0.36, 1.08, 3.58, 10.75 g) of sodium taurocholate the ten obese type II diabetic volunteers (!) in the study by Adrian et al. received rectally via a silastic cannula in 20 ml of 1% (wt/vol.) carboxymethyl cellulose over a period of 1 min after an overnight fast - a small injection with profound effects:

Figure 1: Response of insulin, blood glucose and GLP-1 to rectal administration of different doses of taurocholate to obese type-2 diabetics (based on Adrian. 2013)

As the data in figure 1 shows the injection of deliquescent yellowish crystalline bile acid, most people know for its involved in the emulsification and absorption of dietary fats and fat-soluble vitamins, exerted profound effects on hormonal peptides we have long believed to be produced mainly in response to the ingestion of specific nutrients or the gastrointestinal production of short-chain fatty acids from the latter (Tolhurst. 2013). In particular, the rectal administratoin of sodium taurocholate (the sodium stabilizes the molecule in water) lead to

• dose-dependent increases in plasma concentrations of active GLP-1 and total PYY (not shown in figure 1, but increase paralleled GLP-1) both of which were statistically highly significant (p<0.001) with the highest dose of taurocholate leading to a 7.2x increase in active GLP-1 and a 4.2x increase in PYY
• at the same time plasma insulin increased by 2.6x and the glucose levels decreased progressively over 60 min by up to 3.8 mmol/l

An impressive result which does yet beg the question: Is this good or bad? I mean a 2.6x increase in insulin? That must be bad, right? It certainly would - but if that's a 2.6x increase that does exactly what it's supposed to, i.e. reduce blood glucose levels in obese type II diabetics, it's unquestionably a good thing.

 Figure 2: Food intake 75min after taurocholate administration at different doses; subjects were provided with their favorite meals and advised to eat to satiety (based on Adrian. 2013)

What's yet even better are the downstream effects on subsequent food intake (see figure 2). 75min after the somewhat embarrassing treatment, the subjects had free access to a as much of their favorite food as they wanted. For 2h, their simple task was "eat as much until you are fully satisfied" and the subjects complied. On the occasions where their suppository contained the high dose of taurocholate, the chicken wings, hamburgers, fries and chocolate cakes or whatever these guys indicated were their favorite foods were almost twice as satiating! The 10mol dosage reduced the food intake by roughly 1/4 still and would be in the range of my recommended 'reduce your energy intake by ~20% if you want to maximize fat and minimize lean mass loss' recommendation - yet not as a result of pure willpower, but simply because more was not necessary and much more probably not even possible!
I can control my appetite I don't need these tools

I can see that some of you are now giving a sniff at those gluttonous fatsos who are not able to control their appetite and therefor simply cannot lose weight and I guess for a small minority of dieters that may actually be the case. The emerging research on the far-reaching metabolic effects  of the so-called "satiety hormones" PYY and GLP-1 does yet clearly suggest that gluttony is only part of the reason why the efforts of dieters all around the globe fail time and again. And it is therefore more than reasonable to assume that this satiety induced caloric reduction, contrary to the common will-power based mild to profound starvation,  will actually produce the expected weight loss results as long as it can be sustained over weeks and months.

Figure 3: It's as easy as can be - work against your body, starve yourself, never eat to satiety and lose (top) vs. work with your body, use gut-brain-axis (GBA) modulators and win (bottom)

Direct evidence for this hypothesis comes from yesterday's news, where the reduction in ghrelin, the hunger-inducing counterpart to GLP-1, PYY & co helped the dieters in the high algae fiber group to adhere to their diets, to lose weight and more importantly body fat at a constant rate over the whole 12-week study period (cf. "Sodium-Alginate for 30-40% More Weight Loss and Body Fat Reduction on Mild Caloric Deficit"). 

Taurocholate suppositories, taurine, cholesterol, statins and yet another reason we are fat

Image 2: What do panic buying and overeating have in common? In both cases the affected people or their bodies expect that there is going to be a shortage in the future and they got to squirrel goods or nutrients away.

It doesn't take a rocket scientist or SuppVersity student to figure from the name alone that a molecule which goes by the name "taurocholate" could contain taurine and cholesterol, right? Right! So what happens if you don't eat enough sulfur(-amino acids) which are necessary as a precursor for taurine biosynthesis (Brosnan. 2006), because those are mainly found in yummy high cholesterol foods such as eggs and co? Right! You will neither produce enough taurine nor have enough cholesterol to produce those amounts of taurocholate and other bile acids as would be necessary to reach the enteroendocrine cells in the distal colon, which would then release those peptides that will signal your consciousness that you are satiated and your metabolism to keep burning those damn love-handles because there is plenty of energy coming in and no sign of impeding famine.

The result, a mismatch between energy intake and energy sensing / satiety, will not just have you eat, eat and... eat! as if there was no tomorrow (see image 2), it will also have your body squirrel away every calorie it can save right into your evergrowing adipose tissue. You develop diabetes and hyperlipidemia and your doctor who beliefs in "medical standards" throws a bunch of statins at you. The statins reduce your cholesterol further. There is less substrate for bile acid production. The mismatch becomes even greater, your energy metabolism is tumbling and you are hungrier than ever before... the perfect storm, it's raging!

"Where is the evidence?"

Image 3: What happens when you feed rats 375x more cholesterol than usual, from whole eggs of course? Right, their lipid profile improves! How do you know, did you read my previous blogpost on the study by Yang et al. (Yang. 2013)? If you didn't click on the image to get there.

There is no evidence for a hilarious theory like that? Well let's start with what happened, when we stopped eating nutritious foods, began throwing away egg yolks and started replacing regular foods with cholesterol-free junk... we got fatter: Year by year! Let's go ahead and take a look at the host of scientific evidence for the beneficial effects of taurine on glucose and lipid metabolism (e.g. Park. 1998; Hansen. 2001; Mühlfeld. 2011; De la Puerta; 2010; Nardelli. 2011). And let's finally combine that with the still hushed up pro-diabetic effects of statins (cf. "With >50% Increased Risk to Develop New-Onset Diabetes, Statins are "Starter Drugs" for Post-Menopausal Women"). I guess that's not conclusive scientific evidence, yet and as so often only part of "why we get fat", but it is certainly a promising hypothesis that adds another piece to a puzzle where the gut-brain-axis or gut-endocrine-axis is occupying a place that can hardly be underestimated.

References:

1. Adrian TE, Gariballa S, Parekh KA, Thomas SA, Saadi H, Al Kaabi J, Nagelkerke N, Gedulin B, Young AA. Rectal taurocholate increases L cell and insulin secretion, and decreases blood glucose and food intake in obese type 2 diabetic volunteers. Diabetologia. 2013 Jun 14.
2. Brosnan JT, Brosnan ME. The sulfur-containing amino acids: an overview. J Nutr. 2006 Jun;136(6 Suppl):1636S-1640S.
3. De la Puerta C, Arrieta FJ, Balsa JA, Botella-Carretero JI, Zamarrón I, Vázquez C. Taurine and glucose metabolism: a review. Nutr Hosp. 2010 Nov-Dec;25(6):910-9.
4. Hansen SH. The role of taurine in diabetes and the development of diabetic complications. Diabetes Metab Res Rev. 2001 Sep-Oct;17(5):330-46.
5. Mühlfeld A, Kubitz R, Dransfeld O, Häussinger D, Wettstein M. Taurine supplementation induces multidrug resistance protein 2 and bile salt export pump expression in rats and prevents endotoxin-induced cholestasis. Arch Biochem Biophys. 2003 May 1;413(1):32-40. 
6. Nardelli TR, Ribeiro RA, Balbo SL, Vanzela EC, Carneiro EM, Boschero AC, Bonfleur ML. Taurine prevents fat deposition and ameliorates plasma lipid profile in monosodium glutamate-obese rats. Amino Acids. 2011 Oct;41(4):901-8.
7. Park T, Lee K. Dietary taurine supplementation reduces plasma and liver cholesterol and triglyceride levels in rats fed a high-cholesterol or a cholesterol-free diet. Adv Exp Med Biol. 1998;442:319-25.
8. Stephan ZF, Armstrong MJ, Hayes KC. Bile lipid alterations in taurine-depleted monkeys. Am J Clin Nutr. 1981 Feb;34(2):204-10.
9. Tolhurst G, Heffron H, Lam YS, Parker HE, Habib AM, Diakogiannaki E, Cameron J, Grosse J, Reimann F, Gribble FM. Short-chain fatty acids stimulate glucagon-like peptide-1 secretion via the G-protein-coupled receptor FFAR2. Diabetes. 2013 Feb;61(2):364-71.
10. Yang F, Ma M, Xu J, Yu X, Qiu N. An egg-enriched diet attenuates plasma lipids and mediates cholesterol metabolism of high-cholesterol fed rats. Lipids. 2013 Mar;47(3):269-77. Epub 2013 Jan 11.

3x15g/Day E401, Sodium-Alginate, Increase Weight Loss and Reduction in Body Fat % on Mild Caloric Deficit by 30-40%! The GPA (Gut-Brain Axis) Makes it Possible.

Image 1: The small amounts of sodium-alginate, aka E401 many chocolates and commercially produced foods contain is obviously not enough to ward off obesity. Otherwise the obesity rates should have fallen not risen with the increase in crappy foods.

Aside from the ubiquitous stimulant based fatburners there is another class of weight loss supplements emerging as of late. Those of you who have read Adelfo's Thursday post, here at the SuppVersity, may have seen his plug for Myotropics' WM-HDP based "new Fat Burning Carbohydrate" ThermiCarb(TM). Now as hilarious as it may sound, this resistant starch is in fact as much of a "fat burner" as any of the 1001 currently available stims is. After all, none of those products actively burns fat. What still makes them effective, though, is their ability to shift substrate utilization away from glucose and towards fat, to curb appetite and to deliver the energy you need to do what it takes to shed body fat, i.e. to function normally while eating slightly less and working out.

Contrary to the good old (and certainly not obsolete) stims, these new "fat burners" act on the gut-brain axis, instead of HPA (the hypothalamus-pituatary-adrenal axis), by stimulating the release of a whole host of peptides from the gut. Among those, the  incretin hormones GLP-1 & co. (cf. "Eat More, Burn More and Lose Fat Like on Crack with GLP-1!?") are probably the best understood among these mis-understood "satiety hormones" with their profound  downstream effects on overall energy expenditure, glucose and fatty acid metabolism (Mudaliar. 2013). 

Is alginate, a polysaccharide from marine brown algae, a novel "fat burning fiber"?

Next to designer-starches such as WM-HDP there is also an increasing interest in the effects natural fiber / fiber extracts, such as the 15g alginate from brown algae the obese subjects (0–55y; BMI 30-45kg/m²) in a recent study from the University of Copenhagen in Denmark had to consume before each of their three meals in the course of a 12-week double-blind randomized parallel-intervention (Jenson. 2013), exert on the endocrine signals from your gut.

Image 2: Popsticles are not the only products containing sodium alginate (E401) as a thickener and stabilizer. If you take a closer look at the ingredients of the stuff in the supermarkets, you will notice that  many commercially produced low fat dairy products, ready made sauces, gravies, dressings, puddings, pies and pastry fillings contain it, as well.

What is alginate? Alginate is a gelling polysaccharide (gelling = it forms a gel which passes slowly through your digestive tract) that is extracted from marine brown algae. In seaweed the mannuronic and guluronic acid based components are responsible for the mechanical strength and flexibility. During the regular extraction process alginate is bound to sodium. The result, sodium alginate, has been used a E401 in various foodstuffs to stabilize, gel or viscosify it for years now (Brownlee. 2005). The appetite reducing effects of sodium alginate and other marine-derived fiber are widely known, but the underlying mechanism is still not completely elucidated. According to the current paradigm, it is related to the interaction of sodium-alginate and calcium during the digestive process and the subsequent changes in viscosity of the gastric content, which has been associated with slowed gastric emptying and a reduction of postprandial glucose and insulin response. Of these the latter, i.e. the prolonged influx of glucose, the absence of blood glucose spikes and the overall reduction in insulin levels is currently believed to be at the heart of the observed satiety effects (Cani. 2009).

What is interesting about this study is that according to the self-set goals of the scientists, which lay at the ground of their "Intention-To-Treat analysis" (ITT), which evaluated the changes in body weight and overall body composition, as well as the improvements of metabolic risk factors as a whole, yielded no differences between the two study arms.

Figure 1: Changes in body weight and body composition in response to caloric reduction (-300kcal/day) with or without supplemental alginate (15g/day) after 12 weeks (large graph); actual weight development over the whole 12-week study period (small graph; directly from Jenson. 2013)

If you do yet take a closer look at the actual study data (see figure 1), you will see that there were very important differences between those dieters who simply consumed 300kcal/per day less (control group) and those who followed the exact same calorically reduced dietary regimen yet with an additional 15g of fiber from sodium alginate before every meal (alginate group)!

Lose more weight, more fat and do this at a constant rate beyond week 9!

Despite the fact that onlye the differences between the reduction in total weight and body fat percentage reached statistical significance, this and the absence of the "weight loss plateau" in week 9+ (see figure 1, right) in the alginate group clearly suggest that much contrary to what Jenson et al. had apprehended, the previously demonstrated short-term weight loss benefits of fibrous algae extract and other dietary fiber (Paxman. 2008; Odunsi. 2010; Peters. 2011; Wanders. 2011) did not disappear after an initial adaptation phase. On the contrary! The 40% greater reduction in body weight, as well as the 36% greater reduction in body fat percentage would be of little value if the body weight stagnated after only -6.78kg weight loss in week 9 and left the dieters with an average BMI of 32kg/m² well in the obesity / danger zone.

Figure 2: Changes in glucose metabolism and ghrelin (left) and lipid metabolism (right) in response to caloric reduction (-300kcal/day) with or without supplemental alginate (15g/day) after 12 weeks (large graph); actual weight development over the whole 12-week study period (small graph; directly from Jenson. 2013)

Looking back at the exact weight development in figure 1 (right), we may thus speculate that the observed improvements of the measured markers of blood glucose management and lipid metabolism of which only the HbA1c (not shown in figure 2) showed a statistically significant inter-group difference (+0.01% in control -0.01% in alginate; p < 0.024) would have reached statistical significance after 16-20 weeks. This is particularly true for the insulin levels, for which the difference between control and alginate group is already borderline significant (p < 0.062) after 12 weeks of alginate supported dieting.

Bottom line useful for the obese, safe, well tolerated, but...

Image 3: Duong Nguyen from the first installment of the SuppVersity Student Spotlight at the beginning and end of his amazing 12-week transformation!

As usual we do however have to remember that the subjects in this study were more than just a little chubby, with body fat percentages in the >40% range a reduction of -5.8% (control) and -8.2% (alginate) is easier achieved than a (from a merely mathematical standpoint) equal -12% of the body fat content from 12% to 10%. So, while healthy dieters don't have to care about the minimal, but statistically significantly lower reduction in blood pressure in response to weight loss with sodium-alginate (the scientists ascribe this to the relatively high sodium content of the alginate supplement), the will probably not benefit in the same way as Jenson's obese subjects from the additional 45g of fiber per day. Well, unless, it exerts similar effects effects as they have been observed for hydroxypropyl-distarches (cf. "Waxy Maize Reloaded") on the expression of GIP, GLP-1 and the whole host of the initially mentioned incretin hormones, and adipokines (Sánchez. 2013) and don't just curb appetite and slow digestion.

If it had all those GBA (gut brain axis ;-) effects, seaweed derived sodium-alginate supplements could however make an ideal adjunct to a ~20% reduction in food intake, a reasonable fat loss workout (e.g. "Step By Step Guide to Your Own Workout Routine - Part V: Example Routines - Round 2: Fat Loss Support Routine") and a stimulant-based fat burner of your choice, whenever you strive to cut a few pounds of body weight. I mean, just imagine if Duong (see image 3), who likewise dieted for 12 weeks would have lost 35% more fat mass - yeah you're right, he would probably have been "disgustingly" lean, as Adelfo likes to call it ;-)

References:

1. Brownlee IA, Allen A, Pearson JP, Dettmar PW, Havler ME, Atherton MR, Onsøyen E. Alginate as a source of dietary fiber. Crit Rev Food Sci Nutr 2005;45:497–510.
2. Cani PD, Lecourt E, Dewulf EM, Sohet FM, Pachikian BD, Naslain D, De Backer F, Neyrinck AM, Delzenne NM. Gut microbiota fermentation of prebiotics increases satietogenic and incretin gut peptide production with consequences for appetite sensation and glucose response after a meal. Am J Clin Nutr 2009;90:1236–43
3. Jensen GM, Kristensen M, Astrup A. Effect of alginate supplementation on weight loss in obese subjects completing a 12-wk energy-restricted diet: a randomized controlled trial. Am J Clin Nutr. 2013 Jul;96(1):5-13. Epub 2013 May 30.
4. Mudaliar S, Henry RR. The incretin hormones: from scientific discovery to practical therapeutics. Diabetologia. 2013 Jul;55(7):1865-8. Epub 2013 May 4.
5. Odunsi ST, Vazquez-Roque MI, Camilleri M, Papathanasopoulos A, Clark MM, Wodrich L, Lempke M, McKinzie S, Ryks M, Burton D, et al. Effect of alginate on satiation, appetite, gastric function, and selected gut satiety hormones in overweight and obesity. Obesity (Silver Spring) 2010;18:1579–84.
6. Paxman JR, Richardson JC, Dettmar PW, Corfe BM. Daily ingestion of alginate reduces energy intake in free-living subjects. Appetite 2008; 51:713–9.
7. Peters HP, Koppert RJ, Boers HM, Stro ¨m A, Melnikov SM, Haddeman E, Schuring EAH, Mela DJ,Wiseman SA. Dose-dependent suppression of hunger by a specific alginate in a low-viscosity drink formulation. Obesity (Silver Spring) 2011;19:1171–6.
8. Sánchez D, Miguel M, Aleixandre A. Dietary fiber, gut peptides, and adipocytokines. J Med Food. 2013 Mar;15(3):223-30. 
9. Wanders AJ, van den Borne JJGC, Graaf EJMF. Effects of three dietary fiber on food in real life setting. Appetite 2011;57:544.