Steamed gulf shrimp with vegetables

Few would argue against eating seafood several times a week, except in the case of seafood allergy. Shrimp is a very good option, especially if it is not farm raised.

100 g of shrimp will typically have 20 g of protein, and about 152 mg of cholesterol (this is good for your health). It will also have about 0.6 g of omega-3 fats, and 0.03 g of omega-6; an omega-3 to omega-6 ratio of about 20.

My wife prepared this steamed gulf shrimp with vegetables dish. And it was very, very delicious. Here is her recipe:

- Add a small amount of olive oil and water to a frying pan.
- Add 1 lb of wild-caught peeled gulf shrimp, cabbage, onion, and asparagus (or green beans, as in the photo).
- Cook in low heat for 15 minutes.
- Add spinach and cook in low heat for another 10 minutes.
- Turn off heat, season to taste while mixing; I suggest using garlic powder, cumin powder, and parsley flakes.

Peeled shrimp is usually farm raised, which does not have the same amount of omega-3, or the same ratio of omega-3 to omega-6, as wild-caught shrimp. This small “salad” gulf shrimp was an exception.

Check the package. If it doesn’t explicitly say “wild”, you are better off buying wild-caught shrimp and peeling it yourself. Shrimp peelers are sold in most supermarkets; the one I use looks like a Velociraptor claw.

Adiponectin and tumor necrosis factor-alpha levels after a high saturated fat meal

This is one of those interesting studies where the authors start with some pre-conceived assumptions and end up concluding something else, some way toward the opposite of what they assumed.

My final interpretation of the study results is a bit different though. It suggests that the results are actually the opposite of what the authors originally assumed.

The authors of the study (Poppitt et al., 2008; full reference at the end of this post) start by stating that since “… dietary fat is associated with increased lipid storage, weight gain, and obesity …” it is important to study the effect of dietary fat intake on the blood levels of certain substances that are associated with lipid disorders, weight gain and obesity.

In short, the authors start from the assumption that dietary fat is bad. By the way, this type of indictment of all fats is not very common these days. Usually saturated fat is the target.

Since dietary fat is assumed to be bad for us, that justifies the authors’ goal of studying the effect of dietary fat on certain hormones associated with bad health, including the body fat-secreted hormones adiponectin and tumor necrosis factor-alpha. Low levels of serum adiponectin, and elevated levels of tumor necrosis factor-alpha, are associated with various health complications.

In the study, a high-fat test meal with approximately 59 g of fat (71% of energy as fat) was given at breakfast on two occasions to 18 healthy and lean men. These men had, on average, 23 years of age, a 31-inch waist, and a body mass index of 22.9. In other words, they were young and fit.

Two fatty meal variations were used, one with a lot more saturated fat than the other. Their ratio of saturated:unsaturated fatty acids was 71:29 for the high saturated fat meal, and 55:45 for the other. The table below provides a more detailed picture of the fat composition of the meals. The authors refer to these meals as instances of “acute intake of dietary lipid”.

Lunch, snack and dinner meals were also served to the participants. Those meals were nearly fat-free, with 1 to 3 g of fat only; apparently to help the participants “recover” from the high fat meal. They included plenty of refined grains (e.g., pasta) and fruit juices. Way to go; give these folks refined carbohydrates and sugars galore to help them recover from the “damage” done by the high fat meal!

Blood samples were collected at 0 (baseline), 1, 3, and 6 h for the measurement of various substances, including the body fat hormones adiponectin and tumor necrosis factor-alpha levels.

The figure below shows the variation in adiponectin levels at several times after the meal. The black circles are for the high saturated fat group, and the white circles for the other group. Adiponectin levels do not really start at the same level for both groups, which makes the graph a bit unclear; to better interpret the graph it may be a good idea to simply ignore the first (white) circle at the zero mark on the vertical axis. Also, no hormone levels were negative, of course; the zero on the vertical axis represents a reference value.

As we can see from the figure above, adiponectin levels go up for both groups after the fatty meal, and end up higher than they started for both groups; more for the high saturated fat than for the low saturated fat group. They are at very similar levels at the 24 h mark, but the levels at 24 h for the high saturated fat group appear to be a lot higher than they were right after the fatty meal. (The start point for the high saturated fat group being the first black circle from the left on the graph.) None of the differences are reported as significant. This is not surprising, given the small sample.

The figure below shows the variation in tumor necrosis factor-alpha levels at several times after the meal. This is an even more interesting one, because it suggests a possible negative effect of the low fat meals.

In terms of tumor necrosis factor-alpha levels, the figure above suggests that both groups end up higher than they started, by about the same amount, which is not very good. (With tumor necrosis factor-alpha, unlike adiponectin, the less you have the better - so to speak, the hormone has important functions.) Again, none of the differences, with the exception of one, are reported as significant. The exception is the tumor necrosis factor-alpha level at 6 h for the low saturated fat group, which is significantly lower. But that difference disappears at the 10 h mark, never to be seen again.

Interestingly, note that tumor necrosis factor-alpha levels go up very clearly after the additional meals, which were low fat meals rich in refined carbohydrate and sugars. The variation in adiponectin is not as clearly associated with the additional meals. The points at which those meals were served are indicated by the arrows at the top of the graph; first arrow from left for lunch, second for a snack, and third arrow for dinner.

The conclusion by the authors of the study was that there is “… no evidence from this study of lean, healthy male subjects that the adipose hormone adiponectin is sensitive to acute intake of dietary lipid or to an increase in fatty acid saturation.” They do acknowledge the reduction in tumor necrosis factor-alpha up until the start of the low fat meals, and say that the “mechanism leading to the decrease in TNF-alpha on the high SFA:USFA treatment in our trial is unknown to us.”

My interpretation of this study is that, at least for young and lean men:

- There is some evidence that dietary saturated fat intake leads to increased levels of circulating adiponectin and decreased levels of tumor necrosis factor-alpha in the first few hours after a meal rich in saturated fat; with plenty of palmitic acid in it, by the way, of which animal fat is a great source. These are desirable and health-promoting hormonal responses.

- These is some evidence that meals high in refined carbohydrates and sugars increase levels of circulating tumor necrosis factor-alpha in the hours following the meals. Elevated levels of tumor necrosis factor-alpha are not good news; something that I guess is implied by the name of the hormone.

- There is some evidence that dietary saturated fat intake leads to an increase in adiponectin levels 24 h after a high fat meal, even when it is followed by low fat meals high in refined carbohydrates and sugars. This suggests a protective effect, which is in line with the hypothesis that adiponectin is not only a health marker by also a health-promoting hormone.

Due to the small sample used, none of the conclusions above is based on statistically significant results. More research is needed in the future, with larger samples. I am not sure it will happen though. This study’s findings were obviously accidental, and saturated fat phobia is still widespread.

Adiponectin is highly correlated with body weight, particularly weight associated with body fat mass. So, if you were able to achieve weight loss through a low carbohydrate diet involving a high consumption of saturated fat, there is absolutely no need to change that based on the results of this study.

Plus, saturated fat has the added benefit that it increases HDL cholesterol, the “good” cholesterol.

Reference:

Poppitt, S.D. et al. (2008). Postprandial response of adiponectin, interleukin-6, tumor necrosis factor-α, and C-reactive protein to a high-fat dietary load. Nutrition, 24(4), 322-329.

Adiponectin, inflammation, diabetes, and heart disease

Humans, like many animals, evolved to be episodic eaters and spend most of their time fasting. Body fat is the main store of energy in the human body. Excess dietary carbohydrates and fat are stored as body fat, in specialized cells known as adipocytes. Excess dietary protein is not normally stored as body fat.

Adipocytes can be seen as being part of a very important and distributed endocrine organ, being responsible for the release of many different hormones into the bloodstream. One of these hormones is adiponectin. Other important hormones secreted by body fat tissue are leptin and tumor necrosis factor-alpha.

Among hormones, adiponectin is particularly interesting because it is negatively correlated with body fat mass. That is, unlike other hormones such as leptin and tumor necrosis factor-alpha, a decrease in body fat mass (a well known health marker) is associated with an increase in adiponectin. This has led some researchers to speculate that adiponectin is a causative factor that promotes health, in addition to being a health marker.

Jung and colleagues (2008; full reference at the end of this post) studied 78 obese individuals (41 females) who participated in an exercise program during 12 weeks. The exercise program involved mostly low intensity aerobic activities, such as brisk walking. The individuals also took an appetite suppressant, with the goal of reducing their calorie intake by about 500 kcal per day.

The table below (click on it to enlarge) shows various measurements for the participants before and after the 12-week intervention.

From the table above we can say that there were significant reductions in weight, body mass index (BMI), waist and hip circumference, waist-to-hip ratio (WHR), total body fat, and total fasting cholesterol and triglycerides. However, the participants were still obese at the end of the intervention, with an average body fat percentage of 35.5.

The table below shows the concentrations of various hormones secreted by body fat tissue, as well as other types of tissue, before and after the 12-week intervention. These hormones are all believed to be health indicators and/or health causes.

We see from the table above that the hormonal changes were all significant (all at the P < .001 level except one, at the P < .05 level), and all indicative of health improvements. The serum concentrations of all hormones decreased, with two exceptions – adiponectin and interleukin-10, which increased. Interleukin-10 is an anti-inflammatory hormone produced by white blood cells. The most significant increase of the two was by far in adiponectin (P = .001, versus P = .041 for interleukin-10).

One of the most promising effects of adiponectin seems to be an increase in insulin sensitivity. This effect appears to be unrelated to any effects on insulin secretion. That is, adiponectin seems to act directly on various cells, including muscle cells, increasing their ability to clear glucose from the blood. This effect seems to be one of the underlying, and previously unknown, reasons why loss of body fat improves health in those who suffer from diabetes type 2.

Increased serum adiponectin has been found to be significantly associated with: decreased body fat and particularly visceral fat, decreased risk of developing diabetes type 2, decreased blood pressure, and decreased fasting triglycerides.

Adiponectin appears to also have anti-inflammatory and athero-protective properties.

On average, women have higher levels of serum adiponectin than men.

According to Giannessi and colleagues (2007) administration of adiponectin in mice has shown positive results. Since research on adiponectin is new, it will probably be some time until related drugs are developed. Giannessi and colleagues also note that fish oil and vanadium salts may increase the synthesis and release of adiponectin.

So far it seems that the most effective way of increasing adiponectin levels is weight loss, particularly through body fat loss. Even as new drugs are developed, this will likely remain the most natural and safe way of increasing adiponectin levels.

All of this helps in the identification of missing links between body fat loss and health improvement. It seems that losing body fat has an effect similar to that of supplementation; it increases the blood concentration of a health-promoting substance - adiponectin!

References:

Giannessi, D., Maltinti, M., & Del Ry, S. (2007). Adiponectin circulating levels: A new emerging biomarker of cardiovascular risk. Pharmacological Research, 56(6), 459-467.

Gil-Campos, M., Cañete, R., & Gil, A. (2004). Adiponectin, the missing link in insulin resistance and obesity. Clinical Nutrition, 23(5), 963-974.

Jung, S.H. et al. (2008). Effect of weight loss on some serum cytokines in human obesity: increase in IL-10 after weight loss. The Journal of Nutritional Biochemistry, 19(6), 371-375.