Lose 11% Body Fat in 8 Weeks W/Out Dieting Efforts!? The 'Egg-Approach' to Low CHO Dieting Quintuples Fat Loss

There are 1bn ways to prepare your eggs and the Internet is a rich source of recipes.

You will probably remember the SuppVersity news about the pro-anabolic effects of eggs - whole eggs - from the other day. Now, "gainz" are nice, but as a recent study from the University of Alabama at Birmingham indicates (Goss 2017), they are also a highly useful diet food.

In their recent experimental trial, Amy Miskimon Goss and colleagues investigated the effects of whole eggs, being consumed as part of a low carb diet on the diet-induced changes in body composition, body fat distribution and selected health parameters in aging men and women.

Whole eggs are also an excellent source of dietary protein

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For their randomized clinical trial, Goss et al. recruited 26 men and women aged between  60 and 75yrs. All subjects had a baseline BMI within the "obese" category (30–40kg/m²) and were randomly allocated to consume either ...

• an egg-based lower-CHO/high-fat diet (EBD) containing less than <25% of the energy from carbohydrates, more than 50% from fat and 25% of the energy from protein, or
• a standard CHO-based/low-fat diet (STD) with equal amounts of protein (25%), but 55% of the energy from carbohydrates and only 20% from fat

for 8 weeks. Interestingly enough, participants were not asked to restrict total energy intake. What they had to do, though was to eat the eggs or breakfast bars, the subjects in the EBD and STD group were provided with, respectively.

Figure 1: Overview of the macronutrient composition of the diets (Goss 2017).

The subject's body composition was measured by DXA, their resting energy expenditure (REE) by indirect calorimetry, and insulin, glucose, HOMA-IR and lipids by analyzing the blood of the subjects after an overnight fast, at baseline and after the 8-week intervention.

How did they lose weight if they didn't restrict their food intake? That all subjects lost significant amounts of body fat is a logical consequence of being provided with energy-sufficient meal plans thar reflect either a low-carb, high-fat or a high-carb, low-fat macro composition, when the baseline diet is an obesogenic Western Std. Diet with a high fat and high sugar content. In the absence of detailed food-logs to compare the pre-study intake with the food intake in the intervention study, we do yet have to base this assumption on previous evidence.

As you can see in Figure 1 (and probably already expected in view of the 'ad-libitum' approach), the subjects on the egg-based low carb diet lost more body fat (11.0% vs. 2.3% total fat | p<0.01 for the difference between diets).  Healthwise of even greater importance is that the EBD group also experienced ~3-fold greater loss in unhealthy visceral adipose tissue (aka 'organ fat') compared to the STD group (−23.3% vs −7.1%, p<0.01 for the difference between diets).

Figure 2: Relative changes in total and visceral body fat as measured by DXA scans performed before and after an 8-week high-fat, low-carb (blue) vs. low-fat, high-carb (orange) intervention W/ dietary restriction (Goss 2017).

Against that background, it's at best mildly surprising that the egg+low-carb diet also yielded significantly greater decrease in HOMA-IR (p<0.01); and that only the egg+low-carb group recorded significant decreases in triglycerides and increase in HDL. The changes in lean mass and the subjects' resting energy expenditure did not change.

And there's more new egg research... well, sort of "egg"

That adding eggs can do the most if you use them to replace refined starches and added sugar is also supported by another ahead-of-print paper. The 3-week cross-over (2-wk washout) study one comes from the Midwest Biomedical Research/Center for Metabolic and Cardiovascular Health Objective and evaluated the effects of a substituting refined starches and added sugars (16% of the total energy intake per day) with a combination of egg protein (Epro; 8% total energy intake) and unsaturated fatty acids (UFAs; 8% total energy intake) - which is basically a lower SFA version of eggs from free-ranging hens - on insulin sensitivity (primary outcome) and other cardiometabolic health markers in overweight or obese adults with elevated triglyceride (TG) concentrations.

Choline is also essential if you want l-carnitine to actually work | learn why

The choline advantage: One thing that clearly argues in favor of eggs, though, is that they are one of the best dietary sources of choline which is essential for your metabolic and cardiovascular health and a typical deficiency nutrient in "no egg"-diets (learn more). Furthermore, choline has been shown to promote fat loss when consumed in conjunction with caffeine and carnitine (see "Forgotten Dieting Aids") and stand-alone when it's taken during contest prep dieting (see "2g Choline Double Fat Loss").

As you can see in Figure 3, the twenty-five participants' [11 men, 14 women; mean ± SEM: age, 46.3 ± 2.4 y; body mass index (in kg/m²), 31.8 ± 1.0] Matsuda insulin sensitivity index (MISI) increased 18.1% ± 8.7% from baseline during the Epro and UFA condition and decreased 5.7% ± 6.2% from baseline during the carbohydrate condition (P < 0.001). Similarly, the disposition index (tests the function of the pancreas) increased 23.8% ± 20.8% during the Epro and UFA condition compared with a decrease of 16.3% ± 18.8% during carbohydrate (P = 0.042).

Figure 3: Changes in glucose metabolism and blood lipids (as marker of heart health) in recent crossover study of the effects of replacing refined carbohydrates (16% total energy) with egg-wite + PUFA (Maki 2017).

Of greater importance for heart vs. metabolic health was the incrase in LDL peak particle size of 0.12 nm with Epro and UFA that stood in contrast to a further worsening in form of a decrease of 0.15 nm with carbohydrates (P = 0.019). Similarly, TG and VLDL cholesterol concentrations were lowered by 18.5% (−35.7%, −6.9%) and 18.6% (−34.8%, −7.4%), respectively, after the Epro and UFA condition and by 2.5% (−13.4%, 17.0%) and 3.6% (−12.5%, 16.2%), respectively, after the carbohydrate diet condition (P < 0.002).

Three whole eggs also deliver the most effective "dose" of  egg yolk to improve your triglycerides ↓ and LDL ↓ but HDL ↑ | more

Bottom line: The study at hand stands in line with previous "egg studies" (read them), which highlight that eggs are a nutrient-dense, health-promoting superfood and not the bad "cholesterol bombs" as which they are still portrayed by both, the mainstream media, and "nutrition experts" who haven't upgraded their cookie-cutter approach to nutrition since the 1970s.

In spite of the previously mentioned evidence of the health benefits of eggs, I would like to remind you that other low-carb compatible high protein foods could have yielded similar effects.

It's also worth to note that, in line with previous studies, the effects of the egg diet cannot be ascribed to "any particular metabolic advantage [of low carb dieting] for body fat loss" (Hall 2017), but may be attributed to the ability of 'low carbing' to "decrease hunger, reduce appetite and promote satiety" (Hall 2017; Noakes 2017) - nevertheless, we cannot exclude that other foods with a similarly 50%/50% ratio of protein to fat and an "eggscellent" complete EAA profile could have worked just as well... at least until a follow-up study explicitly compares eggs to other low-carb foods show the opposite | Comment on Facebook!

References:

• Goss, Amy Miskimon, et al. "Effects of an Egg-based, Carbohydrate-restricted Diet on Body Composition, Fat Distribution, and Metabolic Health in Older Adults with Obesity: Preliminary results from a randomized controlled trial." The FASEB Journal 31.1 Supplement (2017): lb320-lb320.
• Hall, K. D. "A review of the carbohydrate–insulin model of obesity." European Journal of Clinical Nutrition (2017).
• Maki, Kevin C. et al. "Replacement of Refined Starches and Added Sugars with Egg Protein and Unsaturated Fats Increases Insulin Sensitivity and Lowers Triglycerides in Overweight or Obese Adults with Elevated Triglycerides." The Journal of Nutrition (2017) First published May 17, 2017, doi: 10.3945/ jn.117.248641
• Noakes, Timothy David, and Johann Windt. "Evidence that supports the prescription of low-carbohydrate high-fat diets: a narrative review." British Journal of Sports Medicine 51.2 (2017): 133-139.

High Dose Caffeine Restores Insulin Sensitivity and Limits Total as Well as Visceral Fat Gain Due to High Sugar Diets

Yes, the study at hand is on caffeine, but the results are relevant for coffee, too.

A decade ago, the medical community though coffee would dehydrate you, would make you insulin resistant and would increase your risk of heart disease. Recent studies show that coffee does not negatively affect your hydration status (Killer. 2014), that higher coffee consumption is associated with reduced diabetes risk and increasing your coffee consumption can reduce your risk of T2DM (Akash. 2014) and that a "daily intake of ∼2 to 3 cups of coffee appears to be safe and is associated with neutral to beneficial effects" on coronary heart disease, congestive heart failure, arrhythmias, and stroke (O'Keefe. 2013).

Against that background it may not be as surprising as it would have been 10 years ago that Joana C. Coelho, et al. (2016) found caffeine to be able to restores insulin sensitivity and glucose tolerance in high-sucrose diet rats. And yet, I personally believe that it is still worth pointing out the results of this study as the high sucrose diet the mice were fed is the same "high sugar diet" about which you will read all over the news that it is to blame for the obesity and diabetes epidemic.

You can learn more about coffee and caffeine at the SuppVersity

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Coffee - The Good, Bad & Interesting

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Caffeine's Effect on Testosterone, Estrogen & SHBG

The Coffee³ Ad- vantage: Fat loss, Appetite & Mood

Caffeine Resis- tance - Does It Even Exist?

Against that background, it is particularly interesting to take a closer look at the data from Coelho's study, because it is the first to actually provide a valid explanation for the observed improvements in glucose sensitivity in response to the ingestion of caffeine.

Figure 1: 16-wk food intake, weight gain, fat gain and visceral fat gain according to caffeine intake (Coelho. 2016).

Now, the bad news is that significant effects were only observed for the highest dose of caffeine, ie..e 1g/L drinking water. That appears to be ridiculously high, but is in fact only "very high". If you do take into consideration that a wistar rat consumes only 100 ml/kg body weight per day, that's a dosage equivalent of 100 mg/kg for a rodent and thus ~16 mg/kg for a human being or ~6-7 cups of coffee (over a 24h period).

University of Memphis: Caffeine can help control the increase in blood lipids and oxidation after inhaling (10 minutes) a high calorie + high fat milk shake, controlled trial involving twelve healthy men shows (Crone. 2016).

Yes, the dosage is high, but actually less may have more benefits, and...  the most relevant benefits (reduced fat gain) were seen at a dosage that would be equivalent to only 4-5 cups of coffee, which happens to be roughly what epidemiological studies show to be in the zone of maximal benefits. Don't mistake this as a recommendation to guzzle liters of coffee, though... and that even if another recent study shows that 400mg of caffeine will lower the fatty acid onslaught and oxidation 12 men experience after consuming a large high fat milk-shake (Crone. 2016)... and speaking of coffee: you may also want to make sure to get a dark roast, because the latter has just been found to improve glucose metabolism and redox balance even if it is low in caffeine (Di Girolamo. 2016). 

While I am not sure how healthy the chronic consumption of these amounts of caffeine actually is. I am aware of several people who get their 6-7 cups of regular coffee per day and are in perfect health. With that being said, the latter may be at least partly due to the the highly beneficial effects of caffeine on the expression of glucose transporter 4 (GLUT4) and insulin receptor expression and phosphorylation (not shown in Figure 2) in the visceral fat depots of coffee connaisseurs.

Figure 2: Effects of different doses of caffeine on GLUT4 and insulin receptor expression in rats (Coelho. 2016).

The above elevations were accompanied by profound increases in protein kinase B (Akt) expression and activity, as well - an observation the scientists regard as being evidence of the fact that "[c]hronic caffeine administration improved whole-body glucose homeostasis and insulin signaling pathways in adipose tissue" (Coelho. 2016).

This conclusion cannot be questioned. What can be questioned, though, is the scientists assumption that this would occur only with high doses of caffeine and in response to increases in GLUT4 and insulin receptor expression in the visceral fat. Why's that? Well take a look at the figure in the bottom line: it shows that significant improvements in glycemia were improved at all dosages. The latter wouldn't have been possible if the lower dosages wouldn't have had an effect on glucose uptake, as well. Whether that's an effect in muscle cells (which would be great), needs further investigation. The previously discussed effects of caffeine on muscle glycogen storage (learn more), on the other hand, would suggest just that: an effect on skeletal muscle, and or a reduction in gluconeogenesis which could, among other things, be triggered by coffee's / caffeine's ability to inhibit the reactivation of glucocorticoids by 11β-hydroxysteroid dehydrogenase type 1" (Atanasov. 2006).

As you can see sign. improvements in glycemia occured even with the lowest amount of caffeine in the drinking water. And that in spite of the fact that the GLUT4 and insulin receptor levels in the visceral fat did not increase significantly... well, maybe those in the rodents' muscle did?

Bottom line: I am not suggesting that the rodent study at hand would provide enough evidence to suggest that everyone should drink at least 4 cups of high caffeine coffee per day. What I do suggest, however, is that the study at hand provides more evidence on potential mechanisms that explain why coffee drinkers are plagued less often by metabolic disease.

With that being said, I would like to remind you that the abuse of caffeine to combat a lack of sleep and/or overtraining may make you dig a deep black hole out of which you will be able to crawl only within weeks of abstinence... and I am talking about abstinence from caffeine and exercise, assuming that it was the combination of both that got your into trouble | Comment on Facebook!

References:

• Akash, Muhammad Sajid Hamid, Kanwal Rehman, and Shuqing Chen. "Effects of coffee on type 2 diabetes mellitus." Nutrition 30.7 (2014): 755-763.
• Atanasov, Atanas G., et al. "Coffee inhibits the reactivation of glucocorticoids by 11β-hydroxysteroid dehydrogenase type 1: A glucocorticoid connection in the anti-diabetic action of coffee?." FEBS letters 580.17 (2006): 4081-4085.
• Coelho, Joana C., et al. "Caffeine Restores Insulin Sensitivity and Glucose tolerance in High-sucrose Diet Rats: Effects on Adipose Tissue."
• Crone, et al. "Impact of Meal Ingestion Rate and Caffeine Coingestion on Postprandial Lipemia and Oxidative Stress Following High-Fat Meal Consumption." Journal of Caffeine Research (2016): Ahead of print. DOI: 10.1089/jcr.2016.0004.
• Di Girolamo, Filippo Giorgio, et al. "Roasting intensity of naturally low-caffeine Laurina coffee modulates glucose metabolism and redox balance in humans." Nutrition (2016).
• Killer, Sophie C., Andrew K. Blannin, and Asker E. Jeukendrup. "No evidence of dehydration with moderate daily coffee intake: a counterbalanced cross-over study in a free-living population." PloS one 9.1 (2014): e84154.
• O'Keefe, James H., et al. "Effects of habitual coffee consumption on cardiometabolic disease, cardiovascular health, and all-cause mortality." Journal of the American College of Cardiology 62.12 (2013): 1043-1051.

Interaction of Fat Cell Size, Protein Intake & Co. W/ Fat Gain + Insulin Res. in Overfed Men + Women in Metabolic Ward

That's rather the low protein variety of overfeeding... but wait, was the high protein diet even "high" in protein? Well high enough to affect liver fat, for sure.

You will probably remember José Antonio's high protein overfeeding study series (learn more) from the articles here and on the SuppVersity Facebook page. The results were quite impressive, but the number of controlled covariates were small and the dietary control was limited to food logs.

In a more recent study, George A. Bray and colleagues from the Pennington Biomedical Research Center of the Louisiana State University System, the George Mason University, and the FL Hospital & Sanford-Burnham Prebys Discovery Research Institute (Bray. 2016) determined the effect of overfeeding diets with 5%, 15% or 25% energy from protein on glycemia + body fat distribution in healthy men and women with add. covariates and in a metabolic ward.

Yes, the high protein intake clogged the liver during overfeeding

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In total, 15 men and 5 women were overfed by 40% (extra calories above maintenance) for 56 days with diets containing

• 5% (LP) of the total energy as protein, 
• 15% (NP) of the total energy as protein, or 
• 25% (HP) of the total energy as protein

Insulin sensitivity was measured using a two-step insulin clamp at baseline and at 8 weeks. Body composition and fat distribution were measured by DXA and multi-slice CT scan ... so far not so different, but the subjects were contained in a metabolic ward, cheating on the diet was thus as impossible, as taking supplements or working out like maniacs.

Figure 1: Diagram that illustrates the 8-weekstudy design; N = 10 male, 5 female subjects (Bray. 2016).

In conjunction with the scientists' analysis of the subjects abdominal subcutaneous fat cell size, which was determined on osmium fixed fat cells, these are two strengths of a study, of which it is yet quite obvious that it also had its disadvantages:

• 

  Review the effects of different macronutrients in overfeeding studies | more

  the protein content of the diet is simply hilarious - that's not just because eating 5% protein, only is nothing but idiotic, but also because 25% of protein is far away from what can be considered "high protein" these days;
• the lack of exercise limits the significance of the results - at least for the majority of SuppVersity readers overeating in phases in which you don't exercise is probably nothing they would even remotely consider.

The scientists observations that neither the subjects' insulin sensitivity and free fatty acids during low and high levels of insulin infusion did not differ after 8 weeks of overfeeding.

Figure 2: Effect of 8 weeks of overfeeding on abdominal fat distribution, ectopic lipid; rel. changes (Bray. 2016).

What did differ, however, were the changes in body fat distribution according to DXA and how the latter depended on the protein content on fat cell size before the overfeeding period. More specifically, ...

• the fat free mass (FFM) and intrahepatic lipid increased more on the high protein, whereas 
• % BF and fasting free fatty acids (FFA) increased more on the low protein diet, while

In addition, the scientists observed that a high initial fat cell size predicted increased visceral fat gains and the FFA suppression during the high-dose insulin clamp.

Figure 3: Relation of Baseline Fat Cell Size to Change in Visceral Adipose Tissue Mass with Eight Weeks of
Overfeeding in heathy volunteers (VAT 0.040 +/- 0.70(FCS); P < .0063 | Bray. 2016)

The subjects' insulin levels at baseline, on the other hand, predicted the increase in subcutaneous but not visceral fat accumulation (see Figure 3) - most intriguingly with low fasting insulin
at baseline correlated predicting higher changes in % fat (for insulin the scientists observed a correlation with r = –0.43; P < .034), but not with other variables. It is thus not surprising that the most insulin sensitive subjects also gained the most subcutaneous fat... or, as the scientists put it: "HOMA IR predicted the increase in DSAT (r = 0.50; P <.016), but not other variables" (Bray. 2016).

Those are important insights of which the authors rightly point out that they clearly indicate that "an induction of insulin resistance with overfeeding is related to fat cell size and requires more than an expansion of adipose tissue stores" (Bray. 2016).

A surprising, but not debatable result of the study at hand is that the high protein diet increased liver fat (HUs;  measured with DXA, too).  The low protein diet, on the other hand, helped to decrease the subjects' liver fat significantly - remember: we are talking about a diet with 40% extra energy on top of the regular diet (Bray. 2016).

Bottom line: Yes, you've read all that in individual articles (albeit often about rodent studies) on SuppVersity before: (1) the more protein, the greater the lean mass gains; (2) the less protein, the greater the ratio of fat to lean mass gains; (3) the fuller your fat cells, the more likely you will gain metabolically unhealthy visceral fat; and (4) the more insulin sensitive you still are, the more metabolically healthier subcutaneous fat you will gain.

What is news, or at least has not been observed in Antonio's study in active individuals (also because they didn't look) is the surprisingly ill effect of high amounts of protein on liver fat (see Figure, right): while the low protein diet reduced the subjects' liver fat sign, the high protein diet triggered a small, but undesirable accumulation of liver fat during overfeeding in normal-weight subjects - not good, but not yet critical and hopefully something you'd not see w/ concomitant exercise or smaller calorie excess | Comment!

References:

• Bray, George A., et al. "Effect of three levels of dietary protein on metabolic phenotype of healthy individuals with 8 weeks of overfeeding." The Journal of Clinical Endocrinology & Metabolism (2016): jc-2016.

Fat-Blocker Effect of Tea Catechins Confirmed (?) in Man - Sign. Abdominal Fat Loss (5-8%) in 12 Weeks W/Out Diet

Tea catechins (which can also be found in black and jasmin tea | see Figure 3) can help you keep particularly unhealthy abdominal fat (Després. 2012) at bay.

It is one thing to have in-vitro and rodent data that green tea can inhibit the digestion of dietary fat (reported previously in the SuppVersity Facebook News); it is another thing, however, to have a human study like the one Makoto Kobayashi and colleagues are about to publish in the peer-reviewed scientific journal Food & Function that shows that the "[i]ngestion of a green tea beverage enriched with catechins with a galloyl moiety (THEA-FLAN 90S) during a high-fat meal reduces body fat in moderately obese adults" (Kobayashi. 2015).

Ok, the abdominal fat loss does not, as the previous quote from the conclusion appears to suggest, occur instantly right after you've consumed your first tea w/ a single meal.

You can learn more about green tea at the SuppVersity

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Will Drinking Tea Solve Your Sugar Problem?

Rather than that, 124 subjects (two of the initially 126 subjects 2 dropped out for personal reasons unrelated to the trial), 53 men, 71 women, who consumed similar, albeit non-standardized diets (see Figure 1 | note: physical activity was also identical) and began the study with body fat levels of ca. 31-35% had to consume the previously mentioned tea beverage that contained tea catechins (250 mL with 215.3 mg green tea catechins containing 211.0 mg green tea catechins with a galloyl moiety) twice or three times daily during mealtimes for 12 weeks, before the significant reduction in body fat became visible.

Figure 1: Macronutrient composition (in g an % of energy) of the non-energy reduced diets the subjects consumed; the values in the left pie chart represent a group average of all three intervention groups. Since the data is based on food records with photographs, it is probably more reliable than in your average diet study (Kobayashi. 2015).

Now, in view of the fact that this is not the first study to demonstrate weight loss effects in overweight subjects consuming green tea or, as in most other studies, green tea extracts, the word "during" and thus the fact that the green tea beverage was consumed with at least two of the three meals per day should be highlighted as a specific feature of the study at hand that is highly relevant to its interpretation.

Figure 2: Detailed analysis of the rel. change in fat area in the abdominal depot of the subjects (Kobayashi. 2015)

It is after all the requirement that the green tea beverage had to be consumed with a (preferable high fat) meal that allows the authors to conclude that the significant fat loss Kobayashi et al. measured by the means of computer tomography predominantly in the abdominal area are the result of an inhibition or slowing of the intestinal fat absorption and thus warrant the conclusion that "the ingestion of green tea beverages enriched with CGM together with high-fat meals may be an effective strategy for reducing body fat in moderately obese adults" (Kobayashi. 2015) - an observation of which I would like to add that the underlying mechanism is not 100% certain.

What about weight and, even more importantly, muscle loss? No, losing lean mass was not an issue in, because weight loss (-0.6 and -0.8% in the low and high dose group, respectively | measured by bio-electrical impedance vs. computer tomography as it was the case for the abdominal fat area) was actually not an issue, either. If you want to measure your success on the scale, green tea is thus not going to be the "diet tool of choice" (unless you use it alongside an energy-reduced diet)... however, if you take into account that the placebo group actually did what the average Westerner does, these days, i.e. gain weight and body fat over the 12-week study period, you may argue that you can still see the results on the scale which could finally stand still after years of displaying subtle, but eventually relevant increases in body weight.

The authors base their conclusion that it is "unlikely that absorbed green tea CGM leads to increased energy expenditure, followed by reduced abdominal body fat area" (Kobayashi. 2015) on two reasonable, but experimentally (in this study) not confirmed assumptions which are that little to no catechins actually made it into the bloodstream, because ...

1. the low caffeine content of the beverage limits the bioavailability of EGCG & co (caffeine enhances its bioavailability | Nakagawa. 2009) and
2. the ingestion of the beverage with a meal has been shown to significantly reduce the bioavailability of green tea catechins in comparison to the fasted state (Chow. 2005).

The assumption that its just a blockade of the digestion of fat becomes even more questionable, if you (re-)read my 2014 article on the carb blocking effects of tea... Well, eventually, though, you may argue that it does not matter if the reduction in abdominal fat was due to thermogenic effects, thermogenic and fat-blocking effects or, as the scientists believe, mediated exclusively an "inhibit[ion] or slowing [of the subjects'] intestinal fat absorption" (Kobayashi. 2015). And let's be honest, I guess you're right. What matters is that there were significant reduction ins abdominal fat (visceral, subcutaneous and total abdominal fat area). Reduction of which the data in Figure 2 tells you that ...

1. 

   Table 1: Catechin composition of the test beverages.

   the fat loss in the abdominal area was dose dependent - even if the differences between the low and high dose group did not reach statistical significance (for the exact catechin composition see Table 1 on the right) - and that 
2. roughly 50% of the benefits were lost within only 5 weeks when the subjects stopped consuming the green tea beverage, even though their diet didn't change at all (in fact, they consumed minimally less energy in the withdrawal phase from week 12-17).

Now, (b) is obviously good news for green tea lovers, but bad news for those who cannot imagine consuming green tea containing beverages "for the rest of their lives".

Green tea forever, it is then!? Well, as usual we have to consider what limits the generalizability of the results. Firstly, we are dealing with a group of people who have more than a few pounds of extra-weight on their hips. An abdominal fat loss of 8% in 12 weeks is thus not impossible, but not exactly likely to be seen in someone who starts at a body fat percentage of 15% or less (which is half what the subjects in the study at hand began with).

Figure 3: Catechin content (mg/10ml) of black, green and jasmine tea prepared from commercial tea w/ different infusion times (Bronner. 1998).

The second thing we have to keep in mind is the beverage itself. As you've previously read, it has been enhanced with catechins with a galloyl moiety (CGMs | EGCG, ECG, GCG, CG). Does this mean that you cannot achieve similar results if you simply drink green tea? Luckily, data from Bronner, et al. (1998) suggests otherwise. As you can see in Figure 3, it would take only 100 ml of commercially available freshly brewed (infusion time 3 min) green tea and even less black tea to achieve similar concentrations of EGCG and the other catechins with a galloyl moiety in your tea. Accordingly, the second obstacle to the gene- relizability of the study is actually irrelevant.

Third- and lastly, there's yet still the fast reversal of the effects which suggests that it is necessary to become a habitual tea drinker to see long-term / lasting benefits of green tea (or as the data in Figure 3 suggests even catechin containing tea in general) on your body weight and, more importantly, body fat you're carrying around | Comment on Facebook!

References:

• Bronner, W. E., and G. R. Beecher. "Method for determining the content of catechins in tea infusions by high-performance liquid chromatography." Journal of Chromatography A 805.1 (1998): 137-142.
• Chow, HH Sherry, et al. "Effects of dosing condition on the oral bioavailability of green tea catechins after single-dose administration of Polyphenon E in healthy individuals." Clinical Cancer Research 11.12 (2005): 4627-4633.
• Després, Jean-Pierre. "Body fat distribution and risk of cardiovascular disease an update." Circulation 126.10 (2012): 1301-1313.
• Kobayashi, Makoto, et al. "Green tea beverages enriched with catechins with a galloyl moiety reduce body fat in moderately obese adults: a randomized double-blind placebo-controlled trial." Food & Function (2016).
• Nakagawa, Kiyotaka, et al. "Effects of co-administration of tea epigallocatechin-3-gallate (EGCG) and caffeine on absorption and metabolism of EGCG in humans." Bioscience, biotechnology, and biochemistry 73.9 (2009): 2014-2017.

Weights or Cardio? What's the Best Visceral Fat Burner + How Often, Long and Intense Do You Have to Train

You don't have to be super fat to have sign. amounts of inter-organ fat.

Visceral or organ fat is the nasty stuff that's "proctecting" your organs from harm... well, as long as it the way you live (bad dietary habits + no exercise) don't increase its volume and weight to abnormal levels.

On the outside, people with high amounts of visceral fat can look anything from significantly obese to normal-weight (particularly if they're wearing the right clothes); and yet, normal-weight obese (skinny fat) individuals, as scientists call these people, do still have a similarly increased risk of diabetes, cardiovascular disease and all the other nasty diseases you can develop when your visceral fat floods your body with pro-inflammatory cytokines.

HIIT is an excellent way to shed both subcutaneous and visceral body fat!

Never Train To Burn Calories!

Tabata = 14.2kcal /min ≠ Fat Loss

30s Intervals + 2:1 Work/Rec.

Making HIIT a Hit Part I/II

Making HIIT a Hit Part II/II

HIIT Ain't For Everyone

Against that background, it stands out of question that the questions Xiao and Fu tried to answer in their latest review of the literature is relevant for millions of people - questions like these:

• How does the type of exercise affect its effects on visceral obesity?
• How much training (volume) does it take to shed visceral fat?
• Do you have to train intense or light to maximize visceral fat loss?

Ah, and obviously there's the question I mentioned in the headline, already: Is strength or aerobic training the optimal visceral fat burner? In view of the fact ...

"[...] there are very few researches focused specifically on the effects of resistance training (RT) on visceral fat, and even these studies have reported different results" (Xiao. 2015)

this is not exactly an easy question to answer. A two-year work by Schmitz et al. (2007) actually found an increase in visceral fat by 7% with RT (although this was significantly less than the 21% increase observed in their inactive controls). Davidson et al.  (2009), found no effect of resistance training on visceral fat and so on and so forth...

Figure 1: While Sigal et al. found no effect on total body fat, both the aerobic and resistance training regimen in their study produced measurable reductions in abdominal visceral fat (Sigal. 2015).

There's still no reason to give up on resistance training as a visceral fat eliminator, though, Davidson et al. had their subjects train only 20 minutes of RT, three times a week, which is probably too little to have a significant effect and and Sigal et al. (2007 | see Figure 1) found similar effects of aerobic and resistance training on visceral fat. Similar results as in the Sigal study were observed by Slentz et al., who found both aerobic and resistance training (3 days/wk, 8 exercises, 3 sets/exercise, 8–12) produces similar anti-obesity effects as aerobic training.

If you want to lose sign. amounts of body fats with strength training (only) you must diet! The most obvious reason that resistance training alone won't help (esp. overweight) people lose body fat is the relatively low amount of energy that's expended during the (often short) workouts in the average study. So, either you train at higher volumes and more frequently, or - and that's the superior approach - you use your diet (25-35% deficit; 2g/kg body weight protein) to lose body fat and (high intensity) strength training to conserve muscle mass | learn more

In conjunction, the results of the few available studies do yet still supports the notion that (in a non-calorically restricted scenario) a low training volume as it was used in the Davidson study may not expend enough energy to trigger sign. reductions in (visceral) body fat.

Whether you will or won't lose visceral fat w/ any form of exercise may thus depend on volume and intensity - for both, it appears as if a threshold would exist.

Some research believe that while any form of exercise will have beneficial effects in reducing total body fat, a higher volume of physical activity would result in a higher reduction of VAT (cf. Friedenreich. 2011). Personally, I tend to agree with McTiernan et al. (2007) and Irwin et al. (2003), though. Both say that you have to train five to six times per week for 45 to 60 min each to see sign. results in the absence of significant energy restriction.

Figure 2: While more exercise (higher duration) helps more for total body fat loss (left), only those of the highly active subjects that also had significant improvements in fitness lost more visceral fat (right | Irwin. 2003).

That there is a minimum of exercise required to produce sign. fat loss in the absence of dietary interventions does yet not mean that "more helps more". If we put faith in the self-reported exercise levels of the subjects in the McTiernan et al. and Irwin et al. studies, though, their results indicate that a mere increase in the training volume does not automatically lead to a greater decrease in visceral fat - for total body fat, however, this may be different (see Figure 2 | left).

Don't forget to diet! The leaner you are, the more important your diet will be. Many TV-shows and magazines still try to fool people to believe that you could get a cover-model look with nothing but (albeit) intense exercise. For most people, i.e. everyone who does not watch his diet strictly, anyway, this is unfortunately not the case. So, if you want to lose fat (visceral or not) start correcting your dietary mistakes first and work on your workout routine later.

In their review, Xiao and Fu argue that a similar "threshold" as it was observed by McTiernan et al. and Irwin et al. for the total exercise volume may exist for the exercise intensity, as well - albeit without being able to define a clear "cut off for exercise intensity":

"A substantial evidence also exists to prove that risk for metabolic syndrome is decreased with increase in physical activity. On the contrary, Gutin et al, . (2002) demonstrated the lack of a significant effect of physical training intensity on decrease in total body fat and visceral fat deposition. Very few studies such as that of Irving et al. have shown the impact of exercise intensity on abdominal visceral fat in obese adults wherein the abdominal fat was a primary outcome parameter. To summarize, studies demonstrating the effect of physical training intensity on visceral fat deposition as a primary objective have been lacking" (Xiao. 2015).

Gender-specific differences, as they have been observed by Redman et al. (2007), who found men lose sign. more visceral fat in response to a combination of aerobic exercise and calorie restriction than women, make it even more difficult to compare the results.

30 Min of Exercise Can Avoid Costly & Unhealthy Gestational Diabetes + Using a Measuring Tape to Judge Visceral Fat Mass. Update: Vitamin D, Age & Obesity | more

Eventually, it turns out that it is - as so often - impossible to give a one-size-fits-it-all answer to the question whether resistance or aerobic training is the better visceral fat burner. If there are no diet- and life-style interventions involved, though, it would appear as if aerobic training has the better scientific backing. Whether that's not a mere result of the comparatively higher energy expenditure is yet about as difficult to answer, as the question whether visceral fat loss really requires 4-5x 40-50 minute exercise sessions per week if you train at more than moderate intensities.

All things considered, it may be a good idea to remember the results of the Irwin study which indicates that anything that improves cardiovascular fitness will also trigger significant visceral fat loss (and improvements in lipid and glucose metabolism). In short, training your fitness will take care of your (visceral) fatness | Comment on Facebook!

References:

• Davidson, Lance E., et al. "Effects of exercise modality on insulin resistance and functional limitation in older adults: a randomized controlled trial." Archives of Internal Medicine 169.2 (2009): 122-131.
• Friedenreich, C. M., et al. "Adiposity changes after a 1-year aerobic exercise intervention among postmenopausal women: a randomized controlled trial." International Journal of Obesity 35.3 (2011): 427-435.
• Gutin, Bernard, et al. "Effects of exercise intensity on cardiovascular fitness, total body composition, and visceral adiposity of obese adolescents." The American journal of clinical nutrition 75.5 (2002): 818-826.
• Irwin, Melinda L., et al. "Effect of exercise on total and intra-abdominal body fat in postmenopausal women: a randomized controlled trial." Jama 289.3 (2003): 323-330.
• McTiernan, Anne, et al. "Exercise effect on weight and body fat in men and women." Obesity 15.6 (2007): 1496-1512.
• Redman, Leanne M., et al. "Effect of calorie restriction with or without exercise on body composition and fat distribution." The Journal of Clinical Endocrinology & Metabolism 92.3 (2007): 865-872.
• Schmitz, Kathryn H., et al. "Strength training and adiposity in premenopausal women: strong, healthy, and empowered study." The American journal of clinical nutrition 86.3 (2007): 566-572.
• Sigal, Ronald J., et al. "Effects of aerobic training, resistance training, or both on glycemic control in type 2 diabetes: a randomized trial." Annals of internal medicine 147.6 (2007): 357-369.
• Slentz, Cris A., et al. "Effects of aerobic vs. resistance training on visceral and liver fat stores, liver enzymes, and insulin resistance by HOMA in overweight adults from STRRIDE AT/RT." American Journal of Physiology-Endocrinology and Metabolism 301.5 (2011): E1033-E1039.
• Xiao, T., and YF FU. "Resistance training vs. aerobic training and role of other factors on the exercise effects on visceral fat." Eur Rev Med Pharmacol Sci 19.10 (2015): 1779-1784.