Dukan Diet

This plan was developed by  NASA to help astronauts lose weight quickly before a mission in space. What is the Cosmonaut regime? Who is he? We take you into space, follow us!
Cosmonaut regime, what is it?
Originally developed by an American doctor for space adventurers, it quickly became a diet program praised by many women in search of a perfect figure.

Cosmonaut diet is a low calorie diet that is low in calories, very strict and very difficult to follow.


The basic rules of the Cosmonaut regime
The first idea to lose weight is to drink water.
Plenty of water. Or tea infusion or coffee. At least 2 liters a day.

It also removes the power of fatty materials such as oil, margarine, butter.

Shelved in favor of sugar sweeteners!
We can dress salads with lemon, mustard or vinegar.

And complete the Cosmonaut regime vitamin supplements and minerals.




Example of the menu system Cosmonaut
Breakfast:
Coffee or tea.

lunch:
3 hard boiled eggs and a tomato or 1 fillet grilled meat (200 g) and a green salad.

dinner:
1 grilled fillet (200g) and a green salad or ham fat York (150 g) and 1 skimmed yogurt.


Cosmonaut system: effectiveness and limitations
This scheme is ultra restrictive.
One can hardly eat anything during the diet.
Suffice to say that it is very difficult to follow ...
Fatigue failures and yo-yo will certainly be felt.
Even if weight loss can be spectacular (almost 3 pounds in 3 days only), watch the boomerang effect!

Milk is a much-needed donation at your local food bank!

Now here are a few more things I've been thinking about . . .

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Here is a reference to help you understand food labels. It is provided by the Academy of Nutrition and Dietetics.

A Guide on How to Read a Nutrition Facts Panel from the Academy

It was about time for an artificial sweetener update, wasnt it?

Alright, I have to admit I am not following the artificial sweetener scene closely enough to have heard about SUCRAM, an artificial sweetener that is composed of saccharin (a classic) and neohepseridin dihydrochalcone, the new kid on the blog, which is yet not officially approved by either the FDA or it European equivalent o be used in the processed junk, most people call "food", these days. If we put some faith into the latest study investigating the effects of this agent, which is apparently already heavily used in animal feeds in Europe it does yet "dramatically reduce enteric disease" and "enhance growth performance in early-weaned piglets." (Daly. 2014)

Whether and to which extent these beneficial effects on gut health are mediated by changes in the gut microbiome is yet still uncertain; and since "uncertain" is a word scientists dont like, Kristian Daily and his colleagues from the University of Liverpool conducted a study to find out, whether the non-negligible health benefits would be brought about by AI <> gut interactions.
To this ends, the scientists employed a DNA-based pyrosequencing technology to investigate the changes in the intestinal microbiota of piglets weaned to a diet supplemented with either a natural sugar, lactose or said artificial sweetener (SUCRAM)

Figure 1: Total and lactobacillus OTU4228 concentrations in piglets on hydrolzysate carbohydrate diet without sweeteners, with lactose or SUCRAM diets and corresponding concentration of lactic acid in the caecal contents (Daly. 2014)

As you can see in Figure 1, both, the addition of lactose and the saccharin/NHDC mix lead to dramatical increases in the caecal Lactobacillus population and could well explain the previously reported "pro gut health" effect of SUCRAM in piglets (Vente-Spreeuwenberg. 2004; Pierce. 2006)

But thats obviously not all thats news-worthy!

I did after all promise you news on products you may be using, as well - aspartame and acesulfame-k, to be precise. Now, while the former is a constant target of public (mostly broscientific) criticism, the latter has been a thorn in my side ever since I have started investigating artificial sweeteners.

Lean more about the "Gut Type Diet" - No Fad, Guaranteed!

And while previous studies only suggested that the effects of acesulfam-k on the pancreas could have pro-obesogenic consequences, a recent model experiment from the Louisiana State University appears to finally prove that acesulfam-k may actively promote the deposition of body fat in the presence of insulin resistance.

Ok, the results have been derived in a Caenorhabditis elegans, a "worm", but one that has long and actually surprisingly successfully been used as a "model for studying the basic biology of obesity" (Jones. 2009) - I know, I am not convinced either, but if the results do actually translate to humans, this would be major (bad) news for the food industry.

In view of the fact that most companies have been pulling acesulfame-k from their products over the past years, anyway, I would not discard the findings Jolene Zheng et al. present in their latest paper in Chemico-Biological Interactions as meaningless, not despite, but rather because a scientists from PepsiCo was part of the research team which observed these significant increases in intestinal fat (=visceral fat of the worm) when the critters were fed with acesulfam-k sweetened coke.
References: 

• Payne, A. N., C. Chassard, and C. Lacroix. "Gut microbial adaptation to dietary consumption of fructose, artificial sweeteners and sugar alcohols: implications for host–microbe interactions contributing to obesity." Obesity Reviews 13.9 (2012): 799-809.
• Pierce, K. M., et al. "The effect of lactose and inulin on intestinal morphology, selected microbial populations and volatile fatty acid concentrations in the gastro-intestinal tract of the weanling pig." ANIMAL SCIENCE-GLASGOW THEN PENICUIK- 82.3 (2006): 311.
• Jones, Kevin T., and Kaveh Ashrafi. "Caenorhabditis elegans as an emerging model for studying the basic biology of obesity." Disease models & mechanisms 2.5-6 (2009): 224-229.
• Vente-Spreeuwenberg, M. A. M., et al. "Effect of dietary protein source on feed intake and small intestinal morphology in newly weaned piglets." Livestock Production Science 86.1 (2004): 169-177.

The Sunday farmers market in Sebastopol, California.

Buying baby squash at the market.

Baby yellow and green zucchini, patty pan and lemon squash.

Squash, onions, tomatoes, garlic and seasoning in the roasting pan.


Sunday I visited my local farmers market in the Sebastopol town square. It was a nice sunny day and there was almost a party atmosphere with happy crowds walking around with their eco-friendly canvas bags. Besides the usual farmers and their wonderful produce, there was a guitar player on stage, a vegetarian tamale stand next to a vendor selling Indian curry. The aromas were amazing! There were bakers selling freshly made whole grain breads (my husband bought a whole grain, walnut sourdough) and farmers selling fresh eggs. You could buy hand made cheeses, flowers, fresh honey and fish that was caught that morning. Why on earth would anyone go to a supermarket when you can have a shopping experience like this?

People in America have gotten so disconnected from their food. Most people don’t even know what food they are eating since it came out of a box that has 20 mysterious ingredients listed, most of which were derived from corn. (For more on this, watch the documentary called, “King Corn”). So I thought I would take you to the market today, buy the ingredients from a local organic farmer, and show you how to make fresh, tasty, roasted baby vegetables and mix them with a hardy, protein and fiber rich whole wheat pasta. As is, the dish is vegan but others could serve this topped with goat cheese or parmesan.

***

Roasted Medley of Baby Squash on Whole Wheat Pasta [Serves 4]
5 cups of mixed baby squash, cut in quarters or eighths
2 cups sliced onions (1 cup yellow and 1 cup red)
2 cups fresh tomatoes, cut in eighths and drained
4 cloves garlic, minced
3 tablespoons fresh basil
1 teaspoon fresh rosemary (or 1/2 teaspoon dry)
1 teaspoon fresh thyme (or 1/2 teaspoon dry)
2 tablespoons extra virgin olive oil
2 tablespoons balsamic vinegar
1 tablespoon honey (or agave syrup)
1 teaspoon salt
1/8 to 1/4 teaspoon black pepper
1/2 pound whole wheat pasta shells (or your favorite shape)

Preheat the oven to 450 degrees. Fill a large pot with water and salt and get ready to boil pasta. Lightly oil a large roasting pan and set aside. Cut the baby yellow and green zucchini in quarters length wise and then in half so you have a large julienne. Cut the lemon and patty pan squash in quarters or eighths depending on their size. Put them in a large bowl. Add the drained tomatoes, garlic and herbs. In a small bowl, mix the olive oil, balsamic vinegar, honey, salt and pepper. Pour this mixture over the vegetables and mix well. Spread the mixture out in the large roasting pan. Bake in the oven for 20 to 30 minutes, or until the squash is soft. Prepare the pasta according to directions while the squash is baking. Mix the roasted squash with the pasta and serve. You can garnish with more chopped basil. Top with nutritional yeast, as a vegan option, or others can top with crumbled goat cheese or parmesan.

Per serving: 357 calories, 8 g fat, 1 g saturated fat, 0 g cholesterol, 10.3 g protein, 62.3 g carbohydrates and 8.8 g of fiber.

Asian foods are low in SFAs. So the researchers had to add it to the pan.

From a physiological perspective, the observation researchers from the Nakamura Gakuen University, the  Akita University, the Chiba University and the University of Copenhagen appear counter-intuitive, why should fat increase the insulin response to a meal. The presence of fat in a meal should slow down the absorption of glucose, right?

Obviously you havent read my previous article on the fallacies of adding fat to glucose in the false believe that the reduced digestive speed would reduce the post-prandial insulin spike ("True or False? Adding Fat to A Carby Meal Lowers Insulin Response." | read more) - a highly suggested read you may want to read either, before or after you devour todays SuppVersity article.
Dont worry, todays article still has something new to offer. While the previously reported data dealt with acute responses to high(er) fat meals, Itoh et al. (2014) whose study is available as an "ahead of print paper" on the website of Nutrition Research, looked at the effects of sub-chronic, not acute high saturated fat intakes.

Figure 1: Graphical overview of the procedure  (Itoh. 2014)

In that, they conducted an intervention study to investigate the insulin and plasma GIP responses in 11 healthy women, including a dietary control. Subjects were provided daily control meals (F-20; saturated fatty acids/monounsaturated fatty acids/polyunsaturated fatty acids [S/M/P] ratio, 3:4:3) with 20 energy (E) % fat, followed by 2 isoenergetic experimental meals for 7 days each. All meals were standard Japanese meals, the recipes for both experimental meals were identical, only a different cooking oil was used.
Talking about "test meals" (I dont like to call them thus, as they were consumed for a couple of days and not just for a "test), these meals comprised 60 E% carbohydrate, 15 E% protein, and 30 E% fat with the fat being distributed as follows:

• in the high saturated fatty acid meal (FB-30): S/M/P, 5:4:1; 
• in reduced saturated fatty acid meal (F-30): S/M/P, 3:4:3

Tests were conducted after two days on the FB-20 meal (pre) and at the end of the FB-30 and F-30 phases (see Figure 1), before and 30, 60, and 120 minutes after a meal tolerance test.

Figure 2: Comparison of glucose, insulin, and C-peptide levels after the control, F-30, and FB-30 meals (Itoh. 2014)

Interestingly, the plasma glucose responses did not differ between F-20 and FB-30 or F-30. The insulin levels, on the other hand, were higher after the FB-30 than after the F-20 (P<.01).

The GIP response, i.e. the response of the non-satiating non-fat burning insulin release triggering brother of GLP-1 (learn more) that does neither reduce hunger, not appetite nor improve glucose control (increased amount of insulin used to store away the same amount of glucose; cf. Edholm. 2010), after the FB-30 was higher than that after the F-30 (P< .05).

"In addition, the difference in the incremental GIP between FB-30 and F-30 correlated significantly and positively with that of the insulin." (Itoh. 2014)

The scientists believe that their results clearly prove, what scientists have believed for quite some time, now: "a high saturated fatty acid content stimulates postprandial insulin release via increased GIP secretion." (Itoh. 2014)
References:

• Boden, Guenther, et al. "Mechanisms of fatty acid-induced inhibition of glucose uptake." Journal of Clinical Investigation 93.6 (1994): 2438.
• Edholm, T., et al. "Differential incretin effects of GIP and GLP‐1 on gastric emptying, appetite, and insulin‐glucose homeostasis." Neurogastroenterology & Motility 22.11 (2010): 1191-e315.
• Itoh, Kazue, et al. "High saturated fatty acid intake induces insulin secretion by elevating gastric inhibitory polypeptide levels in healthy individuals." Nutrition Research (2014).
• Nuutila, P., et al. "Glucose-free fatty acid cycle operates in human heart and skeletal muscle in vivo." Journal of Clinical Investigation 89.6 (1992): 1767.
• Roden, Michael, et al. "Mechanism of free fatty acid-induced insulin resistance in humans." Journal of Clinical Investigation 97.12 (1996): 2859.