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Yes, drastic measures will make the weight melt faster, but even if you tube-feed yourself lean, you will not stay this way without lifestyle changes like an increase in fiber intake.

There are a billion different ways to lose weight, but if you aligned all these ways along in a diagram with two axes: One that describes the degree of invasion in your regular dietary habits and the other indicating the time that's necessary to see results, the two "tricks" discussed in today's waredownloadsoft post would be placed somewhere in the edges of the 2nd and third quadrant.

You don't get that? Well, I guess that's a science guy's way of saying we are dealing with totally different ways of losing weight, of which one, i.e. the use of guar gum to increase the satiety effects of your meals, suitable for long-term weight loss, while the other, i.e. the use of a very low-calorie
protein-based that is enterally fed to obese individuals, being geared towards maximal fat loss in a minimal amount of time - no matter how severe this may mess with your regular eating habits.
In spite of the fact that I hope that few of you are in a situation similar to the one the 364 severely overweight patients (59% women; all with a mean BMI of whopping 46.6 ± 7.2 kg/m²) who participated in a recent study from Italy, I believe that you may be interested to hear how these guys and gals lost 5.4cm of their waists and improved their insulin levels by 11 pts and their glucose levels by 16 pts within only 14 days.

Figure 1: Changes in relevant markers of body comp. glucose and lipid metabolism (Castalado. 2015).

Yeah, the results are impressive, but I doubt that many people like to be fed through a nasogastric tube 24/7, right? Well, that's unfortunately what may be required to ensure that the homemade very
low-calorie (~6 kcal/kg of ideal body weight/day) protein-based formula (2000 mL per day) the scientists used can actually work its full weight loss magic.
Eventually, it should be obvious, though, that a weight-loss strategy like that is not appropriate for someone with only a few extra-kilograms. For people like that "trick" #2 may be of significantly greater interests.

Fiber increases satiety, but more importantly, it also reduces food intake

In the end, it's not actually new that fiber can make you feel more satiated. What is yet by no means clear, however, is (a) whether this is a "one-time thing", i.e. whether the effect will still be there, when you got accustomed to high fiber foods, and (b) whether an acute feeling of increased satiety after a "fiber-upped" food (= foods that are artificially supplemented with fiber) will also make you eat less on subsequent meals.
Both has recently been studied by scientists from Taiyo Kagaku R&D. In three separate studies, Rao et al. determined the whether small doses of partially hydrolysed guar gum (PHGG), a soluble dietary fibre would effect post-meal satiation and subsequent energy intake with acute and long term administration.

"The following three separate studies were conducted: in study 1, healthy subjects (n 12) consumed 2g of PHGG along with breakfast, lunch and an evening snack; in study 2, healthy subjects (n = 24) consumed 2 g of PHGG or dextrin along with yogurt as breakfast for 2 weeks; in study 3, healthy subjects (n = 6) took 6 g each of either PHGG or indigestible dextrin or inulin along with lunch" (Rao. 2015)

The results of the studies confirmed that (1) the acute satiety effect of soluble fiber (in this case guar gum) persists (at least for two weeks) and that (2) slightly larger amounts of soluble fiber will have beneficial effects on energy intake.

Figure 2: Two important findings (1) the appetite suppressive effects actually increase from day 1 to day 7 and (2) the energy intake is reduced even if you take into accout that soluble fiber has calories, too (Rao. 2015).

What's specifically interesting about the last result is that most of the reduction in energy intake occurred in the form of snacks; and in view of the fact that snacking is one of the motors of the obesity epidemic, this is one of the few results from a medium-term study that may actually translate into long-term results.
References:

• Castaldo, Giuseppe, et al. "A 2-Week Course of Enteral Treatment with a Very Low-Calorie Protein-Based Formula for the Management of Severe Obesity." International Journal of Endocrinology 2015 (2015).
• Isken, Frank, et al. "Effects of long-term soluble vs. insoluble dietary fiber intake on high-fat diet-induced obesity in C57BL/6J mice." The Journal of nutritional biochemistry 21.4 (2010): 278-284.
• Howarth, Nancy C., Edward Saltzman, and Susan B. Roberts. "Dietary fiber and weight regulation." Nutrition reviews 59.5 (2001): 129-139.
• Papathanasopoulos, Athanasios, and Michael Camilleri. "Dietary fiber supplements: effects in obesity and metabolic syndrome and relationship to gastrointestinal functions." Gastroenterology 138.1 (2010): 65-72.
• Rao, Theertham Pradyumna, et al. "Post-meal perceivable satiety and subsequent energy intake with intake of partially hydrolysed guar gum." British Journal of Nutrition 113.09 (2015): 1489-1498.
• Weickert, Martin O., and Andreas FH Pfeiffer. "Metabolic effects of dietary fiber consumption and prevention of diabetes." The Journal of nutrition 138.3 (2008): 439-442.

Specifically for teenagers it may be important to work out in both aerobic and anaerobic workouts. So, this would be another reason to favor the combined over the other regimen.

You will probably have overheard the "knowledgeable" trainers at the gym tell their credulous clients, who just told them they "want to lose that belly fat", that the best thing they could do was to "stop spending that much time with weight training" and to do some more (steady state) cardio. Well, in general, there's nothing wrong about steady state cardio - in fact, many studies show that it is superior to resistance training when it comes to "merely" shedding body weight (in the obese). If "weight loss" is still everything you're aspiring, though, you are either new to the waredownloadsoft or another of the "headline skimmers" who happen to ask questions that are answered not just in the article, but actually in one of the red boxes... ah, I am digressing.

So, what I actually wanted to tell you is that a recent study from the Universities of Ottawa and Calgary (Alberta. 2015), clearly contradicts the average commercial gym chain trainer's recommendation and shows that belly fat loss is better achieved with diet + resistance training.
The subjects of the study were youngsters, 304 (! the high number of participants is a huge plus of the study) 14-18 year-old overweight and obese teenagers (mean body fat almost 50%!), to be specific, who were randomized to four different treatments for 22 weeks:

Table 1: Training progression in the Aerobic and Resistance group (Alberga. 2015)

• aerobic training (Aerobic), 
• resistance training (Resistance),
• combined aerobic + resistance training (Combined) or 
• non-exercising control group (Control)

Adolescents,... ok, but unless they're too sarcopenic (=suffer from pronounced age-induced muscle loss) to hit the weights, your overweight clients or you, yourself, should be able to follow the same training programs the adolescents did and see similar results if you fully adhere to the following training prescriptions:

• Resistance: The duration of each session progressed to a maximum of about 45 min. Exercises were primarily performed on weight machines, and when required with dumbbells (lateral raise, shrugs, bicep curls, front raise, preacher curl, dumbbell pullover) or by using one's own body weight as resistance (lunges, sit-ups and abdominal crunches).
  

  Table 2: Overview of the individual workouts in the Resistance group (Alberga. 2015).

  Participants alternated among exercises from groups A1, A2, B1 and B2 shown in Table 2. Participants were asked to rest for ~ 2 min between sets and were instructed on proper breathing techniques.
• Aerobic: Participants randomized to the aerobic training group underwent a 22-week program (Table 1, left) wherein the exercise intensity and duration increased progressively to a maximum of 45 min per session. Exercise was performed on a cycle ergometer, elliptical or treadmill and participants were free to vary the machine(s) used. Exercise intensity was standardized using heart rate monitors (Polar Electro Oy, Kempele, Finland).
• Combined: This group performed the full exercise programs done by both the aerobic and resistance training groups (Table 1, left + right) during each session for a total of 4 times per week for a maximum of 90 min per session.

Figure 1: Changes in subcutaneous (SAT) and visceral (VAT) body fat at different regions; L4L5 represents area between 4th and 5th Lumbar vertebrae; * indicates sign. difference to control; # sign. difference to aerobic (Alberga. 2015).

References:

• Alberga, A. S., et al. "Effects of aerobic and resistance training on abdominal fat, apolipoproteins and high-sensitivity C-reactive protein in adolescents with obesity: the HEARTY randomized clinical trial." International journal of obesity (2005) (2015).
• Dansinger, Michael L., et al. "Comparison of the Atkins, Ornish, Weight Watchers, and Zone diets for weight loss and heart disease risk reduction: a randomized trial." Jama 293.1 (2005): 43-53.
• Thompson, A., and J. Danesh. "Associations between apolipoprotein B, apolipoprotein AI, the apolipoprotein B/AI ratio and coronary heart disease: a literature‐based meta‐analysis of prospective studies." Journal of internal medicine 259.5 (2006): 481-492.
• Walldius, G., and I. Jungner. "The apoB/apoA‐I ratio: a strong, new risk factor for cardiovascular disease and a target for lipid‐lowering therapy–a review of the evidence." Journal of internal medicine 259.5 (2006): 493-519.

Since scientists still judge obesity by BMI values, athletes contribute to the CVD / mortality  "obesity paradox"

Alright, next to "I don't care, I feel good" you will probably have hear or even read statements like "Don't worry if you're obese. The extra fat is protective" or at least claims like "If you're fit, it doesn't matter if you're fat".

In today's waredownloadsoft Special I want to take a closer look at these and other claims that are based on observational data that suggest that either all or at least one of the following "obesity paradoxes" exist: (1) Classic obesity paradox - obesity is protective in some chronic diseases; (2) pre-obesity - overweight is protective in normal populations; (3) fat-but-fit - obesity is not a risk factor for mortality in fit individuals; (4) healthy obesity - a sizeable population of obese adults has normal cardio-metabolic risk profiles (McAuley. 2011).

1. The classic obesity paradox: Ok, let's start with the biggest bogus, i.e. obesity paradox #1 - obesity is protective in some chronic diseases: Yes, you cannot deny that there appears to be a reduced mortality risk in obese vs. lean patients with known or suspected coronary heart disease (CVD). Now, the real problem, though, is that obesity is also an independent risk factor for CHD (Hubert. 1983; Wilson. 2002).
   

   Figure 1: Incidence (‰) of myocardial infarction (top, left), congestive heart failure (top, right) and relative odds of dev. cardiovascular disease in the 1st place acc. to age and weight (% of normal | Hubert. 1983)

   As the data in Figure 1 (bottom) shows the risk of developing cardiovascular disease increases by 13%, 29%, 46% for each 10% extra-weight in men and by 8%, 17% and 26% for each 10% extra-weight men. If you also take into account the incidence of myocardial infarctions (top left) and congestive heart failure (top, right), you will have to admit that it would be stupid to rely on not dying from CVD, because you're fat if you can can avoid developing CVD if you don't get fat in the first place?
   
   In addition, the evidence that normal-weight and even more so underweight CVD patients are at higher risk of not surviving their illness could just as well be a result of reverse causation with the subjects in the normal and low weight range having lost weight due to being sicker than their overweight peers.You don't believe that? Well why do those with the highest weight not have the lowest, but the highest (+88% | Romero-Corral. 2006) CVD mortalities? Convinced? Don't be too sure, there's still one last argument in favor of the existence of an obesity paradox. Who's worse off than someone who is fat and suffers from metabolic syndrome? Well, someone who is not even able to store away the extra energy and suffers from high blood glucose and lipid levels, although he is not obese. If we had sub-group analysis on the normal- and under-weight CVD subjects, I am pretty sure that many will fall into the metabolically deranged skinny fat category. How paradox is it that they don't live longer than their overweight, but in many cases metabolically less deranged peers?

2. The pre-obesity paradox: While you certainly cannot rely to survive all your friends if you're simply the fattest, the pre-obesity paradox which says that people in the overweight, but non-obese pre-obesity zone (BMI 25-29.9 kg/m²) will live the longest is much harder to debunk.
   
   While it is unquestionable that many people who fall into this category suffer from pre-diabetes and pre-hypertension, which in turn are associated with significant increased risk of CVD mortality and all-cause mortality (Tsai. 2008; Ning. 2010). As Karandish and Shirani point out in a recent review "[t]herefore, a gradual increase in mortality risk from pre-obesity to obesity [must be] expected" (Karandish. 2015).
   

   Figure 2: Risk increase for unhealth non-obese and healthy obese individiuals to transit to unhealthy obesity. After each 5 years, those who already made the transition were removed, so the data indicates that w/ a >12x increased risk most of the "healthy obese" became unhealthy obese in only 5 years (Bell. 2015).

   Now, the bad news for those who feel secure in their "pre-obesity" stage is that studies suggest that more than 40% of those "lucky chubbies" will progress to full-blown obesity (Gopal. 2015 | probably also because overweight is linked to inevitable increases in HbA1C and thus diabetes | Nakajima. 2014).
   
   To summarize, I would like to cite the conclusion of a letter to the editor of Obesity Research & Clinical Practice in which the author says that "most of healthy obesity may be a transient state" (Nakajima. 2015) - and that's not a hypothesis. It's based on evidence from studies by Soriguer et al. (2013), Appleton, et al. (2013), Bell et al. (2014 & 2015).
3. The fat-but-fit paradox: You probably won't doubt that fat-but-fit individuals have considerably lower mortality risk compared to normal-weight but unfit individuals. But let's be honest: How many fat-but-fit individuals do you know? None? One? Well, I guess that's because studies show that obesity is a major obstacle to doing what it takes to get and stay fit: exercise (Dalle Grave. 2010; Sallinen. 2009).
   

   Figure 3: Relative risks of (A) all-cause and (B) cardiovascular disease (CVD) mortality by cardiorespiratory fitness quintiles for 40,451 (2657 all-cause and 943 CVD deaths) men and 12,831 (375 all-cause and 90 CVD deaths) women aged 20–100 years without CVD or cancer (Lee. 2010)

   The practical relevance of the fat-but-fit paradox may thus be marginal, but it's of huge theoretical importance, because any investigation that tries to link objective measures of physical activity or BMI to mortality is fundamentally flawed if the scientists don't adjust their data for the fitness of their subjects (Lee. 2010) - what if all the healthy subjects whose survival brought up the original "obesity paradox" were exceptionally fit? What if they were in fact athletes whose increased lean mass tricked the negligent scientists to believe they were obese, because their BMI is elevated? What if the allegedly "lean" CVD-ridden peers were exceptionally unfit, skinny fat, sedentary and diabetic? Well? Right, in any of these cases the paradox would be the mere result of a lack of attention to important details in the statistical analyses of scientists that like to grab the increasingly obese public's attention by assuring them that they are fine.
4. The healthy obesity exists paradox: In the discussion of paradox #1-3, we have already confirmed that you can be obese and significantly healthier than some sick normal-weight individuals. This can, but does not have to mean that you also fullfill the official definition which includes the absence of six common cardio-metabolic risk factors (impaired fasting glucose/diabetes, insulin resistance, high triglycerides, low HDL cholesterol, high blood pressure, and high C-reactive protein) in an individual with a BMI ≥30 kg/m².
   
   The previously discussed evidence that shows that most people rapidly progress from healthy to unhealthy obesity do yet put a huge "?" behind #2 and #3 of the "Health at Every Size" recommendations according to which obese individuals should "trust internal body systems designed to keep us healthy" and "listen to hunger and satiety body signals" - if those mechanisms were fully functional in a world of 24/7 junkfood exposure, no one would be obese - healthy or unhealthy. Compared to yoyo-dieting, though, this strategy has been shown to reduce weight and improve relevant health variables (Bacon. 2002).

References:

• Appleton, Sarah L., et al. "Diabetes and cardiovascular disease outcomes in the metabolically healthy obese phenotype a cohort study." Diabetes Care 36.8 (2013): 2388-2394.
• Bacon, Linda, et al. "Evaluating a" non-diet'wellness intervention for improvement of metabolic fitness, psychological well-being and eating and activity behaviors." International Journal of Obesity (2002).
• Bell, J. A., M. Kivimaki, and M. Hamer. "Metabolically healthy obesity and risk of incident type 2 diabetes: a meta‐analysis of prospective cohort studies." obesity reviews 15.6 (2014): 504-515.
• Bell, Joshua A., et al. "The natural course of healthy obesity over 20 years." Journal of the American College of Cardiology 65.1 (2015): 101-102.
• Calle, Eugenia E., et al. "Overweight, obesity, and mortality from cancer in a prospectively studied cohort of US adults." New England Journal of Medicine 348.17 (2003): 1625-1638.
• Dalle Grave, Riccardo, et al. "Cognitive-behavioral strategies to increase the adherence to exercise in the management of obesity." Journal of obesity 2011 (2010).
• Gopal, J. "Metabolically Healthy Obesity-Is it Really a Distinct Subtype?." Journal of Obesity and Metabolic Research 2.2 (2015): 105.
• Hubert, Helen B., et al. "Obesity as an independent risk factor for cardiovascular disease: a 26-year follow-up of participants in the Framingham Heart Study." Circulation 67.5 (1983): 968-977.
• Karandish, Majid, and Fatemeh Shirani. "Controversies in Obesity Treatment." Nutrition And Food Sciences Research 2.3 (2015): 5-14.
• Lee, Duck-chul, et al. "Review: Mortality trends in the general population: the importance of cardiorespiratory fitness." Journal of Psychopharmacology 24.4 suppl (2010): 27-35.
• McAuley, Paul A., and Steven N. Blair. "Obesity paradoxes." Journal of sports sciences 29.8 (2011): 773-782.
• Nakajima, Kei, and Kaname Suwa. "Excess body weight affects HbA1c progression irrespective of baseline HbA1c levels in Japanese individuals: a longitudinal retrospective study." Endocrine research 0 (2014): 1-7.
• Nakajima, Kei. "Long-term healthy obesity may be exceptional worldwide." Obesity research & clinical practice (2015).
• Ning, Feng, et al. "Cardiovascular disease mortality in Europeans in relation to fasting and 2-h plasma glucose levels within a normoglycemic range." Diabetes Care 33.10 (2010): 2211-2216.
• Romero-Corral, Abel, et al. "Association of bodyweight with total mortality and with cardiovascular events in coronary artery disease: a systematic review of cohort studies." The Lancet 368.9536 (2006): 666-678.
• Sallinen, Janne, et al. "Perceived constraints on physical exercise among obese and non-obese older people." Preventive medicine 49.6 (2009): 506-510.
• Soriguer, Federico, et al. "Metabolically healthy but obese, a matter of time? Findings from the prospective Pizarra study." The Journal of Clinical Endocrinology & Metabolism 98.6 (2013): 2318-2325.
• Tsai, Shan Pou, et al. "The effects of pre-disease risk factors within metabolic syndrome on all-cause and cardiovascular disease mortality." Diabetes research and clinical practice 82.1 (2008): 148-156.
• Wilson, Peter WF, et al. "Overweight and obesity as determinants of cardiovascular risk: the Framingham experience." Archives of internal medicine 162.16 (2002): 1867-1872.

If you oxidize the CHOs from this meal, instead of storing it as glycogen, that's bad news for ability to maintain your body weight over the next 6-months & beyond

You will know (and maybe hate) them, people who are eating whatever they want, whenever they want while still being not exactly shredded, but at least very lean. What do all these people who have an extremely easy time keeping their weight stable in common?

A recent study from the Phoenix Epidemiology and Clinical Research Branch at the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) at the "glorious" National Institutes of Health (NIH) suggests that it may relate to the way they respond to fasting and overfeeding on high carb, low protein and eucaloric diets.
It is by no means news that there is a considerable inter-individual variation in the energy cost of weight gain. Some people gain weight on a caloric surplus of only 10kcal/day, while others stash away hundreds of extra kcals without gaining a single pound of body fat (these figures have only illustrative values and are not meant to be "exact").

"In a prior cross-sectional study, the increase in energy expenditure (EE) with overfeeding and the decrease with fasting were found to be correlated in a small group of 14 male subjects (Weyer. 2011). Our group has previously shown that the EE response to overfeeding varies considerably among individuals but is consistent and reproducible within individuals. This individual contribution explains more of the observed variability in the EE changes with overfeeding than changes to the macronutrient content of the diet (Thearle. 2013). These studies seem to indicate that phenotypic differences may exist in the EE responses to fasting or overfeeding that may affect susceptibility to weight gain. As overeating or caloric restriction are necessary to alter weight, perturbations in energy balance may be needed to uncover responses that signify an energy conserving physiology versus a physiology that is better able to resist weight gain" (Schlögl. 2015).

In their latest study, Schlögl and colleagues extend their previous findings by addressing the question of whether this inter-individual variation in EE changes relates to future weight change. Or, to put it simply: They tried to answer the question

"Will your acute reaction to 24h overfeeding on different diets predict if you can maintain your weight over the next 6 months, or not?"

To answer the question, the 24-h EE during energy balance during fasting and four different overfeeding diets with 200% energy requirements was measured in a metabolic chamber in 37 subjects with normal glucose regulation while they resided in the clinical research unit of the NIH. Each of the diets was administered for exactly 24h with 3-day washouts in-between (breakfast at 07:00, entry into the calorimeter one hour later; further meals were provided inside the calorimeter at 11:00, 16:00, and 19:00 through a two-door airlock):

• a eucaloric reference diet which was 80% of the weight maintaining diet to account for the reduced energy expenditure due to being confined to the metabolic chamber that contained 50% carbohydrates, 30% fats, and 20% proteins
• a fasting trial (FST) in which the subjects sat in the metabolic chamber fasted
• a low-protein diet (LPF) with 51% carbohydrate, 46% fat, 3% protein
• a standard overfeeding diet (SOF) with 50% carbohydrate, 30% fat, 20% protein
• a high-fat, normal-protein overfeeding diet (FNP) with 20% carbohydrate, 60% fat, 20% protein
• a high-carbohydrate, normal-protein overfeeding diet (CNP) with 75% carbohydrate, 5% fat and 20% protein

To be able to assess the long-term weight gain, all participants returned for follow-up visit to the NIH headquarter 6-months after the initial measures.On that occasion, their body weight and composition (DXA | unfortunately, the body fat level was not analyzed seperately) was measured and the change in body weight was correlated with (a) the decrease in 24-h EE during fasting and (b) the increase with the different overfeeding protocols.

Figure 1: 24h energy expression expressed relative to eucaloric reference diet (Schlögl. 2015)

The results of the scientists' correlation analysis were surprisingly unambiguous: A larger reduction in EE during fasting, a smaller EE response to low-protein overfeeding and a larger response to high-carbohydrate overfeeding all correlated with weight gain.

Figure 2: Sign. correlations between change in 24-EE during overfeeding / fasting and weight gain (Schlögl. 2015).

If you take a closer look at the correlations (r-values) and their significance in Figure 2 you will realize that all of them are statistically significant . In other words, there is a significant link between an increased risk of gaining weight in the next 6 months and

• a higher decrease in energy expenditure during fasting (Figure 2; A | this should remind you of the thrifty phenotype theory, cf. Wells. 2011)
• a smaller increase in energy expenditure during low protein dieting (Figure 2; B)
• a higher increase in energy expenditure during carbohydrate overfeeding (Figure 2; C)
• a higher higher reliance on fat during fasting (Figure 2; D)

References:

• Pannacciulli, Nicola, et al. "The 24-h carbohydrate oxidation rate in a human respiratory chamber predicts ad libitum food intake." The American journal of clinical nutrition 86.3 (2007): 625-632.
• Schlögl, Mathias, et al. "Energy expenditure responses to fasting and overfeeding identify phenotypes associated with weight change." Diabetes (2015): db150382.
• Thearle, Marie S., et al. "Extent and determinants of thermogenic responses to 24 hours of fasting, energy balance, and five different overfeeding diets in humans." The Journal of Clinical Endocrinology & Metabolism 98.7 (2013): 2791-2799.
• Wells, Jonathan CK. "The thrifty phenotype: An adaptation in growth or metabolism?." American Journal of Human Biology 23.1 (2011): 65-75.
• Weyer, C., et al. "Changes in energy metabolism in response to 48 h of overfeeding and fasting in Caucasians and Pima Indians." International journal of obesity and related metabolic disorders: journal of the International Association for the Study of Obesity 25.5 (2001): 593-600.
• Zurlo, Francesco, et al. "Low ratio of fat to carbohydrate oxidation as predictor of weight gain: study of 24-h RQ." American Journal of Physiology-Endocrinology And Metabolism 259.5 (1990): E650-E657.

If you belong to the people who simply cannot stay away from HFCS foods and beverages, you may be happy to hear that the equivalent of as little as 10g citrulline or NEAAs in your diet may do much more than "just" fully prevent its negative effects on your liver.

You will probably remember from previous articles I wrote that NAFLD, or rather the development of non-alcoholic fatty liver disease, is one of the earliest markers of metabolic syndrome and beginning type II diabetes. In the Western obesity societies in North America and Europe, NAFLD is among the most common causes of chronic liver disease and its prevalence is increasing rampantly (Marchesini. 2001).

In spite of the fact that its development is most strongly linked to the consumption of a generally unhealthy, energetically dense diet, there are several lines of evidence which suggest that the ingestion of exorbitant amounts of fast-digesting fructose from high fructose corn syrup (HFCS) sweetened beverages or processed foods is one, if not the most reliable motor of its development (Volynets. 2012).
On a molecular level fructose has been shown to trigger the production of fat from glucose in the liver (de novo lipogenesis | DNL). It does so by activating certain enzymes via the sterol regulatory element binding protein-1c (SREBP1c) and/or the carbohydrate-responsive element-binding protein (ChREBP). In conjunction with the corollary hepatic oxidative stress and the subsequent increase in insulin resistance, the onslaught of readily absorbed fructose from processed foods and HFCS-sweetened beverages is thus  like gasoline on the fire of the obesogenic baseline diet some people refer to as the "standard american diet" (learn why the "SAD-diet" is so good at making you fat). On the whole, however, the accumulation of fatty streaks in the liver that's so characteristic of NAFLD is yet only the point of departure of the journey to the land of the super-obese type II diabetics.


Now this journey from slightly overweight to super-obese is a journey of which many previous studies studies already suggested that it could take a very different route if people consumed higher amounts of protein and/or certain amino acids (AAs):

• Theytaz et al. (2012), for example, found a "liver cleansing" increase in VLDL-TG release by the liver with an essential AA-enriched diet, and
• Bortolotti et al. (2012) showed that a protein-enriched diet can effectively reduce the fructose induced lipid accumulation in the liver through increased energy expenditure. 

As Prasanthi Jegatheesan et al. point out, "[t]hese beneficial effects of AAs or proteins may arise through lipid oxidation, decreased DNL, and modulation of genes involved in lipid metabolism" (Jegatheesan. 2015). Since citrulline is the precursor for the renal synthesis of Arg, which is known to improve insulin sensitivity and lipid metabolism, and has been shown to have beneficial effects on the level of plasma triglycerides and fat deposition in the liver, the authors of a recent study speculated that "Cit supplementations might [...] able to limit the development of fructose-induced NAFLD" (Jegatheesan. 2015). Morever, Jegatheesan et al. expected to see similar effects with other nonessential amino acids (NEAA), of which their own previous research had shown that they may offer similar anti-NAFLD effects.
To confirm or falsify their hypotheses, the researchers randomized twenty-two rats into four groups on different diets:

• CNEAA as in control - control diet without added fructose + 1g/kg non-essential amino acids (for humans that's roughly 11g per day | this was the control diet in the study at hand)
• F as in fructose- control diet enriched with 60% fructose without supplements
• FNEAA as in control + fructose - fructose enriched diet (F) + 1g/kg non-essential amino acids (which happens to be the control diet in the study at hand)
• FCIT as in fructose + citrulline - fructose enriched diet (F) + 1g/kg citrulline

In that, it's important to note that the NEAA supplement contained isomolar amounts of the 6 AAs and was isonitrogenous to the Cit diet. So, a mere difference in the nitrogen content of the chow cannot explain the obvious differences that occurred over the course of the 8-week study period.

Figure 1: Relative changes in liver weight, hepatic triglyceride content as well as the liver markers AST, ALT and ALP a marker of kidney health  compared the "control" group (CNEAA | Jegatheesan. 2015)

A period, in which the rodents in the fructose enriched diet group (F) developed NAFLD. A fate the rats in the FCit and the FNEFA group did not share - even though the amount of fructose in their diets was exactly as high as it was in the F group.

Figure 2: Both FNEAA and FCit rodents had a better body composition than the rodents on the NEAA supplemented control diet, but the differences reached statistical sign. only compared to the fructose (F) group (Jegatheesan. 2015)

In that, it is unquestionably worth noting that we are not talking about a mere amelioration of the fructose induced damage. If you look at the data you will notice that the rodents with the alanine, glycine, proline, aspartate, histidine, and serine enhanced fructose enriched diets actually ended up having healthier livers than those on the non-fructose diet... if that's not convincing evidence that the commonly heard, and painfully overgeneralized claim that "fructose is the root cause of all metabolic diseases" is bogus, I don't know.

So, why would you even consider citrulline, if the NEAA combo is better for your liver? 

Well, the reason that the average physique enthusiast, may still choose citrulline as his "fructose buffer" of choice is easy: Firstly, the differences in terms of liver health are not really statistically significant. Secondly and more importantly, though, citrulline triggered a reduction in visceral and total fat mass and a relative increase lean mass that was not observed in the NEAA group. And let's be honest: Isn't this type of body recompositioning effect what many of you are striving for?

What is most astonishing though, is that you could have these fat loss and muscle gain effects not just despite, but maybe even because you're guzzling HFCS drinks all day (obviously we'd have to have a citrulline + baseline diet group to confirm that). If we assume that the results translate 1:1 to human beings, the one thing you had just ~10g of citrulline per day. Is this possible? Well, it is, but let's be honest with ourselves: The inter-group differences between the control and the citrulline + fructose were not statistically significant. So while there were improvements those were not pronounced enough to be of statistical significance even in rodents. It is thus not really surprising that you haven't heard of citrulline as the "get jacked" amino acid very often... even though, evidence that it can help you to get jacked does exist (more).
References:

• Bortolotti, Murielle, et al. "Effects of dietary protein on lipid metabolism in high fructose fed humans." Clinical Nutrition 31.2 (2012): 238-245.
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