Algae Cake: Delicious & Healthy!? Wait Until You Learn that it is a Waste Product of Biofuel Production

Despite the Fukushima disaster and the possible contamination of seafood and algae from the pacific ocean, seaweed still has a very good reputation among the health & longevity "experts" (especially those who happen to sell respective supplements).

Figure 1: Algae cake (left) and differently processed algae (right);
pictures as they appear on homepage of Dr V Sivasubramanian

And though I do not want to argue that there are lots of studies that indicate beneficial effects of eating whole algae or supplementing with certain constituents, I must say that I was somewhat puzzled, when I read about the "terrific" idea, a group of Indian scientists (Singh. 2011) has recently come up with. They want to use algal cake (basically a waste product of the production of biofuel from algae) as ...

[...] extremely valuable, high protein by-product of our system that will be used for the production of nutritional food additives, vitamin supplements, animal/fish feed and other valuable consumer products.

Somehow that reminds me of the economically clever, yet from a health perspective questionable practice of feeding cows and other cattle with fishmeal, another "by-product"  which has traditionally been produced from the waste products of the fishery industry and has - among other health problems - been implicated as a contributing factor to the rise of BSE infection, everyone seems to have forgotten about, these days... But, hey, these are just my 2 cents. If anyone of you has the chance to taste one of these outstanding "cakes" let me know how it did you ;-)

Calorie Restriction vs. Exercise for Optimal Body Composition? Exercise Preserves Muscle Tissue and Prevents Metabolic Downregulation.

Those of you who listened to my comments on set points and reasonable weight loss on Super Human Radio, will already know that - other than Gary Taubes, for example - I am a huge advocate of exercise, when it comes to weight loss, -maintenance and overall improvements in body composition. Data from a recently published study (Soare. 2011), despite being evaluated from an anti-aging perspective, confirms the adequacy of approaching your body composition goals, by dietary modifications and exercise induced increases in energy expenditure, instead of just "eating less calories".

In their study, Soare et al compared 24 subjects who had been on a calorically restricted diet (CR, 1769±348 kcal/d) for an average of 6 years to 24 age- and sex-matched sedentary individuals (control, WD, 2302±668 kcal/d) and 24 body fat-matched exercise-trained (EX, 2798±760 kcal/d) volunteers, who were eating Western diets.

Figure 1: Total body weight, lean mass & fat mass in sendentary control, calorie restricted (CR) and exercise (EX) group. (Data adapted from Soare. 2011)

Although the researchers found that both, "the CR and EX groups were significantly leaner than the control (WD) group" both the greater amount of lean body mass (cf. figure 1) as well as their finding that...

Mean 24-hour, day-time and night-time core body temperatures were all significantly lower in the CR group than in the WD and EX groups (P≤0.01).

...underline the futility of every effort to achieve improved body composition, i.e, to maximize muscle (lean mass), while shedding as much body fat, as possible via (even moderate) caloric restriction.

Two other things are noteworthy, as well. Firstly, the reduction in body temperature, which is indicative of a downregulation of the metabolic rate, may be favorable for a longer, but that does not equate into more livable life. And secondly, the "Taubes-Hypothesis" that exercise is "useless", because "it makes you hungry" (the subjects in the EX group in fact consumed more calories) and you would compensate by eating more, anyway, would be relevant, only, if in fact "a calorie was a calorie" and "only calories" counted; the superior body composition of the exercise group, on the other hand, speaks for itself and does suggest that even Garry himself may benefit from one or another training session in the gym ;-)

Edit: As I hear in an anonymous comment Taubes is supposed to do resistance training. When he was talking to doctor Oz, he did however propose the hypothesis I refer to above and this really bothered me.

Exhaustive Aerobic Exercise Increases Serum Calcium Levels and Dietary Requirements

You probably have heard of the fundamental importance of calcium as a structural component of bones. Yet, calcium is way more than the building block of our bone structure and the concrete the of the hopefully non-existent plaque in your arteries. It is also one of the major players in muscle contraction. Thus, it is not very surprising that a group of Iranian Scientists (Pourvaghar. 2011) found major effects of pro-longed (15min) high intensity aerobic exercise on serum calcium levels of 12 randomly selected student athletes (22.36y; 75kg @ 1.76m):

[…] the participants' mean of serum calcium concentration in the first stage and before Balke exhausting aerobic exercise was measured 98.38 ng/mic L. In the second stage, i.e. after the exhausting aerobic activity, it increased to 114.96 ng/mic L. Research results indicated that the difference in serum calcium concentration between the first and second stages is significant (P= 0.0001).

With the calcium that is appearing in the blood of the athletes being leeched from bones, organs to fulfill the increased calcium needs of active muscle tissue. Due to calcium “consumption” and urinary losses, the scientists speculate, the overall result to be a negative calcium balance.

Figure 1: Serum Calcium levels of athletes before, immediately after and 24h after exhaustive aerobic exercise. (Pourvaghar. 2011)

In view of the fact that, in the 24h after exercise, there is no sudden falloff (only -9.13%) of blood calcium, I would yet advice against extensive calcium supplementation. Previous works from other researchers have conclusively shown that a nutritionally dense, calorically adequate, diverse, calcium-rich diet satisfies the needs of both, the average gymrat and the hard training endurance athletes.

For athletes on a weight-reduction diet, or active gym-goers who – due to whatever other reasons – consume a diet that is low (<1.000mg/d) in calcium supplementing with a bio-available form of calcium, like calcium citrate, could yet be a viable strategy to prevent bone loss and sustain exercise performance.

Fat or Fire, What Comes First? Scientists Answer: Obesity Alone Triggers Inflammatory Signaling in Mice

The metabolic syndrome, i.e. the combination of obesity, inflammation and insulin resistance, is at the center of contemporary medical research. In my appearance on Carl Lenore's Super Human Radio, I already mentioned that from a logical perspective the mainstream belief, inflammation was the root of all evil, must be flawed. How should the reaction to a problem be the cause of the very problem itself? A recent study coming from a group of Korean scientists strengthens my conviction that out of the triad that not inflammation, but rather obesity or - one step further up in the genesis of the pathology - the combination of an unhealthy diet and a sedentary lifestyle is at the heart of the triad we now call the "metabolic syndrome".

Kim et al. investigated the pro-inflammatory signaling cascade in either diet-induced (DIO) or leptin gene deficient (ob/ob) obese mice and found that obesity alone ...

[...] up-regulated the expression of TLR1–9 and TLR11–13 in murine adipose tissues, a phenomenon linked with downstream nuclear factor κB [inflammatory protein linked to linked to cancer, inflammatory and autoimmune diseases, septic shock, viral infection, and improper immune development], interferon regulatory factors, and STAT-1 activation, and up-regulated the expression of cytokines and chemokines via MyD88-dependent and MyD88-independent cascades [activate NF-κB].

Thus, obesity sets the scene for inflammation and inflammation in turn triggers a cascade of unfavorable metabolic and hormonal changes which in and out of themselves result in further weight gain...

Here, we have a self-enhancing pathologic circle, which - and this is probably an even more important result of the study - was especially "effective" in the group of diet-induced obese mice:

The magnitudes of the obesity-induced up-regulation of the TLR1, TLR4, TLR5, TLR8, TLR9 and TLR12 genes in the visceral adipose tissue were greater in the DIO mice than in the ob/ob mice. Similarly, the expression of the IFNα and IFNβ genes significantly increased in the adipose tissues of the DIO mice but did not change in the adipose tissues of the ob/ob mice.

So, its not in your genes, but in your hands, feet and mouth to ward off the plague of the 21st century: Exercise and eat healthy to get lean and/or stay lean and stave off inflammation and diabetes.

Supplemental (!) Coconut Diet Reduces Waist Circumference in Men more Than in Women While Leaving Lipid Profiles Unchanged

I take the recent New York Times Article on coconut oil as clear evidence of the fact that the health benefit of tropical oils is getting more and more public attention. Studies that establish the many anecdotal reports you can find all over the Internet may even speed up this process and thus I am happy to report the findings of a Malasian study (Liau. 2011) that clearly underlines that the "bad" saturated fat cannot be so "bad" after all.

The scientists had a group of 20 healthy, but obese Malay volunteers consume an additional 30 mL of coconut oil (approx 2 tablespoons) per day taken in three divided doses, half an hour before each meal (as far as digestive side effects are concerned, this was the best tolerated dose as assessed before the actual study) and found...

that only waist circumference [WC] was significantly reduced after one month of VCO with a mean reduction of 2.87 +/-4.95 cm.

The high standard deviation of this data may well be attributed to the fact that there was no additional control of the dietary habits of the volunteers. The study says subjects "continued their weight loss efforts", but you probably know these "efforts" often turn out to be hardly comparable. I also feel that the real-world significance of the scientists statistical assessment "WC reduction was only seen in males" must be reevaluated, especially in view of the fact that "the reduction [meaning in cm WC] was larger in females" and the reduction in females with BMI <30 (4.8 +/-6.1 cm), other than in females with BMI >30 2.61 +/-2.17) was statistically significant (for more data cf. figure 1).

Figure 1: Comparison of mean differences in anthropometric measurements and lipid profile values in 7 males and 13 females after VCO consumption. (Liau. 2011)

I refrain from commenting on the reasons and invite readers to come up with their own theories, why someone who has gotten to a BMI of >30 (!!) may have problems losing weight on an uncontrolled intervention. What this should tell you, however, is that you may safely assume that 2 x tablespoons of coconut oil (~30ml) à day may be a worthwhile addition to your well-planned diet & exercise regimen.

On a side note: Who knows how much centimeters the volunteers had lost if the had just replaced some of the "good" seed oils in their diets? Well, I guess in view of the fact that the scientists seemed surprised that the bad saturated fats in coconut oil did not ruin their volunteers fatty acid profiles, they probably considered it unethical to ask their participants to completely replace corn with coconut oil ;-)

Review of Intervention Studies Shows: Weight Loss Success Independent of Meal Frequency

"Eat 3 large meals à day!", "Eat smaller meals every 2 hours!", "Eat a single meal and fast the rest of the day!" If you have been trying to find information on how to lose weight effectively, you probably heard all these "expert" advises. What if I told you that a recent review of 25 weight loss interventions shows that it simply does not matter!

In an extensive review of the literature, Palmer et al. (Palmer. 2011) conclude:

Manipulating the EF [eating frequency] of a client seeking weight management is unlikely to provide any additional benefits to weight, body composition or health. The theoretical benefits of manipulating EF may not be sustained in the real life clinical setting as a change to EF may be difficult to maintain over the longer term. Current evidence does not support many of the theories that encourage manipulating EF for weight management. Focus needs to be placed on dietary weight management strategies that are achievable and sustainable over the longer term.

Better body composition? Only inconclusive evidence. Better glucose tolerance in non-diabetics? Definitely not. Decreased risk of heart disease? Unlikely. Less hunger? At least not with three vs. six meals. Bottom line: Another myth debunked!

Low Fat Dairy no more! Milk Fat Protects Women from Myocardial Infarction.

Do you like your 0.1% yogurt? No? Well, what if I told you that it ain't even healthy? A recent study from Sweden (Warensjö. 2011) shows that milk fat is heart healthy! Particularly in women.

The study population comprised roughly 1000 Swedish men and women, whose anthropometric, biomarker fatty acid, physical activity, and dietary data were collected and comparisons were made between people with previous myocardial infarctions (cases) and healthy age-mates (controls).

In women, proportions of milk fat biomarkers in plasma phospholipids were significantly higher (P < 0.05) in controls [i.e. healthy individuals] than in cases and were, in general, negatively, albeit weakly, correlated with risk factors for metabolic syndrome. [...] After multivariable adjustment for confounders, the inverse association remained in both sexes and was significant in women. In agreement with biomarker data, quartiles of reported intake of cheese (men and women) and fermented milk products (men) were inversely related to a first MI [myocardial infarction] (P for trend < 0.05 for all).

So, you better ditch your low fat diary products and grab some full-fat cheese and yogurt (preferably from grass-fed cows). Believe me, they also taste much better!

L-Arginine Biscuits Exhibit Ameliorated Insulin Response. A Viable Alternative for People with Metabolic Syndrome!?

"L-Arginine ameliorates insulin resistance and has beneficial effects on blood pressure", "Fat people love cookies and tend to develop insulin resistance!" - if these two thoughts get together in the head of an Italian scientists, a new product is born: the L-Arginine Biscuit!

In a recent study Emanuela Setola (Setola. 2011) investigated the effect of a biscuit with 6.6g arginine on selected metabolic parameters of 7 healthy subjects. The results are encouraging:

A significant increase of nitric oxide (NOx) and cGMP levels were significantly increased with Biscuit +L-ARG 6.6 g and Powdered L-ARG as compared to Biscuit. AUC NOx and cGMP were significantly increased (p<0.04vs Biscuit). Percentage incremental increase of post-ischemic blood flow significantly increased with Biscuit +L-ARG 6.6 g and Powdered L-ARG, suggesting a functional effect of L-ARG added to the food preparation. Further, at 240 minute mean arterial blood pressure and peripheral vascular resistances slightly declined with Biscuit +L-ARG 6.6 g without reaching a statistical significance. At metabolic levels, the addition of L-ARG to a biscuit decreased insulin levels in the presence of similar glycemic levels, in particular a significant decrease of AUCinsulin during the test with Biscuit +L-ARG 6.6 g in comparison to Biscuit alone was found (p<0.05).

The last result, i.e. the decreased insulin release is probably the most interesting finding of this study and was further investigated by the researcher:

From the results of glucose and insulin, two indices were derived: a Modified Matsuda, (index of whole-body insulin sensitivity) and the Disposition Index (index of the product of insulin sensitivity and first phase insulin secretion). We were able to define that both indices were significantly increased with 6 Biscuits having 6.6 g of L-Arginine while intermediate values were found when 3 Biscuits (3.3 g) were eaten as compared to Biscuits without L-Arginine addition.

After all, I think it would be better to avoid cookies and biscuits completely, but if you just cannot resist, you may well add some arginine to the dough for this years Christmas baking.

Go for Gold: Golden Kiwifruit Outperforms her Green Sister in Terms of Antioxidant Potential

Groundbreaking research ;-) at the Faculty of Pharmaceutical Sciences at the Teikyo University in Tokyo, Japan, did now reveal that Kiwis, especially the golden variate outperforms other highly acclaimed health foods in terms of their antioxidant potential.

Comparison of the anti-oxidant effects in vitro demonstrated that kiwi fruit had stronger anti-oxidant effects than orange and grapefruit, which are rich in vitamin C; gold kiwi had the strongest anti-oxidant effects. Kiwi fruit inhibited oxidation of biological substances in the human body. In particular, kiwi fruit may inhibit early lipid oxidation.

While it is common knowledge that Kiwis contain a lot of vitamin C, the scientists underline that most of its beneficial effects come from the various forms of polyphenols in the fruits.

Fig. 1: Inhibition of Lipid Oxidant by Fruit Juices (Iwasawa. 2011)

So, next time you see some of these hairy little Chinese gooseberries at your local grocery store, grab some golden ones and bump up your antioxidant defenses.



On a side note: According to Dr. Smith from the Life Extension Foundation, Kiwi is also the common food with the highest amount of PQQ ("the new CoQ10" LEF is promoting) you can possibly find - unfortunately, you would probably have to eat truckloads to get the desired effect ;-)

The Great Feast: Overeating With a Macronutrient Emphasis on Carbs Suppresses GH Levels Via Hyperinsulinemia

An interesting study done by scientists from the Department of Internal Medicine (A.L.B.) at the University of Michigan (Cornfold. 2011) reveals a direct influence of overeating (+75% over maintenance) and the associated rise in insulin on growth hormone levels.

Cornfold et al. found that GH levels of seven (formerly ;-) healthy, nonobese men (body mass index, 24 ± 1 kg/m²; age, 25 ± 1 yr) "declined nearly 80% by d 3 of overeating".

Figure 1: Mean plasma GH concentration every 20 min for 24 h before overeating
(baseline), ond3of overeating, and at the end of the 2-wk overeating period. Inset,
The average plasma GH concentration at baseline, d 3, and 2 wk of overeating.

In view of some people's "eat all that cannot run away fast enough" mass gain diets, it is noteworthy that the decline in GH concentration is not an initial reaction. As it is shown in figure 1, GH response stayed way below baseline for the whole 2 weeks the subjects ate their standardized meals containing 70 kcal/kg fat-free mass/d (~4000 kcal/d; 50% carbohydrate, 35% fat, and 15% protein).

So, what can we conclude from that? A dirty / extreme bulk with a high carb intake will ruin your GH levels, spike your insulin levels and set the stage for fantastic, or should I say "fatastic", mass or rather fat gains.

Rat Study: High Carb Diet Induces Hepatic Steatosis and Increases Heart Fat by 43%

For a large part of the 1980s and 1990s fats have been considered the "source of all evil". Now, it is our carbohydrate consumption which is held to be responsible for diabetes, obesity and the other ugly faces of "the metabolic syndrom". A recent study by a group of scientists from Sao Paulo (Haubert. 2010) seems to confirm this "revised" hypothesis.

Over a period of 21 days, the scientists fed a group of rats (experimental) a 70% carbohydrate diet with astonishing or rather shocking results (cf. table 1)

 

Within three weeks the rats developed a fatty liver and their heart fat mass increased by 43%. While the scientists did not provide much information about the overall underlying mechanism of these changes, they emphasize the pronounced decline in tissue vitamin E produced by the high carb consumption. In how far additional vitamin E may have prevented some of the fat accumulation yet remains unknown and would warrant further investigation.

Even Individuals on a "Healthy" Diet May Benefit from Supplemental Fiber

Fiber has been advertised for years as a universal health promoter. It curves appetite, reduces cholesterol and improves digestion - but is it really necessary to supplement with additional fiber, if your intake in fibrous veggies etc. is already high? A recent study by scientists from Australia (Pal. 2010) suggests that it may not be necessary, yet beneficial.

Figure 1: Changes in body weight (A); BMI (B); % body fat (C) and waist circumference (D).
From left to right: Control, FIB, HLT, HLT-FIB

Studying a cohort of 72 overweight and obese individuals with a BMI between 25 and 40 kg/m² and age between 18 and 65 years, the researchers found that over a time period of 12 weeks in which the subjects either practiced their "normal" eating habits or changed to a healthy food diet (HFT), supplemented with fiber (FIB) or switched to a healthy food diet that was supplemented with fiber (HFT-FIB)...

[...] weight, BMI and % total body fat were significantly reduced in FIB and HLT–FIB groups, with weight and BMI significantly reduced in the HLT group compared with control at 12 weeks. HLT–FIB and HLT groups had significant reductions in TAG and insulin compared with control at 6 and 12 weeks, and in insulin compared with the FIB group at 12 weeks. The HLT–FIB, HLT and FIB groups all had significant reductions in total cholesterol and LDL-cholesterol compared with control after 6 and 12 weeks.

As can be seen from figure 1 (above) the addition of fiber to an already healthy diet did in fact improve the overall beneficial results of the change in dietary habits. Bottom line: Firstly, eat healthy! Secondly, consider using a fiber supplement only if your diet is already in check.

Dietary Oxidized Frying Oil Impairs Pancreatic Insulin Release. Vitamin E Helps!

It certainly is no coincidence that a recent study on the detrimental effects of oxidized frying oil (OFA) was published in the British Journal of Nutrition. Afterall, it suggests that the British are at risk of dying out, if they just listened to their appetite and kept over-consuming "Fish and Chips".

After feeding rats with either soy (HF) or oxidized frying oil (HO) over a period of 8 weeks the researchers found:

[...] mice in the HO group showed glucose intolerance and hypoinsulinaemia, and their islets showed impaired glucose-stimulated insulin secretion (P,0·05; HO group v. LF and HF groups). Significantly higher oxidative stress and a lower mitochondrial membrane potential were observed in the islets in the HO group compared with the LF and HF groups. Immunoblots showed that the reduction in insulin levels in HO islets was associated with activation of the c-Jun NH2-terminal kinase and a reduction in levels of pancreatic and duodenal homeobox

Furthermore, they found that, "when dietary OFO-induced tissue vitamin E depletion was prevented by high-dose vitamin E supplementation (500 IU(1·06 mmol all-rac-a-tocopherol acetate)/kg diet; [...] the OFO-mediated reduction in islet size and impairment of glucose tolerance and insulin secretion were significantly attenuated."

So, obviously it is the interplay of oxidation and lack of antioxidants (in this case vitamin E) which collectively initiate these metabolic changes, which consequently are at the bottom of what is often called "the metabolic syndrome". Bottom line: Beware of oxidized fats and support your antioxidant capacity by healthy food choices and supplements.

Anti-obesity & Anti-diabetic effect of Trehalose in Rats on a High Fat Diet

I know, I know, rats on a high fat diet are a topic on their own: "Are they a valid model for metabolic disease in man?" etc. - Be that as it may, the findings of scientists from the Biomedical Institute, Research Center, Hayashibara Biochemical Laboratories in Okayama (Arai. 2010) suggest that, of all things, a sugar(!) molecule may help prevent the negative effects of a high fat diet on fat mass and insulin resistance, which are commonly observed in the rat-model of the typical western-world high-fat diet.

Other than rats on a glucose [Glc], a maltose [Mal], a high-fructose corn syrup, or a fructose [Fru] rich high-fat-diet [HFD], the rats which were fed the natural alpha-linked disaccharide trehalose did not exhibit the typical signs and symptoms subsumed under the keyword "metabolic syndrome":

After 7 weeks of HFD and saccharide intake, fasting serum insulin levels in the Tre/HFD group were significantly lower than in the Mal/HFD and Glc/HFD groups (P < .05). Furthermore, the Tre/HFD group showed a significantly suppressed elevation of homeostasis model assessment–insulin resistance compared with the Mal/HFD group (P < .05) and showed a trend toward lower homeostasis model assessment–insulin resistance than the Glc/HFD group. After 8 weeks of feeding, mesenteric adipocyte size in the Tre/HFD group showed significantly less [fat] hypertrophy than the Glc/HFD, Mal/HFD, high-fructose corn syrup/HFD, or Fru/HFD group. Analysis of gene expression in mesenteric adipocytes showed that no statistically significant difference in the expression of monocyte chemoattractant protein–1 (MCP-1) messenger RNA (mRNA) was observed between the Tre/HFD group and the distilled water/standard diet group, whereas a significant increase in the MCP-1 mRNA expression was observed in the Glc/HFD, Mal/HFD, Fru/HFD, and distilled water/HFD groups.

While these results certainly appear promising, I better add that the laboratory that did the study is financed by the Hayashibara company, the same company which recently developed a new technique to produce or rather to extract trehalose commercially. So treat these results with a grain of skepticism, if you understand what I mean ;-)

Overweight Boys More at Risk of Obesity Related Health Problems than Girls

In a recent study from Egypt, Hassan et.al. took anthropometric measures of adiposity from 150 pupils between the ages of 7 to 18. Along with data on body composition and serum total lipids profiles the scientists intended to find correlation between obesity and adverse health effects at younger age. The results are interesting in that no correlation was found between lipid profile and body composition in the adolescent group (12-18 years). On the other hand, in the younger children , ...

For young age [7-11 years], triglycerides and HDL-C are correlated to most of the body composition and anthropometric parameters in boys and not in girls.

The scientists speculate on whether the different fat distribution pattern in young boys (centrally dominant) could be one of the underlying reasons for this observation. Be that as it may, I consider this another good reason to encourage boys (and girls, alike) to act out their natural desire to move and exercise before they  become PlayStation cambling couch potatoes.