Treatment of edema by joy

In my last post I discussed the Romantic Love Diet. For those who lost weight via this method the following post is redundant. For the rest the post adds support to my over-riding concept that having lots of joy is vital to long term weight loss.

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Activation of PPAR-alpha peripherally helps relieve edema. (1) indicates that increasing brain palmitoylethanolamide (PEA) can activate PPAR-alpha peripherally.

(2) indicates that human fat cells produce PEA in quantity. Suggesting that as a person drops weight they produce less PEA and may become more prone to edema.

Egg yolk has the highest concentration of PEA in commonly eaten foods. However, very little, if any, PEA is absorbed from our diet. And what is absorbed does not normally make it into our brains. (Yes, I have links to support these statements.)

So what is a swollen girl to do? Have fun! And LOTS of it. (3) points out the role being engrossed in life and love has in elevating brain PEA.

Maintaining weight loss is very few people can do it since it naturally leads to depression due to lowering of PEA. Which is relieved by eating lots of junk food. For the less than 5% of dieters who do restrict calories long term they normally accumulate water weight - particularly if they are female. If depression can't get them then misery at not dropping weight due to water retention probably will. The fix for people who wish to maintain weight loss is to live a more joyful life.

1. J Pharmacol Exp Ther. 2007 Jun 12
Acute intracerebroventricular administration of palmitoylethanolamide, an endogenous PPAR-{alpha} agonist, modulates carrageenan-induced paw edema in mice.
D'Agostino G, La Rana G, Russo R, Sasso O, Iacono A, Esposito E, Mattace Raso G, Cuzzocrea S, Lo Verme J, Piomelli D, Meli R, Calignano A.
Dept Exp Pharmacol University Naples Federico II.
Peroxisome proliferator-activated receptor alpha (PPAR-alpha) is a nuclear transcription factor. Although the presence of this receptor in different areas of CNS has been reported, its role remains unclear. Palmitoylethanolamide (PEA), a member of the fatty-acid ethanolamide family, acts peripherally as an endogenous PPAR-alpha ligand, exerting analgesic and anti-inflammatory effects. High levels of PEA in the CNS have been found, but the specific function of this lipid remains to be clarified. Using carrageenan-induced paw edema in mice, here we show that i.c.v. administration of PEA may control peripheral inflammation through central PPAR-alpha activation. A single i.c.v. administration of PEA (0.01-1microg), 30 min before carrageenan injection, reduced edema formation in the mouse carrageenan test. This effect was mimicked by GW7647 (0.01-1microg), a synthetic PPAR-alpha agonist. Moreover, central PEA administration significantly reduced the expression of the proinflammatory enzymes COX-2 and iNOS and significantly restored carrageenan-induced PPAR-alpha reduction in the spinal cord. To investigate the mechanism by which i.c.v. PEA attenuated the development of carrageenan-induced paw edema, we evaluated IkB-alpha degradation and NF-kB p65 activation in the cytosolic or nuclear extracts from spinal cord tissue. PEA prevented IkB-alpha degradation and NF-kB nuclear translocation confirming the involvement of this transcriptional factor in the control of peripheral inflammation. The obligatory role of PPAR-alpha in mediating PEA's effects was confirmed by the lack of the compounds anti-inflammatory effects in mutant mice lacking PPAR-alpha. In conclusion, our data show for the first time that PPAR-alpha activation in the CNS can control peripheral inflammation.
PMID: 17565008

2. http://www.obesityresearch.org/cgi/content/abstract/15/4/837
Obesity 15:837-845 (2007)
...N-palmitoylethanolamine is the most abundant cannabimimetic compound produced by human adipocytes, and its levels are significantly down-regulated by leptin but not affected by adiponectin and PPAR- agonist ciglitazone. N-palmitoylethanolamine itself does not affect either leptin or adiponectin secretion or PPAR- protein expression in adipocytes.

Discussion: This study has led to the identification of human adipocytes as a new source of endocannabinoids and related compounds. The biological significance of these adipocyte cannabimimetic compounds and their potential implication in obesity should deserve further investigations.

3. http://www.nutraplanet.com/product/1057/pea.html
PEA is a naturally occurring substance found in such items as blue-green algae, salami, bologna, and of course, chocolate. In recent years, it has also become an extremely popular ingredient in numerous dietary supplements, ranging from weight loss products to ‘whole health’ products.

Often dubbed “The love molecule” PEA, is a compound naturally produced by the brain, is responsible for the feeling of experiences associated with pleasure and mental awareness. For example, when one is absorbed by an activity like painting, sculpting, or reading a fascinating book, when the world around seems suspended and nothing can disturb us, when worries vanish and hunger goes away, in such moments PEA is being produced by the brain. Likewise, PEA is released in the brain when one experiences the feelings of love and joy. For this reason, PEA has been coined “The love molecule.” When taken orally, PEA is known to readily cross the blood-brain barrier and become immediately available in the brain.

In the brain, PEA is believed to act by having a greater affinity for the re-uptake mechanism for dopamine in presynaptic vesicles. Therefore, when present in the brain, PEA is captured into the presynaptic vesicles and occupies the space normally taken by dopamine. This leads to an increase in free-circulating dopamine in the presynaptic terminal and a higher concentration of dopamine diffusing into the synaptic cleft, therefore enhancing dopaminergic transmission.

This ability to modulate dopaminergic transmission provides PEA with interesting properties in increasing concentration and elevating mood.

PEA has also been shown to enhance norepinephrine transmission in the brain. Norepinephrine is also involved in the experience of joy. Enhancing norepinephrine transmission in the brain increases the experience of joy and reduces appetite. For example, if an animal is implanted with an electrode in an area of the brain concentrated in norepinephrine, and this electrode is activated by a pedal that the animal has access to, the animal will disregard food and water and will press the pedal relentlessly until exhaustion to elicit an electrical impulse in this area of the brain.

Finally, PEA also carries another interesting benefit. As mentioned before, PEA is produced by the brain when one is fully absorbed into an activity like painting, sculpting or reading a fascinating book. At such a time, the world seems to disappear around us, and we are no longer hungry. This phenomenon is not an anorectic effect in which hunger completely disappears but happens because our attention is taken away from the feeling of hunger. In this manner, PEA acts as an appetite suppressant. Therefore, through its ability to reduce appetite, PEA is an effective supplement to be taken as part of a comprehensive weight-loss program.


Nerissa

Artificial sweeteners induce weight gain

Studies on people who drink diet sodas shows that "something" in diet sodas induces these people to gain weight (1).

The "something" is the artificial sweeteners that are in the diet drinks. These stimulate alpha-gustducin (2). This is a taste receptor that allows us to taste sweetness. It is in our intestine in addition to on our tongue.

In our intestine, once stimulated, it increases sugar absorption. Artificial sweeteners may stimulate it more than actual sugar or conversely may not increase the compensatory normal elevation in glucagon-like peptide-1 (not in the literature so just a guess by me). Meaning when we use artificial sweeteners we often end up absorbing more sugar and more calories. Result = a tendency to gain weight.

This same effect should happen whether the artificial sweetener is in diet drinks or anything else we consume. Acesulfame K (acesulfame potassium or K) and Splenda (sucralose) are particularly bad in this regard.

1. http://www.cbsnews.com/stories/2005/06/13/health/webmd/main701408.shtml Diet Soda Drinkers Gain Weight Overweight Risk Soars 41 Percent With Each Daily Can Of Diet Soda J
June 13, 2005 (WebMD)
People who drink diet soft drinks don't lose weight. In fact, they gain weight, a new study shows.

The findings come from eight years of data collected by Sharon P. Fowler...

For regular soft-drink drinkers, the risk of becoming overweight or obese was:

26 percent for up to 1/2 can each day
30.4 percent for 1/2 to one can each day
32.8 percent for 1 to 2 cans each day
47.2 percent for more than 2 cans each day.

For diet soft-drink drinkers, the risk of becoming overweight or obese was:

36.5 percent for up to 1/2 can each day
37.5 percent for 1/2 to one can each day
54.5 percent for 1 to 2 cans each day
57.1 percent for more than 2 cans each day.

...something linked to diet soda drinking is also linked to obesity. ...

2. J Physiol. 2007 Jul 1;582(Pt 1):379-92
Sweet taste receptors in rat small intestine stimulate glucose absorption through apical GLUT2.
Mace OJ...

Sweet taste receptors in rat small intestine stimulate glucose absorption through apical GLUT2. Natural sugars and artificial sweeteners are sensed by receptors in taste buds. ...

Intestinal brush cells or solitary chemosensory cells (SCCs) have a structure similar to lingual taste cells and strongly express alpha-gustducin. ...

Artificial sweeteners increase glucose absorption in the order acesulfame potassium approximately sucralose > saccharin...artificial sweeteners are nutritionally active, because they can signal to a functional taste reception system to increase sugar absorption during a meal...
PMID: 17495045

Nerissa

calorie restriction and leaky gut syndrome

Every time my weight drops into the range I desire I develop leaky gut syndrome. Which means I feel like dog meat until I regularly eat more. This has lead to an endless cycle of dropping weight, feeling bad, regaining weight...

Least you think I'm some anorexic nut case my BMI fluctuates around about 24 +/- 1. I want to get down to about BMI 21 to 22 which still is safely out of the "please hold me down and stuff food into my mouth" anorexic range.

Why does calorie restriction (CR) trash our guts out? Two reasons:

First, CR elevates the so-called anti-inflammatory hormone adiponectin. High adiponectin is a really good thing for our health per many references. Unfortunately, adiponectin is PROinflammatory in our gut (1).

Second, CR lowers insulin. In many ways this is great for our health. Unfortunately, low insulin is associated with INCREASED gut permeability (2).

Surf the net and you can find many ideas for dealing with leaky gut. A treatment I've come up with is the following:

Combine a scoop of Citrucel (methylcellulose) with 1/2 glass of lemonade, 400 mg of magnesium citrate and a tablespoon of coconut oil and drink it just prior to bedtime. The methylcellulose binds most pathological bacteria (via binding to their type 4 fimbriae; PMID: 9811650), the lemonade has anti-inflammatory properties, the magnesium lowers permeability of the intestine (PMID: 16180088) and the coconut oil is great for killing various pathological bacteria (too many references to list).

1. Gastroenterology. 2007 Feb;132(2):601-14
Adiponectin deficiency protects mice from chemically induced colonic inflammation.
...APN deficiency is associated with protection from chemically induced colitis. APN exerts proinflammatory activities in the colon by inducing production of proinflammatory cytokines and inhibiting bioactivity of protective growth factors. Thus, in colitis, APN exerts an opposite role compared with atherosclerosis.
PMID: 17258715

2. Clin Hemorheol Microcirc. 2006;34(1-2):259-63
Permeability response of the rat mesenteric microvasculature to insulin.
...insulin reduces mesenteric venule permeability differently in males and females. Further studies are needed to differentiate the permeability responses with respect to age and gender.
PMID: 16543645

Nerissa