Leaky Gut & Gluten Belly: Bacterial Firebugs Translocate from Your Gut to Your Ever-Growing Visceral Fat Depots

Image 1: Gluttony or a victim of bacterial translocation from an unrecognized gluten-sensitive leaky gut (img from COPD Lighthouse)

"Leaky gut", for decades one of those concepts, the belief in which divided self-proclaimed "real scientists" from their "hippie" counterparts, has eventually found its way to mainstream science. What began with a few tentative studies into the role of a pathologically increased gut permeability in Crohn's disease and co., is about to become a recognized research area with about 150 related publications within the first 9 month of 2011, alone. Out of these 150 publications, a study by Professor Pierre Desreumaux, and his colleagues from the Universitè Lille Nord de France (Desreumaux. 2011) is unquestionably among those, which could have a major impact on the established image of the gut and its biota as an isolated system that sustains the rest of the body with nutrients and has - due to the insulating epithelial layer - little or no direct impact on all the ailments and illnesses by which the Western civilization has been befallen in the course of its quest for highly palatable, optically pleasant, economic and convenient (franken-)food.

The study comprised 22 patients with Chron's disease, 17 patients with ulcerative colitis and 21 controls, who were normal weight, had no history of diabetes mellitus and were not being treated with speci fic medications known to modulate visceral fat. All patients had been scheduled for operations, during which - with their consent - the required subcutaneous/mesenteric fat specimens were taken and the ileal and colonic transparietal biopsies were performed.

Figure 1: CRP mRNA expression [arbitrary units] in mesenteric and subcutaneous fat pads of control, Crohn's disease (CD), and ulcerative colitis (UC) patients (data adapted from Desreumaux. 2011)

While the result that the mRNA expression of c-reactive protein (CRP) in the Crohn's disease group was 83x higher than in the patients with ulcerative colitis (UC) and 3000x higher than in the control group, alone would probably have been worth the whole procedure, a way more interesting result is that the 83x increase over the UC group is fat-depot specific. This means, only the mesenteric fat that is situated right next to the organs of the intestinal tract produces this 83x exaggerated amount of the acute phase protein CRP that is released in response to acute profound inflammation and has been implicated as a marker for peripheral vascular disease (Abdellaui. 2007), liver inflammation (Rodrigez-Leal. 2006), and other unwanted metabolic consequences of the rampant obesity-pandemic (Oda. 2008). This novel observation led the scientists to believe that CRP expression may be enhanced by inflammatory and bacterial stimuli related / subsequent to the pathologically increased gut permeability in Chron's patients.

Image 6: Could Glutamine be
the cheap colostrum?

Can you take measures to decrease your gut permeability and spare your visceral fat e.coli and other bacterial infections? Yes you can! And if you are a diligent student of the SuppVersity, who does not miss a single "course" (i.e. blogpost), you already know that

• glutamine (e.g. dos Santos. 2010), and
• colostrum (Marchbank. 2011)

have been shown to increase gut integrity and to reverse the negative effects of strenuous exercise (such as heavy weight lifting and marathon running ;-) on intestinal permeability.

And in fact, Desreumaux et al. were able to show that in Crohn's disease patients, bacterial translocation, which is usually defined as the migration of bacteria from the gastrointestinal tract to mesenteric lymph nodes and then to peripheral organs such as the liver and spleen, can also affect the mesentric fat pads and increases during experimental ileitis (i.e. inflammation of the ilium, of which a permanently increased mucosal permeability is a characteristic feature; Kroesen. 2008):

Bacterial translocation to mesenteric adipose tissue occurred in 80% of indomethacin-treated rats [model for inflammatory bowel diseases] compared with 11% of control rats. Higher rates of bacterial translocation to mesenteric lymph nodes were also noted in rats following intraperitoneal administration of indomethacin when compared to control animals (67% vs 22%, p < 0.089). The rates of bacterial trans-location were broadly similar in mesenteric adipose tissue and mesenteric lymph nodes (80% vs 67%) in indomethacin-treated rats, as well as in control animals (11% vs 22%).

With 27% the rate in the Crohn's patients was lower, yet still more than two 2x higher than in the "healthy" controls (13%). Basically, this means that a healthy gut keeps >87% of the bacteria from wreaking havoc on your visceral fat depots (and other organs) a "leaky" one, on the other hand, may allow up to 80% of these tiny firebugs to make themselves at home in the fat tissue next to your digestive organs. Now, that would not be a problem, if the local "fire" your new subtenant are sparking within those fat pads would not results in chronic and systemic inflammation (the scientists were able to show a linear relation between visceral CRP and systemic CRP levels) and thus predispose you to obesity, diabetes, heart disease, Alzheimer's, cancer and all the other plagues of the 21st century.

What's Worse: YoYo-Dieting or Constant Gluttony? What Happens During Weight Cycling? And Why Does Every Diet Make You Fatter? Lots of Questions, a Couple of Answers

Image 1: To eat or to diet, what's worse?

Despite the fact that the magazines are still full of "X pounds in Y weeks" diets, more and more people begin to realize that "diet hopping" and even "dieting" in the conventional sense, i.e. following a special, usually very strict and non-sustainable nutritional regimen for a very short amount of time, are futile. But can calling a halt before you blow up like a balloon from time to time actually be worse than letting yourself go all-day, everyday? According to the results of an experiment that has been conducted at the Institute of Biology of the State University of Rio de Janeiro, the results of which have just been published in the open access journal PLoSOne, the answer to this question must be: YES, it can! And that may be true, even when you are not starving yourself!

Even "healthy" weight cycling turns out to be profoundly unhealthy!

Now, the unfortunate news first: We are, as so often dealing with a rodent study - one that was done conducted with 80(!) 3-months old C57BL/6 mice. "Wow! 80 mice? That's plenty!" Yeah, initially it may sound like that, but in view of the fact that their number was decimated every 8 weeks, there would not have been the necessary 4x8 rodents left at the end of the 24-week study period for the final evaluation of the four experimental groups, which were

• standard chow (SC; 15kJ/g) - rodents in this group received the standard chow (76% energy from carbohydrates, 14% energy from protein, and 10% energy from fats) for the whole study period
• high fat diet (HF; 21kJ/g) - rodents in this group received a fattening hypercaloric diet (26% energy from carbohydrates, 14% energy from protein, 50% energy from animal lard and 10% energy from soy bean oil 
• SC ↔ HF - rodents in this group received standard chow for the first 8-week cycle, high fat diet for the 2nd 8-week cycle and standard chow for the third and last 8-week cycle
• HF ↔ SC - rodents in this group received high fat diet for the first 8-week cycle, standard chow for the 2nd 8-week cycle and high fat  for the third and last 8-week cycle 

If we go back to the initial question, the HF group would be our 24/7, 365 days a year eat everything the worst Western diet you can imagine has to offer, while the animals in the group SC ↔ HF and HF ↔ SC group would be representative of

• the high school football player who turns to a sedentary lifestyle and bad eating habits when he goes to college, is partying all night, bear pizza, etc. eventually, he realizes he got fat, and diets again (SC ↔ HF ↔ SC) and
• the obese kid who eventually turns to physical culture, works out, eats health and loses weight, when he starts college, to then fall back into his old bad habits and starts letting himself go, when he marries and has kids (HF ↔ SC ↔ HF)

I know this is a little far-fetched and as we are going to see later, mice are not exactly the best model to study things like that, but still, the way the weight of the rodents, who had free access to the respective chow they were on during the whole experimental period, developed is quite telling:

Figure 1: Despite intermediate fat loss the increased feed efficiency (=weight gain per kcal) that is especially pronounced in the HF phases of the weight cycling groups quashed the previous weight loss. If age effects had not become a problem this effect would have been more obvious in a 4th cycle.

And the message the data in figure 1 is sending is quite clear: Dieting, as in changing your eating habits only intermediately, is useless, at best! - "at best", because it becomes increasingly difficult to lose and constantly easier to gain weight or, as Barbosa-da-Silva et al. put it:

[...] after three consecutive WC [weight cycles], the reduction of BM is less marked during the SC cycle, as well as the increase of BM is more prominent during HF cycle (Barbosa-da-Silva. 2012).

Now, we probably would not have had to do a 24-week rodent study to know that, right? Right! Notwithstanding, though, the beauty of working with rodents - instead of Biggest Losers, for example - is that they usually don't complain much when you slaughter them, so that the scientist could not only measure the serum leptin (figure 2, left), triglycerides, cholesterol, insulin and glucose levels, but also count the number and measure the size of the adipocytes in their visceral fat pads.

Figure 2: Leptin expression and adipocyte density per area of adipose tissue mass after the 1st, 2nd and 3rd weight gain/loss cycle (data adapted from Barbosa-da-Silva. 2012)

And as you can see in figure 2 (right) the weight cycling induced quite profound effects on the adipose tissue morphology; effects that are similar to what we have seen in previous discussions on the underlying causes of the yoyo effect (see "Nasty Insights into the YoYo-Effect"). You have to keep in mind, though, that you would be comparing apples and oranges if you compare the two weight cycling groups with each other, as one group has always just lost weight, when the other has gained weight so that in one group the adipocytes will  be depleted, when they are filled to the seams in the other one. If there had been a fourth cycle in the course of which the fat cells of the SC ↔ HF group would have been repleted, we may thus safely assume that the absolute size-differences, which reached statistical significance only in the HF ↔ SC group after the third cycle (violette bar in figure 2, right), would have been similar or even more pronounced after 32 weeks and 4 cycles in the then HF dieting SC ↔ HF (note: one of the reasons the researchers did extend the experiment for another 4 weeks was that even now, age-related effects and obesity related morbidities would have reduced the significance of the data).

Adipocyte morphology, leptin expression, fat pad restructuring and body fat that sticks

Apropos significance, you ay remember from the "previously mentioned post" on this issue that one of the currently discussed hypothesis that could  (at least partly) explain why formerly obese people are not just having a really hard time to lose weight, but also, and often even more so, to keep that weight off, relates to what I have previously labeled "relative leptin defiency" (too little leptin production per adipose tissue mass) or, and this would be an alternative hypothesis, "leptin resistance" (more than enough leptin in the blood, but the signal transmission does not work).

The first thing we can say based on the data Barbosa-da-Silva acquired on the absolute fluctuations of leptin in the blood of the rodents (figure 2, left) ist that previously made conclusions about the effects of weight gain, weight loss and energy intake on leptin, like

1. weight loss and fasting are associated with reduced leptin levels, 
2. weight gain is associated with an increase in leptin concentration 
3. chronically increased leptin can lead to leptin resistance
4. meals and according to meal composition or short-term swings in energy balance such as fasting or overfeeding induce swings in systemic leptin levels

appear to be accurate. To check whether there is evidence for my "relative leptin deficiency" hypothesis, especially in weight cycling groups, I ploted the ratio of serum leptin to body fat in figure 3 (left):

Figure 3: Leptin levels in serum per body fat (left), leptin expression in adipose tissue (middle), and sectional area of adipocytes of the different groups (based on Barbosa-da-Silva. 2012)

And what is interesting is that in this calorically non-restricted scenario, the respective "relative leptin deficiency" occurs only in the SC ↔ HF group during the third and last cycle, when their relative leptin levels which should actually be identical to the SC group (we must compare them to the SC group, because the current diet will influence leptin expression as well) are 36% lower than they "should" be. In the same third cycle, the HF ↔ SC group (remember, those are our "formerly obese kids") have 21% more leptin in their blood than they "should" - given their current adipose tissue mass.

Some food for thought - Though not directly related to the topic, there is one thing pertaining to the heavily debated "CLA post" from last week (cf. "CLA Destroys Body Fat"), I want to mention. If we assume that the CLA-induced adipose tissue apoptosis Kim et al. observed in their recent study is as rodent-specific as the natural death and rejuvenation of adipose tissue Cinti et al. observed in the study I cite relating to the limited adipose tissue growth in rodents, this would not just indicate that taking copious amounts of CLA would not help to reverse the damage you may have done during previous "diets", but could also explain why conjugated linoleic acid supplements don't work in humans (or horses; see yesterday's news).

Now this segues directly into the allegedly somewhat counter-intuitive conclusion that anything that soothes the raging inflammation in your fat cells may ameliorate the downstream detrimental effects on glucose and lipid metabolism, but will, on the other hand, help your fat cells to survive or maybe even proliferate in amidst the TNF-alpha induced cytokine storm (Prins. 1997), which would otherwise kill them. Now with the current paradigm of "inflammation = bad" this may sound hilarious. In the the end, it does yet only echo the title of a 1999 paper by Hube and Hauner, "The role of TNF-alpha in human adipose tissue:  Prevention of weight gain at the expense of insulin resistance?" (Hube. 1999) and would provide us with a mechanistic explanation of several otherwise non-explicable phenomena such as the profound fat loss in rodents who lack the master antioxidant glutathion (see "Inflammation Is the True Fat Burner"),,, but as indicated: This is just some food for thought ;-)

In combination with the leptin overshoot (+153%) in the "former football players on their college binge", this data would suggest that we are not dealing with "relative deficiency" and "leptin resistance" but rather with a complex mixture of both, where the latter is probably a result of repeated overshoots like the one we see in the SC ↔ HF group after their first high fat feeding cycle (2nd cycle, 154% elevated leptin levels).

Relative leptin deficiency, systemic resistance and now local differences?

And as if things were nor already complicated enough, there are also potentially important differences between circulating leptin levels and local leptin expression in isolated fat pads figure 3 (middle; compare data to figure 2, left, 3rd cycle). Thus, the drop in leptin levels upon "fasting" in the (SC ↔ HF, 2nd cycle  and HF ↔ SC, 3nd cycle) is systemic, but does not reflect the expression of leptin in the intra-abdominal tissue. This stands in line with my previous dissertation on "relative leptin deficiency" and the differences between...

• intra-abdominal (easy to shed on a diet), and 
• subcutaneous (esp. in the lower body compartment difficult to shed on a diet)

...adipose tissue in "Nasty Insights into the YoYo-Effect" (a similar depot-specificity has been reported for pre-adipocytes, i.e. developing fat cells, as well - intriguingly only in 9 out of human subjects (=81%); cf. Niesler. 1998). Due to the fact that the expansion of adipose tissue in rodents appears to be limited and the cell-turnover high (contrary to humans, where you get the impression that obesity is only limited by death and the cell-turnover - if it exists at all - must be very slow), these effects are probably even more pronounced in humans than in mice. Consequently, it can be expected that the diet / feasting induced upward shifts of the body fat set point are more pronounced and their morphological reversal either more time-consuming (probably true for the visceral body fat) than in rodents or simply impossible (could be the case for parts of the subcutaneous body fat) in human beings.

Image 1 : Lose 20lbs now, gain 25 back and have 5 stick with every diet! We still don't understand exactly why, but by now it should be clear, diets like the "Kendra diet" are rather part of the problem than viable solutions

Implications: Despite the fact that we still don't really understand what's happening, when we are trying to shed the body fat we have acquired in times of gluttony, the few novel insights we have gained from the study at hand should make it even more obvious that "classic" dieting does not hold the answer to the obesity problem. Neither on an individual, nor on a societal level. Instead of "eat less, exercise more", the main message should read: "Don't ever think of dieting, again! Revamp your life, your activity profile and the way you eat and wait for things to fall in place." After all, the "formerly obese kids" in the HF ↔ SC group were not too bad off, when they had returned to a (for rodents!) healthy diet in the 2nd cycle. We may even speculate that the difference the rodents in the control group (SC) would not have been significant anymore, if the scientists had kept the HF ↔ SC rodents on standard chow for another 8 weeks.

The same group is however living (now dead ;-) proof that the notion that you could diet today, look better tomorrow and then return to what has gotten you into misery before is not just illusive, but outright life-threatening. Since caloric restrictions, which are still at the heart of 99% of the mainstream diets, will probably magnify the amplitude (i.e. the up and down) of the yoyo effect and its negative metabolic consequences, it appears reasonable to assume that the yoyo-dieter will eventually be worse off than the "happy fatso" who has been eating whatever he wanted for all his life and dropped dead morbidly obese with a heart attack at 45. After all, it seems likely that he (or she!) will not even live to the 45th year before he falls victim to the very same fate and that after not despite, but rather because of all the temporary austerities... now, this may be like choosing between pest and cholera, and the third option, i.e. following the path of physical culture would alway be my first choice, but honestly, if I had to choose, I'd rather be the fatso who enjoyed his 45 years of pizza, pasta and chocolate pie than the frustrated yoyo dieter.

References

• Barbosa-da-Silva S, Fraulob-Aquino JC, Lopes JR, Mandarim-de-Lacerda CA, Aguila MB. Weight Cycling Enhances Adipose Tissue Inflammatory Responses in Male Mice. PLoS ONE 2012; 7(7): e39837.
• Cinti S, Mitchell G, Barbatelli G, Murano I, Ceresi E. Adipocyte death defines macrophage localization and function in adipose tissue of obese mice and humans. J Lipid Res 2005; 46: 2347–2355.
• Hube F, Hauner H. The role of TNF-alpha in human adipose tissue: prevention of weight gain at the expense of insulin resistance? Horm Metab Res. 1999 Dec;31(12):626-31.
• Kim JH, Kim J, Park Y. trans-10,cis-12 Conjugated Linoleic Acid Enhances Endurance Capacity by Increasing Fatty Acid Oxidation and Reducing Glycogen Utilization in Mice. Lipids. 2012 Jul 11.
• Niesler CU, Siddle K, Prins JB. Human preadipocytes display a depot-specific susceptibility to apoptosis. Diabetes. 1998 Aug;47(8):1365-8.  
• Prins JB, Niesler CU, Winterford CM, Bright NA, Siddle K, O'Rahilly S, Walker NI, Cameron DP. Tumor necrosis factor-alpha induces apoptosis of human adipose cells. Diabetes. 1997 Dec;46(12):1939-44.
• Zhu. Ncb5or in Fatty Acid Desaturation and Metabolic Diseases. Zhu Diabetes Research Group. University of Kansas School of Health Professionals. < http://www.alliedhealth.kumc.edu/school/research/zhu/more_info.html > retrieved July 22, 2012

Topical Fat Loss: Capsaicin Cream Blunts Weight Gain in Rodent Model and Increases Leptin, Adiponectin, Lipolysis and Fatty Acid Oxidation in Visceral Fat Depots

Image 1: If you infused your ice-water with an extract of those, that could supercharge your "cold thermogensis" (see "Ephedra vs. Cold Thermogensis" ;-)

Those last 1-2lbs of stubborn fat have been and still are the focal point of countless of discussions among trainees, trainers and  magazines even average Joes and Janes who would not even remotely consider to go to the gym to get rid of those love handles - interestingly, all these groups are similarly susceptible to one message: "Revolutionary breakthrough in topical fat loss: "Whatever-Our-Marketing-Department-Came-Up-With-Burn will obliterate the stubborn body fat that's still covering your abs, obliges, butt, and whatever else you hate about yourself in record time!" Sounds and, as the countless disappointed testimonies on the Internet confirm, is usually too good to be true.

How many scoville (SHU) does it take to burn 1lbs of body fat?

A soon to be published study by researchers from the University of Ulsan in Korea does however show that many of the companies which advertise with the afore "cited" slogans could in fact be on the right track - at least with respect to one of the key ingredients many of those topical fat-burners contain: Capsaicin, a major pungent molecule that is found in hot chilies and other peppers and has already been shown to exert direct effects on isolated adipocytes in vitro (Kang. 2007; Hsu. 2007) and anti-obesity activity in animal models (Yoshioka. 1999; Zhang. 2007). Interestingly enough, epidemiological (Wahlqvist. 2001) and controlled human trials (Bloomer. 2010) suggest that these effect do - despite the often-touted differences in the thermogenic capacity of humans and rodents - in fact manifest in all the usual steps of scientific experimentation in the medical field, i.e. the petri dish, the animal model and the controlled, randomized, placebo-blinded human trial.

From the mouth onto the skin

As far as its topical usage is concerned the main focus of scientific research has yet been on the ameliorative effects of capsaicinoids on painful neuropathies and neuralgia (Harding. 2001; Roberts. 2011) and Lee et al. claim that their study is the first one to investigate the effects of in vivo application of 100mg of a 0.075% hydrophillic capsaicin cream applied to the shaved abdominal skin of pre-fattened mice who were pair-fed (=equal caloric intake for rodents in both groups to exclude reduced appetite as a cause for the observed effect) for 7-weeks.

Figure 1: Body composition (left) and adipocyte size (right) after 7-weeks on HFD with our without topical application of 100mg 0.075% capsaicin cream to the abdomen of obese mice (based on Lee. 2012)

As the data in figure 1 clearly shows, the topical application of capsaicin elicited similar beneficial effects on the blood lipids (not shown) as its oral ingestion in a previous HFD rodent trial (Kang. 2010). What is however particularly striking is that it did at the same time totally blunt further increases in body weight and reduced body fat storage in both the mesenteric, as well as the epididymal, visceral fat depots. The latter went hand in hand with profound changes in the adipocyte morphology of both fat depots which shifted from fewer large, to many small adipocytes - a feature which is usually associated with lower adipocyte inflammation and thus reduced risk of cardiovascular disease & co.

Topical application, systemic effects?

Both results, the improved lipid profile, as well as the reduction in visceral (intra- not super-abdominal) obesity appear to suggest that the effects of the capsaicin cream was by no means as localized as the producers of respective "supplements", would have it.

Figure 2: Adiponectin, leptin, TNF-alpha, lipoprotein lipase, UCP-2 and PPAR expression in mesenteric fat pads of the animals at the end of the 7-week study period (based on Lee. 2012)

The localized decreases in TNF-alpha, a central regulator or inflammation and the profound increases in adipokine expression (adiponectin + leptin), lipoprotein lipase, as well as UCP-2 and all three varieties of the peroxisome proliferator receptors (PPARs), Lee et al. observed in the mesenteric fat pads of the animals do yet confound this theory - capsaicin is, at least partially, a topical fat burner in the literal sense.

Caution! Stimulant-laden fire hazard!

Aside from the fact that its certainly non-negligible effects on visceral fat should not be of great interested for any avid trainee who is following a wholesome whole-foods diet, as those last slabs of body fat that are covering your abs belong to your subcutaneous and not visceral fat depots, there are two more things you should be aware of before you (most likely) waste your money on one of those products.

1. The capsaicin itself will make the body part you rub the product on look like a tomato on fire and burn worse than stinging nettle and that usually for hours!
2. The systemic effects of the stimulants most of these products contain can become an issue especially for leaner folks, as the dosages are usually adjusted for customers with a thick "insulation" that has to be penetrated, first. 

If you still feel that you have to give one or another of those preparations a shot, start with a moderate dose first and wait for a couple of hours to see what it does (don't expect it to do anything to your body fat in that time - if your waistline goes down within the first days of application that's simply water loss!).

My personal recommendation would still be to keep away from any of these products. Regardless of your personal tolerance to stimulants or the specific composition of the different formulas that are currently on the market - 99% of the feedback I have heard and read about states that these products are much better money- than fat-burners  ;-)

References:

1. Bloomer RJ, Canale RE, Shastri S, Suvarnapathki S. Effect of oral intake of capsaicinoid beadlets on catecholamine secretion and blood markers of lipolysis in healthy adults: a randomized, placebo controlled, double-blind, cross-over study. Lipids Health Dis. 2010 Jul 15;9:72.
2. Kang JH, Kim CS, Han IS, Kawada T, Yu R Capsaicin, a spicy component of hot peppers, modulates adipokine gene expression and protein release from obese-mouse adipose tissues and isolated adipocytes, and suppresses the inflammatory responses of adipose tissue macrophages.FEBS Lett. 2007;581:4389-96. 
3. Kang JH, Goto T, Han IS, Kawada T, Kim YM, Yu R. Dietary capsaicin reduces obesity-induced insulin resistance and hepatic steatosis in obese mice fed a high-fat diet. Obesity (Silver Spring). 2010 Apr;18(4):780-7.
4. Lee GR, Shin MK, Yoon DJ, Kim AR, Park NW, Yu R, Han IS. Topical application of capsaicin reduces visceral adipose fat by affecting adipokine levels in high-fat diet (HFD)-induced obese mice. Obesity (Silver Spring). 2012 Jun 18. doi: 10.1038/oby.2012.166. [Epub ahead of print]
5. Hsu CL, Yen GC Effects of capsaicin on induction of apoptosis and inhibition of adipogenesis in 3T3-L1 cells.J Agric Food Chem. 2007;55:1730-6. 
6. Wahlqvist ML, Wattanapenpaiboon N Hot foods--unexpected help with energy balance? Lancet. 2001;358:348-9.
7. Yoshioka M, St-Pierre S, Drapeau V, Dionne I, Doucet E, Suzuki M, Tremblay A Effects of red pepper on appetite and energy intake.Br J Nutr. 1999;82:115-23. 
8. Zhang LL, Yan Liu D, Ma LQ, Luo ZD, Cao TB, Zhong J, Yan ZC, Wang LJ, Zhao ZG, Zhu SJ, Schrader M, Thilo F, Zhu ZM, Tepel M Activation of transient receptor potential vanilloid type-1 channel prevents adipogenesis and obesity.Circ Res. 2007;100:1063-70.

30 Min of Exercise Can Avoid Costly & Unhealthy Gestational Diabetes. Carbohydrate Oxydation Determines Appetite After Workouts. Using a Measuring Tape to Judge Visceral Fat Mass. Update: Vitamin D, Age & Obesity.

85 sessions (general fitness class, three times/week, 55-60 min/session from weeks 8-10 to weeks 38-39 of pregnancy are nothing but healthy for mother + child (Barakat. 2013)

Obese mothers with gestational diabetes are more than just a financial burden. That's what the SuppVersity Figures of the Week clearly indicate.

According to a recently published paper from the National University of Ireland Galway woman who develop gestational diabetes during pregnancy (mostly due to pre-existing extra fat-pounds; not BMI), produce 34% higher health-care costs (Gillespie. 2013). Just as the 75% increase in the necessity to have the kids being delivered by cesarean section, this would still be tolerable, though, if their poor offspring did not also have a increased risk of being born with pathological ventricular hypertrophy (Ullmo. 2007) and a 214% higher likelihood of having to be admitted to the neonatal unit, which, in turn, is associated with "increased and/or aberrant adiposity, in addition to postnatal growth retardation" (Gianni. 2012).

Another good reason to (a) get healthy (and contrary to what the soothing news in the mainstream media will tell you this involves having normal body fat levels), before you even think of bringing a baby into this world and (b) not dropping your exercise regimen all-together, when you're pregnant:

 "A supervised program of moderate exercise performed throughout pregnancy is not a risk of preterm delivery for heal thy pregnant women." (Barakat. 2013) 

This, by the way, works not only in type II, but also type I diabetic mothers, whose chance of developing gestational diabetes and/or even more hazardous extreme spikes and troughs in blood glucose can be reduced from 19% to ZERO with only 30 min of light exercise per day (a self-paced walk in the park is enough!) and making the right food choices (Kumareswaran. 2013).

• Related D-News from Japan: Vitamin D deficiency in Japan comes with current smoking, being female, lack of regular walking and low dietary vitamin D intake, study shows (Yoshimura. 2013).
  

  Overall, 81.3% of the subjects in the study from the University of Tokyo were vitamin D insufficient - only 1.2%, though, had a full-blown deficiency, defined as 25OHD levels below 10 ng/ml.
  Being fat is a critical determinant of baseline vitamin D levels and the response to vitamin D supplement in older Irish adults (Forsythe. 2013).

  "In older adults, vitamin D status was inversely associated with BMI (kg/m2), WC (cm), FM (kg and %), FMI (kg/m2) and FM:FFM (%) at baseline (r − 0·33, − 0·36, − 0·33, − 0·30, − 0·33 and − 0·27, respectively, all P values < 0·01). BMI in older adults was also negatively associated with the change in 25(OH)D following supplementation (β − 1·27, CI − 2·37, − 0·16, P = 0·026)."

  What's surprising, though, is the fact that this correlation of which I have previously argued that is is probably based on the pro- and anti-inflammatory effects of obesity and vitamin D and initiated by being fat, not vitamin D deficient, was not present in the younger study participants.
  
  Just as a review I mentioned only a couple of days ago said: There is still much to learn about vitamin D - in that case D2 & D3 - and how their enzymatic hydroxylation influences both our baseline levels as well as their metabolic downstream effects (read more)

• Exercise does not make you hungry, per se, but the more carbs you burn during your workout the hungrier you're gonna be afterwards (Hopkins. 2013) That's the main finding of a recent study from the Leeds Trinity University in the UK.
  
  

  

  There comes a time, when getting fat and sick is no longer only about making the "wrong" food choices or a non-warranted urge to eat. A time, when neither the apple nor granny's pie will satisfy your hunger, and your cells will be starving within a nutritious cocktail of partially oxidized fatty acids and sticky glucose molecules... yet still, or I should say, exactly for that reason simply "cutting calories" won't solve the problem. Learn more about how this state is creeping up on the obesity generation (read more)

  According to the data the researchers gathered in the course of a bout of cycling individually tailored to expend 400 kcal (EX) or a time-matched no exercise control condition in a randomized, counter-balanced order,
  

  "[...] there was a marked individual variability in compensatory EI. The difference in EI between EX and the control condition ranged from -234.3 to 278.5 kcal. Carbohydrate oxidation during exercise was positively associated with postexercise EI, accounting for 37% of the variance in EI (r=0.57; p=0.02)" (Hopkins. 2013)

  That's particularly interesting, because the average total energy intake did not differ significantly between the exercise and the control condition (666.0±203.9 vs 664.6±174.4 kcal, respectively) in the overweight and obese women with a mean BMI of 29.6±4.0 kg/m².
  
  These observations provide further evidence of the detrimental effects of metabolic inflexibility, a classic characteristic of developing or full-blown metabolic syndrome and a state in which your body is heavily (in the worse cases almost exclusively) reliant on glucose as a substrate - a paradox, in view of the fact that thee aberrant insulin resistance of obese individuals has their cells starve in a state of glucose abundance (learn more)

• Toss your scale and use a measuring tape! Nothing predicts metabolic risk and high risk visceral fat as adequately as the circumference of your midsection (Grundy. 2013)
  
  As a SuppVersity reader you should actually have banned your scale into the depth of your "things I will never need again (!)"-cupboard, once you achieved a normal body weight (on a side note: I don't have a functional scale). From the many questions I receive on a daily basis, I do yet know that some of you are either hesitant to do that or fill inclined to get it back out from time to time to ruin their days and results by stepping on the scale at least thrice a week. If that's you, I suggest you take a peak at the results of a recent study from the Clinical Nutrition and Center for Human Nutrition and the Division of Cardiology of the University of Texas Southwestern Medical Center in Dallas.
  
  To find out whether or not a simple measuring tape by the means of which you would assess the circumference of your waist (WC) would be an adequate measure of total abdominal fat (TAF), abdominal subcutaneous fat (ASF) and intraperitoneal fat (IPF) Scott M. Grundy and his colleagues correlated the measuring tape data with results they had obtained from magnetic resonance imaging (MRI) and found an excellent correlation between WC and total abdominal fat (R² = 0.81 − 0.88) "with progressively lower correlations with ASF (0.65–0.82) and IPF (0.29–0.85)" (Grundy. 2013)
  

  

  Figure 1: Median intra-abdominal fat (median in kg), waist circumferences and corresponding intraperitoneal to total abdominal fat rario (IP/ABS x10) for quintile 1-5 of total abdominal fat in men (left) and women (Gruny. 2013)

  As hinted at in the arrow in figure 1 the accuracy of the waist circumference as a means to quantify the body fat levels and metabolic risk does not only depend on gender, but also on ethnicity, with African American men and women having lower median IPF masses than Whites and Hispanics, in general, but high(er) greater amounts of subcutaneous. In view of the fact that unlike IPF, ASF correlated only with HOMA2-IR, whereas elevated IPF values were also reliable predictor of high triglyceride levels, as well - African Americans may be at a slightly, but probably not significantly lower risk of developing heart disease (high triglycerides are a neat predictor here) than Whites and Hispanics of whom the latter tend to carry the most vicious visceral fat per cm on their waists.

Believe it or not, but that's it for today! I know that was fast and therefore I'll provide you with a couple of additional facebook news, you may be interested in.

• 

  The fact that simply dropping the weight and lying around for weeks could lead to fat gains is actually not that surprising right? So what can be done to make constant progress without overtaxing the system? One of the answers certainly is P-E-R-I-O-D-I-Z-A-T-I-O-N and the Step By Step Guide to Your Own Workout Routine is the series, where you can learn about planning your training schedule in the long and short run to maximize your results and accommodate it to your personal goals (read more)

  Is giving up physical culture worse for your health than being a sedentary slob in the first place Rodent study suggests there is propensity for increases in visceral fat gain during 4-week detraining that surpasses in previously trained rats that of the sedentary controlled (read more)
• Fooled again 2.0: By one way or another Subway bamboozles customers to believe their junkfood was less junky than that of the competition. According to a recent Harvard study, adolescents dining at Subway underestimate the caloric value of their nutrient deficient junk food by more than 500kcal! That's... (read more)
• The "starve yourself to live longer"-bubble is bursting! Now scientists realize that even in yeast, what you eat is more important than how much you eat and that the simple addition of a pH buffer can go a long way (read more)
   
• SuppVersity Suggested Read: Prolotheraphy? Can you actually HEAL those chronically painful tendons, ligaments and cartilage without having to resort to a butcher's... ah, I mean a surgeon's knife? My buddy Sean Casey just posted part II of his scientifically grounded answer (read more).

Now that you're through with these as well, all that's left to be said is: "Have a nice weekend, everyone, and don't forget that the SuppVersity is open on Sundays, as well!"

References:

• Barakat R, Pelaez M, Montejo R, Refoyo I, Coteron J. Exercise Throughout Pregnancy Does Not Cause Preterm Delivery. A Randomized, Controlled Trial. J Phys Act Health. 2013 May 10.
• Forsythe LK, Livingstone MB, Barnes MS, Horigan G, McSorley EM, Bonham MP, Magee PJ, Hill TR, Lucey AJ, Cashman KD, Kiely M, Strain JJ, Wallace JM. Effect of adiposity on vitamin D status and the 25-hydroxycholecalciferol response to supplementation in healthy young and older Irish adults. Br J Nutr. 2012 Jan;107(1):126-34. 
• Giannì ML, Roggero P, Piemontese P, Orsi A, Amato O, Taroni F, Liotto N, Morlacchi L, Mosca F. Body composition in newborn infants: 5-year experience in an Italian neonatal intensive care unit. Early Hum Dev. 2012 Mar;88 Suppl 1:S13-7.
• Gillespie P, Cullinan J, O'Neill C, Dunne F; ATLANTIC DIP Collaborators. Modeling the independent effects of gestational diabetes mellitus on maternity care and costs. Diabetes Care. 2013 May;36(5):1111-6. 
• Kumareswaran K, Elleri D, Allen JM, Caldwell K, Westgate K, Brage S, Raymond-Barker P, Nodale M, Wilinska ME, Amiel SA, Hovorka R, Murphy HR. Physical Activity Energy Expenditure and Glucose Control in Pregnant Women With Type 1 Diabetes: Is 30 minutes of daily exercise enough? Diabetes Care. 2013 May;36(5):1095-101. 
• Ullmo S, Vial Y, Di Bernardo S, Roth-Kleiner M, Mivelaz Y, Sekarski N, Ruiz J, Meijboom EJ. Pathologic ventricular hypertrophy in the offspring of diabetic mothers: a retrospective study. Eur Heart J. 2007 Jun;28(11):1319-25.
• Yoshimura N, Muraki S, Oka H, Morita M, Yamada H, Tanaka S, Kawaguchi H, Nakamura K, Akune T. Profiles of vitamin D insufficiency and deficiency in Japanese men and women: association with biological, environmental, and nutritional factors and coexisting disorders: the ROAD study. Osteoporos Int. 2013 May 15.

Liposuction Shifts Fat from Subcutaneous to Visceral Fat Depots and Reduces Energy Expenditure by 5%!

Image 1: Without exercise and a healthy diet your fight against body fat is as desperate as Heracles fight against the Hydra without the help of his nephew Iolaus.

After yesterday's blogpost on the Biggest Losers, who - upon closer scrutiny - were not so bad of, as many people in the health and fitness community would have it, we will take a look at a more convenient and (accordingly *sigh*) increasingly popular way to get rid of the nasty lovehandles: Liposuction, or the costly reduction of subcutaneous body fat with a hopefully 100% sterile vacuum cleaner ;-) Aside from the risks that are directly related to the operation, a group of Brazilian researchers right from the mecca of plastic surgery, Sao Paulo, has just published a paper (2 days ago, to be precise) on another, hitherto totally overlooked side effect that arose subsequent to a small-volume tumescent abdominal liposuction (1240.3ml) in the sedentary half of 36 physically inactive (i.e. not engaged in any form of regular physical activity program for at least 6 months), yet non obese women (20 –35yr) who participated in the study (Benatti. 2012)

Remove it here, regrow it there. Body fat resembles the Hydra from Greek mythology

In order to control the outcome of the operation itself and its long(er) term consequences in the presence or absence of a physical exercise program that was conducted for four months starting 2 months after the OP (this yields a total duration of 6 months for the whole study), the Fabiana Benatti and her colleagues assessed the total body fat and fat-free mass of the participants via hydrostatic weighing and used computer tomographs to determine the size of the individual fat depots.

Figure 1: Changes in body composition relative to baseline (data calculated based on Benatti. 2012)

As you can see in figure 1 the comparatively reasonable exercise program the subjects in the training group (TR) performed three times per week during the last four months of the follow-up period and which consisted of a...

• 5-min warm-up followed by 
• strength exercises: 8 exercises for the major muscle groups, 3 sets of 12 reps, and
• aerobic exercise on the treadmill: 30-40min at 75% of the VO2max

led to further reductions in subcutaneous fat mass. From a non-aesthetical perspective, it is yet more important that the three weekly exercise sessions prevented the vicious repartitioning effect from the subcutaneous to the visceral body stores, the cosmetic surgery had on the adipose tissue of the the women in the sedentary group (NT) in the course of the 4 months after their surgery.

Could it be that taking the easier way out is always a bad idea?

Image 2: Does look nasty, is not without risk and not effective in the long run - liposuction.

These results are interesting, because they do confirm the long-touted notion that plastic surgery would be pretty useless, if it is not combined with an adequate exercise and nutrition program. Moreover, the novel finding that the compensatory effects, i.e. the regrowth of body fat, does not take place in the subcutaneous fat depots, but in the vicinity of the organs, i.e. in the dreaded visceral adipose tissue stores, sheds an even more unfavorable light on a convenient, yet expensive, ineffective and - as this study shows - profoundly unhealthy attempt to "looking good naked".

The further reduction in subcutaneous fat and the absence of this highly unfavorable "repartitioning effect", on the other hand, speak to the effectiveness of a combined strength and endurance training program for female and, as we know from countless of other studies, also male weight loss - and that in the absence overtly restrictive eating.

Clear results with surprising effects on CVD risk and  energy expenditure

Still, there are a few downsides and shortcomings to this study that should not be overlooked. Firstly, the scientists did not evaluate the body fat distribution in the upper body, specifically the breasts. Whether there may have been a repartitioning effect from the abdominal to the upper body (e.g. breast, back and arms) subcutaneous fat depots, thusly remains to be elucidated. Moreover the increase in total LDL count, the scientists observed in the non-training group was not accompanied by increases in ApoB levels, which are considered as a relatively reliable marker for the number of the allegedly artery-clogging small LDL particles. Whether the women in the study are thusly actually facing an increased risk for cardiovascular disease or simply carry ~10% more visceral body fat around is about as questionable as the underlying cause of the reduction in energy expenditure that went hand in hand with the loss of ~1kg of subcutaneous body fat in the absence of a reduced caloric intake.

Figure 2: Significant (non-training, p = 0.01) and non-significant (training, p = 0.82) changes in doubly labeled water measured energy expenditure 6 months after liposuction (data adapted from Benatti. 2012)

In the end, the data in figure  2 relates directly to what we have seen in yesterday's analysis of the metabolic effects of a -60% reduction in body fat (cf. "Metabolic Consequences of Extreme Weight Loss"). If we assume that the 7-day food diaries provide an accurate estimate of the energy intake (if anything those logs usually underestimate / the participants underreport energy intake) and rely on the exactness of the relatively reliable doubly labeled water method you already know from yesterday's Biggest Loser study, the ~100kcal reduction in energy expenditure in the study at hand cannot be induced by restrictive eating (and in the non-training group obviously not by excessive exercise ;-), so that the Brazilian scientists conclude that...

our data suggest that the fat loss per se plays a role in decreased energy expenditure because no changes in food intake, lean mass, or leptin levels were observed.

And call for "[a]dditional studies" to "comprehensively explore the underlying mechanisms of the liposuction-induced decrease in energy expenditure". In view of the fact that these results could be of fundamental importance not only for the lazy plastic surgery patient, but also for the hard-training physical culturist who strives to push his / her body fat levels lower and lower, you can be certain that the SuppVersity is the place, where you are going to read about the results of future investigations into the underlying mechanisms first!