Dukan Diet

The economy is all whacked out right now and its scary. Im not watching the news.

I get an email almost every day asking if I am saving money by using my CrockPot daily.

No. What I am doing is not normal. Most people do not try to do what Im doing in the crockpot. We are pretty much breaking even on the grocery bills, thanks to BlogHerads. I am grocery shopping more than I ever have before, and am cooking way too much food. I am also buying ingredients that cost more than I would normally spend because Im trying so many new things.

But you can save money. You dont need to cook a different something every single day. You can cook a big pot of beans, stew, or a casserole and eat it for a few days in a row. You can stock your freezer with homemade broth, stock, and cream of something soup. You can freeze your own cooked beans. You can make yogurt. You can make baby food. You can cook a whole chicken and pick off the meat for future meals. You can even make playdough, crayons, or use the crockpot as a footbath (not really. this one is just for fun.)

When I was first married, I stunk at cooking. I still kind of do, but at least the crockpot allows me a bunch of wiggle-room. I would make Taco Soup every other week, and Adam and I would stretch the food to last for days by making burritos, or adding it on top of rice.

Ive put together a round-up of money-saving CrockPot ideas for you. I will continue to add more posts when I come up with them.

homemade chicken broth
homemade beef stock
homemade cream of mushroom soup

Myrons famous whole chicken
lemon and herb chicken
rotisserie-style chicken

How to make canned beans
or refried beans
How to make yogurt
How to make babyfood
Playdough recipe
Recycle crayons in your crockpot
Recycle Candles, too!
Use your crockpot as a rice cooker
Make homemade chicken nuggets in the crockpot
Skip the coffee house and make pumpkin spice lattes at home or peppermint mochas.
Having a party? Stretch your wine by turning it into mulled wine.

Extra food? Make fried rice in the crockpot!
You can make applesauce or apple butter, or homemade granola.

And my favorite way to use my crockpot: the lazy way. Plop in a hunk of frozen meat---it really doesnt matter what kind---and cover it with a bottle or jar of your favorite sauce. Cook on low all day, and serve the shredded meat over rice or pasta. Ive used spaghetti sauce, barbecue sauce, A-1, salad dressing, and bottled marinades.

If you are concerned about the amount of energy consumed by using a crockpot (which is a very valid concern!) here is a pamphlet put out by First Energy Corp., in Ohio. The chart on page 5 says that a crockpot uses $0.02 power per hour.
Heres another energy usage list put out by the Northeast Utilities System, that says the monthly cost of using a slow cooker is $1.17.

For more frugal dinner ideas, visit Erin at $5 Dollar Dinners.

Slow Cooking During a Recession
Meal Planning With the CrockPot
Alphabetical Listing of Recipes
Frequently Asked Crock-Pot Questions
Help! My CrockPot Cooks Too Fast!
An Important Note About Safety
My New Years Resolution

The brain is fed and oxygenated by capillaries that penetrate its grey matter, but the cells and proteins of the blood are kept separated from the brain by the cells and matrix of the vessel walls, the blood brain barrier (BBB). That barrier can be breached by inflammation that lowers the heparan sulfate composition and stretches the matrix.

The blood can be considered a large organ with liquid surrounding the cells of the tissue instead of extracellular matrix composed of proteins and polysaccharides. Organs are typically surrounded by a basement membrane made of laminin, entactin (nidogen), collagen and perlecan (a heparan sulfate proteoglycan). These components are secreted by the adjacent cells, and the proteins and polysaccharide (heparan sulfate) bind to each other in multiple ways and hold the tissue together. The cells lining blood vessels, endothelial cells, are connected to each other by tight junctions and the space between the cells is filled with the extracellular matrix of the endothelial cells, the equivalent of the basement membrane of the blood.

Inflammation leads to an alteration in the structure of blood vessels that produces the gross symptoms of inflammation: swelling, reddening, warmth and pain -- the blood vessels dilate or stretch. Persistent or chronic inflammation of vessels can lead to changes in the composition of basement membranes and one notable change is a decrease in the heparan sulfate proteoglycan.

In my own research on the molecular impact of inflammation, one of my students, April Reimers, induced inflammation in cultures of cartilage secreting cells, chondrocytes, using a glucan (similar to the glucan elicitor that I used thirty years earlier to stimulate disease resistance in plants.) She used real time reverse transcriptase PCR to follow the expression of the genes involved. The inflammation transcription factor, NFkB, was turned on (as judged by a compensating induction of its inhibitor IkB) and proteins and enzymes involved in the expression of heparan sulfate proteoglycans were shut down. Our interpretation was that inflammation reduces some heparan sulfate proteoglycans. Since there are at least a dozen different HSPGs with different patterns of expression, we would expect there to be some exceptions from the general suppression caused by inflammation.

Inflammation caused by many different diseases opens up capillaries to provide access of the immune system to damaged tissue. Breakdown of the integrity of an endothelial barrier with an inflammatory decrease in HSPG in kidneys is observed as proteinuria (loss of protein into the urine) due to high blood sugar of diabetes. Breakdown of the capillaries also disrupts blood flow to extremities and is responsible for amputations in diabetics with poor control of blood sugar. Inflammation of intestinal blood vessels and HSPG reduction occurs in protein lossing enteropathy (loss of blood protein into the lumen of the intestines) as a result of heart reconstruction to repair congenital structural defects. The same thing happens to the BBB when vessels of the brain experience inflammation.

Breaching of the BBB is an essential initiating event in many diseases of the brain. Subsequent flareups of symptoms may signal repeat compromise of the barrier between the blood and the brain. The reduction of the barrier, including a decrease in HSPG, permits transit of antibodies, other proteins, e.g. the beta amyloid peptides of Alzheimer’s disease, and lymphocytes from the blood into the brain. The region of the brain that is inflamed and the nature of the interaction between the blood components and the brain determine the symptoms. Examples would be the autoimmune attack on the myelin sheath of nerves in multiple sclerosis and the aggregation of fibers of beta amyloid peptides with heparan sulfate on the surface of neurons in Alzheimer’s disease.

Shutting the blood brain barrier would seem to be the first step in disease treatment, but in some cases, the BBB must remain breached for medication to reach the brain -- the BBB is also a barrier to drugs. If the BBB is to be repaired, then inflammation must be stopped. In most cases, this is accomplished by anti-inflammatory drugs. In some cases, such as protein lossing enteropathy, heparin therapy can reverse symptoms. A very effective supplement to reduce chronic or in some cases acute inflammation is an anti-inflammatory diet. The components of these diets are discussed elsewhere on this blog. These diets have been used effectively in the treatment of MS, Alzheimer’s and many other degenerative and autoimmune diseases.

If you want other to see your pump, you got to be ripped. If not, why care about reductions in BMR?

If you remember my posts about the first generation, arginine-based pre-workout products you will be aware that the only pump they produced was the word "pump" in their name or product description. The reason was and still is simple. The mere provision of l-arginine, which is a precursor to nitric oxide does not lead to an increase in nitric oxide production. Why? Well, think of a building a house: Just buying some concrete wont make you a proud home owner, either ;-)

The bad thing: Arginine didnt work. The good thing: This means it didnt decrease your BMR, either

Against that background its quite astonishing that arginine and citrulline based pre-workout products have dominated the top-seller lists of the big supplement vendors for decades. A fact thats probably partly due to other potential benefits of these amino acids, of which one - you as a SuppVersity reader know that - could be fat loss | learn more about the potential fat loss effects.
With more and more people openly declaring that they would no longer waste money on "good tasting, but expensive and disfunctional products", they industry was yet pressed to develop alternatives. Luckily, our body has two options it can chose from, when producing nitric oxide.

Fortunately, the industry has developed better alternatives...?

You know option #1, the arginine ➲ nitric oxide pathway, and - with all the hype and hyperbole that surrounded the introduction of the first nitrate supplements - I am pretty sure, you know the other one as well, the nitrate-nitrite ➲ nitric oxide pathway

Figure 1: The Arginine- and the Nitrate-Nitrite - NO pathway are the yin and yan of nitric oxide production (Lundberg. 2008).

As the illustration (Figure 1) I have "borrowed" from a comment by Jon. O. Lundberg et al. (2008) illustrates quite nicely, the arginine and nitrite nitric oxide pathway are the yin and yan of NO production.

With the "yan", i.e. the nitrate-nitrite ➲ nitric oxide pathway being a relatively "new kid on the NO block", that recycles (=reduces) inorganic anions nitrate and nitrite to form bioactive NO in blood and tissues during physiological hypoxia.

It goes without saying that there is a bottle neck to this process as well, but the rate limiting availablility of oxygen which hampers the argine-based NO generation by NOS becomes limited as oxygen levels fall is actually a signal for the nitrate–nitrite ➲ nitric oxide to really kick in.

There is more yin and yan, here

If you take a closer look at the results of a study in the America Journal of Clinical Nutrition (Figure 2), you will yet have to realize that there is "more yin and yan", here than youd probably hope for. According to the data scientists from the venerable Karolinska Institutet in Stockholm, Sweden, present in their paper, "[d]ietary inorganic nitrate reduces the RMR." (Larsen. 2014)

Figure 2: VO2 consumption (marker of fatty acid oxidation) and basal metabolic rate (BMR) relative to means (left), thyroid hormone (T3, T4) levels after 3-d dietary intervention with sodium nitrate (Larsen. 2014)

Whut? Yes, you read Larsen et al. right: In their randomized, double-blind, crossover study, in the course of which the Swedish scientists measured the resting metabolic rate (RMR) of 13 perfectly healthy 18–49 y olds (17 women) via indirect calorimetry after a 3-d dietary intervention with sodium nitrate (NaNO3 @ 0.1mmol/kg body weight) or a placebo (NaCl), Larsen, Schiffer, Ekblom et al. observed a statistically and (probably) physiologically significant reduction BMR reduction of 4.2% which correlated strongly to the degree of nitrate accumulation in saliva (r²= 0.71) and fits in nicely with the reduced O2 consumption of which Bailey et al. were the first to observe it in response to nitrate supplementation during exercise (Bailey. 2009).

Interestingly, these effects were not - as you may have been speculated - brought about by changes in thyroid hormone status. And the subjects insulin sensitivity, glucose uptake, plasma concentration of isoprostanes, as well as their total antioxidant capacity were unaffected, as well.
Reference:

• Bailey, Stephen J., et al. "Dietary nitrate supplementation reduces the O2 cost of low-intensity exercise and enhances tolerance to high-intensity exercise in humans." Journal of Applied Physiology 107.4 (2009): 1144-1155.
• Hotta, Yuji, et al. "Oral l‐citrulline supplementation improves erectile function and penile structure in castrated rats." International Journal of Urology (2014).
• Larsen, Filip J., et al. "Dietary inorganic nitrate improves mitochondrial efficiency in humans." Cell metabolism 13.2 (2011): 149-159.
• Lundberg, Jon O., Eddie Weitzberg, and Mark T. Gladwin. "The nitrate–nitrite–nitric oxide pathway in physiology and therapeutics." Nature Reviews Drug Discovery 7.2 (2008): 156-167.
• Neuzillet, Y., et al. "A randomized, double‐blind, crossover, placebo‐controlled comparative clinical trial of arginine aspartate plus adenosine monophosphate for the intermittent treatment of male erectile dysfunction." Andrology 1.2 (2013): 223-228.

Does a (very) high fish oil diet entail the risk of going rancid - in spite of all its short-term health benefits?

Dont worry, I am not addressing the prostate cancer issue, again. In a way, I am still going to resume a discussion, you should be familiar with from my article "Sesame Powered High Omega-6 Diet Boosts Endurance Performance in Rodents - High Omega-3 Diet Sucks" | read more. Its the notion that the extensive incorporation of easily oxidizable (or already rancid) omega-3 fatty acids into metabolically highly active tissues, such as our musculature, will only be beneficial until a certain optimal threshold level is reached. Beyond this point, any further increase of the long-chain PUFA content becomes as problematic as the overabundance of other fatty acids.

This article is about balance!

By now, you should have realized that this post is all about balance, the critical balance of stable saturated and unstable (poly-)unsaturated fatty acids - not in your diet, but in cells & tissue.
Recent evidence of the importance of these numbers comes from a study that was conducted by researchers from the INRA UMR in Montpelier, France (Feillet-Coudray. 2013). It is, as you may have suspected, a rodent study. With a study duration of 12 weeks and the aspiration to investigate the long-term effects of diets containing 50 or 300 g lipid/kg  in the form of either lard or fish oil, this was yet more than a concession to financial constraints.

In the life of a rodent, three months are equivalent to several human years (some sources would say 5 years, but I would not bet on that). A similar study in man would thus take several years - years in the course of which all study participants would have to be locked away in a metabolic ward to ensure that they eat nothing but what the scientists serve them.

Figure 1: Total fatty acid (FA) composition of the LIVER and MUSCLE (mg FA/g tissue; Feillet-Coudray. 2013)

Against that background it is unlikely, but not impossible that we will see similar changes (see Figure 1) in the muscle and liver lipid levels of a human subject within only 3 months, even if he or she would reduce his or her overall fat intake to almost zero while upping the amount of fish oil in the diet into the 50g+ range. For 99% of the existing human studies this means that they are 100% irrelevant in view of the long (and if I write "long", I mean "long" like in years!) term high dose fish oil intakes and the corresponding changes in the fatty acid content and ratios of muscle, liver and other tissue.

No changes in muscle fatty acid make-up. How Come?

Apropos changes! If you look a the data in Figure 1 you will realize that the fatty acid make-up of the musculature in the study by Feillet-Coudray et al. did not change at all. In view of the significant changes in the fatty acid composition of the liver, this appears to be counter-intuitive and if we recall the study design and results of the previously cited study by Ayre et al. (1997) probably a result of the comparatively high omega-6:omega-3 ratio of the purported "fish oil" diet, which contained only 15g of omega-3 fatty acids per kg, and a whopping 21.7g of omega-6s. With an additional 25g of monounsaturated and 27.4g of saturated fats it is thus by no means an "omega-3", let alone "fish oil" diet as the one in the Airy study, which lead to major performance impairments in muscular endurance (and probably strength, which was yet not measured in the Ayre study | learn more).

Figure 2: Fatty acid composition of the test diets (Feillet-Coudray. 2013)

If you take a closer look at Figure 2 you will realize that - compared to the allegedly unhealthy lard diet" - the major difference is not, as people who still believe lard contained almost exclusively saturated fats could believe, the saturated-to-polyunsaturated fatty acid ratio, but simply the absence of significant amounts of omega-3 fatty acids in the mixed control and lard diets (one good reason to supplement a lard only diet with reasonable amounts of fish oil; e.g. 1g per day or 4g twice a week).

Not exactly representative of the contemporary diets, but still meaningful

From a scientific point of view the significant, but still small differences may be a limitation. From a practical point of view, the omega-3 : omega-6 ratios are however more realistic than those of a real fish oil only diet:

• CONTROL & LARD ~ 7:1 vs.  FISH ~ 3:2 
• SAD ~ 15:1 vs. HIGH N3 ~ 1:1 - 3:1

What they are not, however, is representative of the difference between the SAD (standard American) and a high omega-3 diet (HIGH N3).
As close as the FISH diet may be to the often hailed "optimal 1:1" ratio, the CONTROL and LARD diets both contain much more omega-3s / less omega-6s than the SAD diet. Against that background its actually quite astonishing that

Meta-Analysis Says: Fish Oil Does Not Help You Lean Out! Plus: Its Still Worth Having Fatty Fish 1-2x/Week | more

• all rats developed liver steatosis associated with moderate liver injury when fed the 30 % lipid diets
• the rats in both the CONTROL and FISH group did so without getting obese (only the rats "on" the 30% LARD diet became obese; 11% higher body weight, 32% more body fat)
• both FISH (+30%) and LARD (+103%) had elevated insulin levels compared to the rodents on the 30% CONTROL diet; despite higher insulin levels, the effective glucose uptake in the FISH group was normal, while it was already compromised in the LARD group

Its yet not all surprising and unexpected. The FISH diet did produce the expected improvements in total cholesterol and the HDL:LDL ratio. In spite of the -35% (vs. CONTROL; -47% vs. LARD) lower triglyceride levels, "[t]he fish-oil 30 % lipid diet failed to prevent the development of hepatic steatosis" (Feillet-Coudray. 2013) - an effect which may be mediated by concomitant increases in liver lipid oxidation, of which the researchers write that it

Additional Read: "Fish Oil Compromises, Fish Improves Adiponectin Levels in "Overweight, But Healthy" Individuals. Neither Promotes Weight or Fat Loss Within a 4-Week Study Period" | more.

"[...] was increased with the fish-oil diet in comparison with the mixed and the lard diets. Within the 5 % lipid diets, the liver TBARS level was increased by 22 % with the fish-oil diet compared with the mixed diet, whereas within the 30 % lipid diets, the liver TBARS level was increased by 104 % with the fish-oil diet compared with the mixed diet." (Feillet-Coudray. 2013)

It turned out that there was a direct correlation of pathological lipid oxidation and the amount of omega-3 fatty acids in the liver (p < 0·001; r = 0·319). Accordingly, the...

"glutathione peroxidase activity was decreased with the fish-oil 30 % lipid diet in comparison with the lard 30 % lipid diet" (Feillet-Coudray. 2013)

The answer to the the question I raised in the caption of the image in the title of this article, i.e. "Does a (very) high fish oil diet entail the risk of going rancid - in spite of all its short-term benefits?" is "Yes, it does!".
References:

• Ayre KJ, Hulbert AJ. Dietary fatty acid profile affects endurance in rats. Lipids. 1997 Dec;32(12):1265-70 (learn more) 
• Browning, Lucy M., et al. "Compared with Daily, Weekly n–3 PUFA Intake Affects the Incorporation of Eicosapentaenoic Acid and Docosahexaenoic Acid into Platelets and Mononuclear Cells in Humans." The Journal of nutrition (2014): jn-113.
• Feillet-Coudray C, Aoun M, Fouret G, Bonafos B, Ramos J, Casas F, Cristol JP, Coudray C. Effects of long-term administration of saturated and n-3 fatty acid-rich diets on lipid utilisation and oxidative stress in rat liver and muscle tissues. Br J Nutr. 2013 Nov;110(10):1789-802.