1) Prolonged bleeding times:

This has been less established, but there is some data indicating that high intakes of EPA and DHA have the capacity to extend bleeding times. This story came to the surface after excessively long bleeding times and increased incidence of hemorrhagic stroke were observed in Greenland Eskimos (2-3). Their omega-3 intake reached levels of 13.7 g/3000 kcal/day (4). High doses of EPA+DHA may decrease platelet aggregation and therefore may influence bleeding time. However, a review that examined the link between bleeding after cardiovascular procedures and fish oil intakes, found no significant risk of bleeding (5). Nevertheless, in some individuals combined intakes exceeding 3g of DHA+EPA a day, may result in excessive bleeding (6).

2) Suppressed immune response

A suppressed immune response may be helpful for people suffering from an autoimmune –or inflammatory disease. However, this does not apply to healthy elderly people. In a study from Thies and colleagues, healthy elderly subjects were submitted to a 12-week trial in which they daily received capsules filled with 4g placebo oil (an 80:20 mix of palm and sunflower seed oils) or blends of placebo oil and 2g ALA, 770 mg GLA, 680 mg AA, 720 mg DHA, or 1 g EPA + DHA (720 mg EPA + 280 mg DHA). Total fat intake from the capsules was 4 g/d. Only the addition of 280 mg of DHA to 720 mg of EPA reduced natural killer cell activity with 48% (7). This significant reduction in NK cell activity was fully reversed 4 weeks after finishing supplementation. In another study conducted by Rees et al, healthy young and older men received 9 placebo capsules (corn oil) or 9 capsules containing oil that provided 1.35, 2.7, or 4.05 g EPA/d for 12 weeks (8). Only in the older men, EPA supplementation caused a dose-dependent decrease in neutrophil respiratory burst. From these 2 studies, we can conclude that for healthy elderly people or people with an already weakened immune system, taking high dosages of fish oil may not be such a good idea. Natural killer cells and neutrophils both belong to the innate immune system and form our first line defense against pathogens. Thus, taking high intakes of EPA+DHA may hamper your immune response.

Conclusion:

There is some data available showing that reasonable intakes of fish oil (1-3g of EPA+DHA/day) is beneficial for our health, but don’t overdo it. For healthy people it is just not necessary to take more than 3g of EPA+DHA per day. According to the FDA, intakes up to 3g of combined EPA+DHA can be considered to be safe, so why would you take more and risk side effects ?

Excerpt image by Jonas N

Bibliography:

1. Kris-Etherton, P.M., W.S. Harris, and L.J. Appel, Fish consumption, fish oil, omega-3 fatty acids, and cardiovascular disease. Circulation, 2002. 106(21): p. 2747-57.
2. Ostergaard Kristensen, M., Increased incidence of bleeding intracranial aneurysms in Greenlandic Eskimos. Acta neurochirurgica, 1983. 67(1-2): p. 37-43.
3. Dyerberg, J. and H.O. Bang, Haemostatic function and platelet polyunsaturated fatty acids in Eskimos. Lancet, 1979. 2(8140): p. 433-5.
4. Bang, H.O., J. Dyerberg, and H.M. Sinclair, The composition of the Eskimo food in north western Greenland. The American journal of clinical nutrition, 1980. 33(12): p. 2657-61.
5. Office of Nutritional Products, Labeling, and Dietary Supplements, Center for Food Safety and Applied Nutrition, US Food and Drug Administration. Letter responding to a request to reconsider the qualified claim for a dietary supplement health claim for omega-3 fatty acids and coronary heart disease. Docket No. 91N-0103. February 8, 2002.
6. Harris, W.S., Expert opinion: omega-3 fatty acids and bleeding-cause for concern? The American journal of cardiology, 2007. 99(6A): p. 44C-46C.
7. Thies, F., et al., Dietary supplementation with eicosapentaenoic acid, but not with other long-chain n-3 or n-6 polyunsaturated fatty acids, decreases natural killer cell activity in healthy subjects aged >55 y. The American journal of clinical nutrition, 2001. 73(3): p. 539-48.
8. Rees, D., et al., Dose-related effects of eicosapentaenoic acid on innate immune function in healthy humans: a comparison of young and older men. The American journal of clinical nutrition, 2006. 83(2): p. 331-42.

Our appetite is regulated by a part of the brain, called the hypothalamus. This organ senses changes in appetite regulatory hormones such as leptin, cholecystokinin (CCK), peptide YY (PYY) and ghrelin. When leptin is secreted by fat tissue, hunger is suppressed. Besides fat tissue, also the gastrointestinal tract is capable of secreting hunger suppressors (e.g. CCK, PYY) and hunger promoters (ghrelin). It is already known that drastic reductions in energy intake result in direct compensatory alterations, such as reductions in energy expenditure, leptin and CCK, and increases in ghrelin and appetite. These changes promote weight regain, and the researchers of this study wanted to examine whether these acute disruptions in appetite regulating hormones also persists over a longer time period.

Fifty overweight or obese adults (BMI: 27-40 kg/m², average weight: 95kg) participated in a radical 8-week during weight loss program (500-550 kcal/day, Optifast). Body composition measurements and appetite regulatory hormones were measured at the start of the trial, after 10 weeks and after 62 weeks (one year after initial weight loss).

Only 34 participants were able to finish the 62-week trial. After 10 weeks, the dieters achieved a mean weight loss of 13.5 kg (14% of initial weight). As expected, this reduction in bodyweight led to significant reductions in leptin, peptide YY, cholecystokinin, and to increases in ghrelin. Consequently, an increase in subjective appetite occurred. One year after this initial weight loss, the participants regained 5.5 kg of weight, and the levels of most appetite-regulating hormones were still significantly worse compared to their values before the start of the diet.

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The authors conclude that “Long-term strategies to counteract this change may be needed to prevent obesity relapse.” I am of the opinion that most people participating in a weight loss program, need to diet sensible. They should therefore stay away from crash diets of 500-550kcal per day. It is logical that at such low daily energy intakes, the body’s hunger regulatory hormones become severely disrupted and the price will be paid eventually.

Excerpt image by Viveraehealth1

Source:

Sumithran, P., Prendergast, L. A., Delbridge, E., Purcell, K., Shulkes, A., Kriketos, A., et al. (2011). Long-term persistence of hormonal adaptations to weight loss. New England Journal of Medicine, 365(17), 1597-1604.

Angiotensin I-converting enzyme (ACE) catalyzes the conversion of the inactive angiotensin I in the blood to the active angiotensin II. The active form makes the blood vessels contract, which builds up the pressure in the arteries causing high blood pressure (hypertension). Dark chocolate is rich in flavanols (e.g. catechin, epicatechin) and procyanidins, and it is suggested that these compounds have beneficial effects on cardiovascular disease. High blood pressure is one of the risk factors for cardiovascular disease, so one of the aims of the study was to investigate the effect of dark chocolate on ACE activity.

Sixteen healthy subjects, both male and female, were recruited for this study. They were not allowed to use nicotine containing products and medical and/or herbal drugs in the 2 weeks leading up to trial. In the last 2 days before the start of the study, they had to stay away from chocolate and other products containing similar compounds such as many types of berries, coffee, wine, tea and some types of fruit and vegetables. All participants consumed 75 grams of dark chocolate with a minimal cacao content of 72%, within approximately 5 minutes. To measure the effect of chocolate consumption on ACE activity, blood samples were taken before ingestion and after 30 minutes, 60 minutes and 3 hours. Blood pressure was also assessed at the same time intervals.

An 18% inhibition of ACE activity was observed three hours after dark chocolate ingestion, which is comparable with the effect seen in prescription ACE inhibitors. This effect might be due to the catechins in the chocolate, since their plasma values peak 2-3 hours after ingestion. No effect on blood pressure was observed, since blood pressure regulation is a long-term process and also because the healthy subjects had normal blood pressure values to start with.

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However, this study clearly demonstrates that dark chocolate consumption is capable of reducing ACE activity, in a magnitude similar to prescription ACE inhibitors. An optimal dose hasn’t been determined yet and chocolate isn’t exactly low in calories and fat either. Nevertheless, chocolate can be part of a healthy diet as long as the cocoa content is at least 70% and it is consumed in moderation. You can also use raw cocoa powder, which is lower in calories.

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Source:

Persson, I. A. -., Persson, K., Hägg, S., & Andersson, R. G. G. (2011). Effects of cocoa extract and dark chocolate on angiotensin-converting enzyme and nitric oxide in human endothelial cells and healthy volunteers-A nutrigenomics perspective. Journal of Cardiovascular Pharmacology, 57(1), 44-50

Resveratrol is a compound that is naturally found in the skin of red grapes, peanuts, dark chocolate and red wine. It is produced when their plants are being attacked by pathogens. Resveratrol can also be produced chemically. In animals it has been demonstrated that resveratrol, similar to calorie restriction, directly or indirectly activates a protein called SIRT1, which promotes metabolic function and healthy aging. So, the researchers of this study wanted to investigate the metabolic effects of resveratrol supplementation in human subjects.

Eleven healthy, obese men were randomly divided into two groups. One group received 150 mg of trans-resveratrol daily, the other group ingested a placebo for 30 days. After a 4 week wash-out period the groups and treatments were swapped for an additional 30 days. Just as a reference: 150 mg of resveratrol equals to 150 glasses of red wine, so the dose used in this study can’t be obtained from the diet and requires supplementation. Obese subjects were chosen because of their higher risk of developing type 2 diabetes. Body weight, energy expenditure, fat storage, blood pressure, mitochondrial function and plasma markers among other measures were measured before and after each treatment.

Resveratrol significantly reduced blood glucose levels, improved insulin sensitivity (HOMA index) and lowered plasma triglyceride levels.  Resveratrol supplementation also reduced several markers of inflammation, blood pressure, sleeping and resting metabolic rate. There was also a shift in fat storage from liver to skeletal muscle along with an increase in mitochondrial function and SIRT1 production in the muscle, however no change in body weight was observed. Most of these metabolic changes are also seen during calorie restriction and/or endurance exercise. They also checked for side effects, but no adverse effects of supplementation were found.

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It seems that 30 days of resveratrol supplementation mimics the metabolic effects observed during calorie restriction, at least in healthy, obese men. It should be noted that these effects were modest compared to the effects of diet and exercise. Furthermore, it appears that resveratrol should not be used as a weight loss supplement, since it wasn’t able to increase 24-hour metabolic rate. Weight loss requires an increase in calories burned, therefore metabolic rate needs to go up. Moreover, they conclude that: “future studies should investigate the long-term and dose-dependent metabolic effects of resveratrol supplementation in order to further establish whether resveratrol supplementation has the potential to overcome the metabolic aberrations that are associated with obesity in humans”.

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Source:

Timmers, S., Konings, E., Bilet, L., Houtkooper, R. H., Van De Weijer, T., Goossens, G. H., et al. (2011). Calorie restriction-like effects of 30 days of resveratrol supplementation on energy metabolism and metabolic profile in obese humans. Cell Metabolism, 14(5), 612-622.

Creatine is naturally produced in the liver and kidneys from the amino acids L-arginine, glycine, and L-methionine. Besides the fact that creatine can be produced in our body, most if it is ingested from animal products (e.g. meat and fish). Creatine is then stored as creatine phosphate and 95% is located in skeletal muscle pools, hence the use as a sports supplement. Creatine phosphate is also present in high amounts in other tissues such as the brain, heart and testes. The sports performance enhancing effects of creatine supplementation are well known, less is known about the role of creatine on cognition and brain function.

It is known that when brain activation goes up, fuel supply (ATP) may become limited. Creatine phosphate is able to supply a phosphate group to ADP to reform ATP in a very fast way, so more ATP is readily available in the mitochondria and cytosol of the brain. Therefore, the researchers wanted to know if mental performance could be improved if the creatine stores in the brain were increased by oral supplementation.

In the study from Rae et al., 45 subjects were recruited from both vegetarian students (27) and vegan students (18), because their creatine stores tend to be lower and less variable. Subjects received 5g creatine monohydrate daily, the placebo treatment existed out of 5g maltodextin administration per day, both for 6 weeks. Participants were randomly assigned to both treatments in a cross-over design with a 6 week washout period in between both treatments. Subjects completed two cognitive tests before and after each treatment. The results demonstrated that creatine supplementation significantly improved both working memory (backward digit span: 8.5 digits vs. 7 compared with placebo) and intelligence (Ravens’s Advanced Progressive Matrices), which both require speed of processing.

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It appears that that creatine monohydrate is capable of improving mental performance in vegetarians and vegans. The dose they used (5g/day = 2kg of meat/day) can’t be achieved by eating animal products, so it could be that even omnivores might benefit from creatine supplementation.

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Source:

Rae, C., Digney, A. L., McEwan, S. R., & Bates, T. C. (2003). Oral creatine monohydrate supplementation improves brain performance: A double-blind, placebo-controlled, cross-over trial. Proceedings of the Royal Society B: Biological Sciences, 270(1529), 2147-2150

Circulating glucose is the primary fuel source for the brain. It is known that a mild decrease in circulating glucose causes hunger. This study also looked into the effect of normal circulating glucose on certain brain regions and its subsequent influence on high-calorie food intake. The use of brain imaging (fMRI) allowed them to investigate the brain of 14 healthy (5 obese and 9 non-obese) participants. Seven individuals were used as a control. Brain imaging was combined with a stepped hyperinsulinemic euglycemic-hypoglycemic clamp (a technique to control blood glucose levels) after a standardized meal, consumed 2 hours in advance. The desire for high-calorie foods after changes in circulating glucose was measured by the use of different food and non-food images.

They found that a slight reduction in blood glucose levels to 67 ± 1 mg/dl, activates limbic-striatal brain regions (image = blue parts) and this increases the desire for high-calorie foods. However, normal circulating glucose levels (88 ± 2 mg/dl) trigger the medial prefrontal cortex (image = red and yellow parts), an area of the brain known to regulate emotions and impulses, causing a reduced interest in food. Interestingly, this later effect was lacking in obese individuals (see image).

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This study has shown that blood glucose levels are able to reduce or increase our desire for high-calorie foods by affecting different regions in the brain. Foods packed with sugar and other high glycemic carbohydrates spike the secretion of insulin, which is followed by drops in circulating glucose stimulating the desire for high-calorie foods. Sadly enough these foods are omnipresent in our fast food society. Keeping circulating glucose constant appears to be a good strategy to reduce high-calorie food intake, at least in lean individuals. This can be achieved by the use of regular and smaller meals. Another option is the use of complex carbohydrates over their refined counterparts. This study also indicates that there might be a biological difference in appetite suppression between lean and obese individuals, causing more difficulties for obese people to control their desire for high-calorie foods.

Excerpt image by celebrity-diets.org

Source:

Page, K. A., Seo, D., Belfort-DeAguiar, R., Lacadie, C., Dzuira, J., Naik, S., et al. (2011). Circulating glucose levels modulate neural control of desire for high-calorie foods in humans. Journal of Clinical Investigation, 121(10), 4161-4169.

What do we need?

• 3 oz. (85 g) of water-canned tuna, drained and flaked
• 1 omega-3 egg, hard cooked and chopped
• Half a bag (100 g) salad/vegetable mix
• 1 table spoon (15 g) of mayonnaise made from olive oil
• Half a can (105 g) of yellow unsweetened corn
• A pinch of salt and pepper

Instructions:

Combine all of the ingredients in a bowl and mix well. Season it up with a pinch of salt and pepper.

Enjoy!

Nutrition facts per serving:

• Calories: 370 kcal
• Protein: 33 g
• Carbohydrates: 13 g
• Fat: 20 g
• Fiber: 6 g
• Sodium: 700 mg

So, I realized that MRP bars could make my life a lot easier and I went online to look for one rich in quality ingredients. After a while searching, I found out that most of the MRP bars contain inferior protein sources (e.g. gelatin),are loaded with sugar, high-fructose corn syrup and saturated fats. Most of the time they are also low in fiber and filled with compounds you can’t pronounce the names of. Consequently, they pack the bars with vitamins and minerals to make them look good and to make up for the inferior ingredients used. The low-grade ingredient of most MRP bars has put me of from buying them for years. Since MRP bars need to be able to replace a meal, it is important that the ingredients that are used are of great quality.

The requirements for a complete meal replacement bar, besides a great taste:

A decent amount of high quality protein:

In my opinion, every meal should contain a decent amount of high quality protein. A good MRP bar should contain at least  15-20g of protein, preferably from whey, casein, milk or soy protein. Avoid the ones that contain gelatin and other inferior protein sources.

Sufficient amount of fiber:

Fiber supports the intestinal system and it helps you feeling full. If a bar replaces a meal, fiber has to be present. Around 5-10 grams of fiber per bar should be sufficient.

Quality carbohydrates and fats to fill up the desired amount of calories:

Try to look for bars that are low in sugar and high-fructose corn syrup. The carbohydrates should come from sources such as (dried) fruits, honey, oats, wheat or rice. Choose these ingredients over sugar alcohols, since they tend to induce some gastrointestinal side effects in some people. In regard to fats, it is important that the bar is free from trans fats, low in saturated fats and rich in healthy fats. The fats in a MRP bar should mainly come from nuts and seeds. The amount of calories a bar should contain depends on the person’s weight, age, height and lifestyle and is therefore very individual.

Vitamins and minerals:

Most MRP bars are loaded which huge amounts of vitamins and minerals. They should not be dosed too high; around 25% of the RDA is more than enough. If the producer of the bar uses quality ingredients, no additional vitamins and minerals should be added.

There are only a few MRP bars that can replace a meal. Most of them are the low-carb protein bars. When protein bars are rich in carbohydrates, they tend to become energy bars and are loaded with fast digesting carbohydrates. In addition to the home-made bars, I only found 2 commercially available bars that can be used as a good meal replacement.

Quest protein bars:

• 20g of high-quality proteins (whey protein isolate, milk protein isolate)
• Minimal amount of ingredients
• High quality ingredients
• Gluten Free
• BUT: Very high amount of fiber per bar (so don’t use more than 2 bars per day!)

George Spellwin’s Raw Protein Bars:

• 26 grams of high quality whey protein
• Minimal amount of ingredients
• High quality ingredients
• No conservatives
• BUT: It’s a mix of dry ingredients, so you need to add the peanut butter, honey or sugar-free syrup yourself. Therefore, the shelf life is limited to 30 days in the refrigerator.

So there you have it, protein bars can be used as a meal replacement. But before you buy one, you need to check their list of ingredients. I do want to emphasize that you should prefer a solid meal or shake over a meal replacement bar. Quality MRP bars are not cheap, but they should be solely intended as emergency backups for situations in which you can’t have or bring a meal or shake with you.

Excerpt image by changa_lion

This study was based on the theory that cancer cells rely on glucose more than normal cells. So, they inserted both mouse and human carcinomas in various mice strains. These mice either received a low carbohydrate – high protein diet (16% carbs, 58% protein and 26% fat) or a normal Western diet (55% carbs, 23% protein and 22% fat). They corrected for caloric restriction by designing diets with the same amount of calories. They did this by increasing the protein content rather than fat, because a high fat diet might promote tumor growth, while a high protein diet may support the immune system.

They found that both mouse (figure 1) and human (figure 2) carcinomas grew slower in mice consuming the low carbohydrate – high protein diet, compared to the high carbohydrate – low protein diet (Western diet = 5058). This effect was independent of weight loss, since no weight difference between both groups was observed. Additionally, the low carbohydrate diet led to lower blood glucose, insulin and lactate levels, compared to the high carbohydrate group. Moreover, they found a positive correlation between plasma insulin levels and tumor size, thereby verifying the hypothesis that glucose supply could be associated with tumor growth.

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They also investigated the combinatory action of a low carbohydrate diet and specific drugs (mTOR inhibitor CCI-779 and COX-2 inhibitor, Celebrex). The low carbohydrate diet induced an additive effect, especially in combination with Celebrex, which is a powerful anti-inflammatory drug.

Furthermore, the effect of both diets was also investigated on genetically engineered mice predisposed to breast cancer. Almost 50% of the mice on the high carbohydrate diet developed breast cancer and gained weight within their first year of life, whereas no tumors or weight gain were found in mice on the low carbohydrate diet. Remarkably, only 1 mouse on the Western diet completed a normal life span of roughly 2 years, while more than 50% of the mice on the high protein diet achieved or surpassed their normal life span.

In conclusion, it seems that a simple change in a subject’s diet (reducing carbohydrates and increasing protein) can reduce the development and progression of cancer, with or without drugs, at least in mice. This study illustrates a novel way to treat cancer, but more importantly as stated in the paper:  “further investigation in humans is warranted especially in combination with existing therapies”.

Excerpt image by superbproteindiet.com

Source:

Ho, V. W., Leung, K., Hsu, A., Luk, B., Lai, J., Shen, S. Y., et al. (2011). A low carbohydrate, high protein diet slows tumor growth and prevents cancer initiation. Cancer Research, 71(13), 4484-4493.

The claims made regarding CEE compared to CM are:

Improved stability and a higher creatine uptake in the muscle:

In 2007, researchers from Kingston University compared the stability of CEE with CM. They found that CM was more stable than CEE (1). Adding an ethyl group to creatine reduces its stability in an acid environment and speeds up the unwanted conversion of creatine to creatinine. In addition, Giese and Lecher showed that in mild aqueous conditions, which are common during digestion, CEE is mainly a precursor for creatinine instead of creatine (2). Another study, from Katseres et al., demonstrated that the presence of CEE in the blood is too short to reach the muscle, indicating an impaired stability (3).

A lower stability of CEE is probably an indication for a reduced uptake of creatine in the muscle. Spillane et al., found a significant increase in creatinine levels in the blood from subjects that used CEE compared to those that used CM, both in combination with resistance training. In addition, the CM group had a higher creatine content in the muscle compared to the CEE group (4). So, CM is more effective in increasing muscle creatine stores and less creatine is converted to creatinine.

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More muscle mass, no bloat and an increase in strength and power:

The study of Spillane et al. also showed that CEE supplementation did not led to bigger gains in body mass nor fat-free mass. CEE even caused a trend towards more bloat (greater extracellular water content) compared to CM. In addition, CEE was also less effective in increasing strength and power (4). These findings were demonstrated in a double-blind randomised trial of 7 weeks, in which 30 male resistance trainees ingested either CEE, CM (Creapure) or a placebo. They used a loading phase of five days in which the dose was approximately 20g per day, followed by a daily maintenance dose of 5g for 42 days.

Conclusion: CEE = hype

These studies show that creatine ethyl ester cannot support its claims. It seems that CEE is less ergogenic than creatine monohydrate. It won’t reduce bloating and it won’t improve body composition over CM. In addition, CEE has a higher degradation to creatinine and this may cause some safety concerns. Considering the price of CEE, which is much higher than that of CM, there is not a single reason left to choose CEE over CM.

Excerpt image by supplementnews.org

Bibliography

1. Child, R., Tallon, M.J. (2007). Creatine ethyl ester rapidly degrades to creatinine in stomach acid. Paper presented at the International Society of Sports Nutrition 4th Annual Meeting, Las Vegas, NV, June 12, 2007
2. Giese, M. W., & Lecher, C. S. (2009). Non-enzymatic cyclization of creatine ethyl ester to creatinine. Biochemical and Biophysical Research Communications, 388(2), 252-255.
3. Katseres, N. S., Reading, D. W., Shayya, L., DiCesare, J. C., & Purser, G. H. (2009). Non-enzymatic hydrolysis of creatine ethyl ester. Biochemical and Biophysical Research Communications, 386(2), 363-367.
4. Spillane, M., Schoch, R., Cooke, M., Harvey, T., Greenwood, M., Kreider, R., et al. (2009). The effects of creatine ethyl ester supplementation combined with heavy resistance training on body composition, muscle performance, and serum and muscle creatine levels. Journal of the International Society of Sports Nutrition, 6