January 2016 Blog with Durk and Sandy

—Yogi Berra

—Jean Cocteau

—Robert Heinlein

—Ambrose Bierce

—Sandy (not a poet, just like to play with words)

(D&S Comment: Nothing has changed
other than the weapons technology.)

[D&S Comment:
A Good Fence makes a good neighbor,
And sure is worth the Labour!]

—Anon Y Mous

—Moshe Dayan

—Durk Pearson

(D&S Comment: The above is just a thought as we watch developments in Europe, while Putin is on the sidelines plotting to take advantage of it. Of course, Obama has been sold to the highest bidder (hint: not the U.S. taxpayers) and the European militaries will not be doing anything to interfere with a takeover of Europe by Islamic extremists demanding Sharia law. Meanwhile while our traitorous President wants to import hundreds of thousands of Islamic immigrants—just funded yesterday (12-17-15) by our helpful Congress—immigrants who will be thoroughly background checked,* avers Kerry. Think of this as hiring a thousand agents provocateur. Ever get the feeling that this is not a case of stupidity or ignorance, but of a plan to dismantle the America we were born in? Thank the Second Amendment activists for seeing to it that we have not been disarmed.)

—lost source

All in this paragraph was reported
in Wonkblog by Christopher Ingraham.

QUICKIES

Chen et al. Activation of TRPV1 channel by dietary capsaicin improves visceral fat remodeling through connexin43-mediated Ca2+ influx. Cardiovasc Diabetol.14:22 (2015).

The above paper discusses the stimulation by capsaicin (hot pepper) of the burning of fat by adipocytes in visceral fat. Niacin, a TRPV1 agonist, signals brown fat and other types of cells to use fat as a fuel rather than glucose, though we do not have a reference at hand that niacin signals such a switch in fuel use in adipocytes in the heart nor do we know whether capsaicin does that in the heart. This could be important as the heart is highly dependent on fat burning for the production of energy. See Virtue et al. A new role for lipocalin prostaglandin D synthase in the regulation of brown adipose tissue substrate utilization. Diabetes. 61:3139-47 (2012). Prostaglandin D synthase is activated by niacin during the niacin flush. For more, see Sandy Shaw’s niacin flush paper in the August, September, and October Life Enhancement website. Li et al. TRPV1 activation impedes foam cell formation by inducing autophagy in oxLDL-treated smooth muscle cells. Cell Death Dis. 5:e1182 (2014).

Foam cells are a major part of the atherosclerotic process. Here, the researchers used smooth muscle cells derived from mice. Capsaicin was used to activate TRPV1.

Suggestion: Take capsaicin capsules as a daily supplement

VITAMIN D3 promotes the recovery of amyloid beta clearance by phagocytes in ALZHEIMER’S DISEASE macrophages derived from human patients.

Reference

• Mizwicki et al. Genomic and nongenomic signaling induced by 1alpha,25(OH)2-vitamin D3 promotes the recovery of amyloid-beta phagocytosis by Alzheimer’s disease macrophages. J Alzheimer’s Dis. 29(1):51-62 (2012)

DAYDREAMS: NOREPINEPHRINE facilitates what is called “task unrelated thoughts” or (more commonly) daydreams.

Reference

• Smallwood et al. Insulation for daydreams: a role for tonic norepinephrine in the facilitation of internally guided thought. PLoS ONE. 7(4):e33706 (2012).

LYCOPENE—A CAROTENOID WITH POWERFUL ANTI-INFLAMMATORY POWERS

The data in a paper (Rafi, 2007) indicated potent anti-inflammatory effects of the carotenoid lycopene that, as part of a natural chemical pathway, inhibits COX. Via its two forms COX1 and COX2, COX converts arachidonic acid to inflammatory prostaglandins, such as the powerful inflammatory prostaglandin E2 (PGE2) (though under some conditions PGE2 can be anti-inflammatory). PGE2 is a known factor in virtually all inflammatory diseases, including cardiovascular disease, cancer, diabetes type 2, arthritis, inflammatory bowel disease, epilepsy, Alzheimer’s disease, and many others.

COX-1 is constitutively expressed, while COX-2 is an inducible enzyme that “mediates acute and chronic inflammation, pain, and cellular repair mechanisms.” (Rafi, 2007) The authors believe that the results of data from studies of lycopene “suggest that inhibition of COX2 may be effective in preventing infammatory-associated cancers.” (This suggestion, from 2007, was supported by later work.) The authors concluded: “Therefore, using lycopene or [lycopene-containing] tomato-based products to regulate the production of NO and COX-2 may be classified as a therapeutic approach for the treatment or prevention of chronic inflammatory disease.”

Sandy Gets Some Relief From The Pain Of Her Arthritic Knees With Lycopene

Unfortunately, Sandy has a moderate case of knee osteoarthritis. We had run out of lycopene and after a few days to a couple of weeks she had noticed more pain in her knees. The day she went back on lycopene (we both used 15 mg a day, though Sandy has upped hers to 30 mg a day now that she has felt the difference), she was aware of much more comfort in walking. The best way to take it is with the fattiest meal of the day, as it is absorbed best with fats.

It is also interesting that lycopene is another one of the natural products that inhibits formation of inflammatory prostaglandins. See (Shaw, 2015) “Why the Niacin Flush May Be Surprisingly Beneficial to Your Health” by Sandy Shaw for a discussion in Part I under the subheading “What Is the Niacin Flush? of inflammation and the prostaglandins that play such a major role in it, particularly PGE2 and PGD2. PGD2 is prostaglandin D2 that is released, causing the niacin flush, and which counters the effects of inflammatory PGE2 when released as a pulse, but there are many ways other than taking niacin to interfere with PGE2-induced inflammation. Lycopene is one such effective antiinflammatory nutrient.

Note that COX-2 inhibitors such as Celebrex are widely used for treating arthritis and, unlike the prescription COX-2 inhibiting drugs, there is no evidence that lycopene increases the risk of cardiovascular disease. Indeed, lycopene reduces the risk, possibly (at least in part) because of its powerful antioxidant activity.

Sandy Shaw (2015) paper, Part I, is found in the Life Enhancement website, www.life-enhancement.com, August 2015.

Reference

• Rafi, Yadav, Reyes. Lycopene inhibits LPS-induced proinflammatory mediator inducible nitric oxide synthase in mouse macrophage cells. J Food Sci.72(1):S69-S74 (2007).

NEUROGENESIS CAN BE OVERDONE JUST LIKE EXERCISE
IT IS INITIATED BY ELECTRICAL ACTIVATION OF NEURAL STEM CELLS, SAME TYPE OF ELECTRICAL ACTIVITY THAT TRIGGERS EPILEPTIC SEIZURES

Like any physiological process, there is a level at which too much neurogenesis can lead to adverse effects (Hsieh and Schneider, 2013). The effects of various levels of electrical activity on neurogenesis have been described (Hsieh and Schneider, 2013) as follows: “It may be that the neurogenesis response of stem progenitor cells to [electrical] activity is an adaptive mechanism to maintain regional homeostasis: increasing stem cell production when local circuitry activity levels are low, and restoring quiescence when activity levels are high.” The point here is that when activity levels are too high, you have electrical activation that becomes pathologically high as occurs during an epileptic seizure. As the authors go on to explain: “A potential ‘cost’ of excitable stem cells is inappropriate activation after pathological forms of activity, such as seizures.”

The authors also describe a possible excitation signal as follows: “A possible mechanism for excitation-neurogenesis coupling is GABA-mediated depolarization, previously described in mouse embryonic neuronal progenitor cells. Depolarization causes an increase in intracellular Ca2+ concentration similar to that evoked in cultured neural stem/progenitor cells. This excitation signal is relayed to the genome wherein the transcription factor NeuroD is rapidly activated to promote neurogenesis.” “…excitation signaling in the form of GABA is also necessary to drive the functional integration of newborn neurons.”

In another paper (Veyrac, 2013), the authors explain, “Newborn DGCs [dentate granule cells] are initially tonically activated by ambient depolarizing GABA….” Following hyperpolarization (by process that includes expression of glutamate receptors), “…they are hyperexcitable, display properties of ehanced synaptic plasticity, and are prone to integrate the existing hippocampal neurocircuitry.”

Importantly, the authors point out, “As their functional maturation progresses, however, newborn DGCs compete to survive, leaving the majority eliminated by cell death. Several behavioral manipulations, in particular hippocampal dependent learning, can regulate their rate of survival.” In this paper (Veyrac, 2013), the authors identify the Zif268/egr1 gene as controlling the selection, maturation, and functional integration of adult hippocampal newborn neurons by learning.”

Immediate Early Genes Are Transiently And Preferentially Induced In Newborn DGCs During Their Critical Period Of Maturation

Zif268/egr1 is one such immediate early gene and, as explained in the paper, actively controls the survival of newborn DGCs during their critical period of maturation in the first 2-3 weeks of their birth.”

The requirement for excitation during the early phase of newborn neuronal maturation may be a reason that the decline in arachidonic acid in cell membranes of the brain with aging is a negative factor in cognition (McGahon, 1997). Despite the fact that the metabolic products created by arachidonic acid are often involved in damage due to excessive inflammation, arachidonic acid is there for some reason(s) and this might be one of those reasons. Rice oil is relatively rich in arachidonic acid. Perhaps this is one reason that the Japanese who live in Japan, who consume a lot of rice and use rice oil in cooking, may live longer than those in other countries.

DHA Protects the Brain Against Inflammation

As we have written before, one way to protect the brain against arachidonic acid-associated inflammation is to take supplementary DHA, docosahexaenoic acid, as found in fish oils. (Basselin, 2012).

References

• Hsieh and Schneider. Neural stem cells, excited. Science. 339:1534-35 (2013).
• Veyrac, Gros, Bruel-Jungerman, et al. Zif268/egr1 gene controls the selection, maturation and functional integration of adult hippocampal newhorn neurons by learning. Proc Natl Acad Sci U S A. 110(17):7062-67 (2013).
• McGahon, Clements, Lynch. The ability of aged rats to sustain long-term potentiation is restored when the age-related decrease in membrane arachidonic acid concentration is reversed. Neuroscience. 81(1):9-16 (1997).
• Bresselin, Ramadan, Rapoport. Imaging brain signal transduction metabolism via arachidonic acid and docosahexaenoic acid in animals and humans. Brain Res Bull. 87(2-3):154-71 (2012).

LIVE LONGER AND ENJOY BETTER ORGASMS, TOO?

ORGASM: How the Brain Makes You Feel SOOOOO Good
by Sandy Shaw

HYPOTHESIS: ORGASM is like a small, self-limited epileptic seizure in terms of temporal electrical activity, that takes place in the “pleasure center” area of the brain and also in the lower part of the spinal cord. Feeling good is an important part of what makes life worth living and orgasms make you feel so good.

It is known that people experiencing epileptic seizures may also concurrently have orgasms. An early paper Sandy got after she hypothesized that orgasm might be a sort of small epileptic seizure provides support for that hypothesis (Heath, 1972). It is surprising how some of the oldest papers in a field provide information that has not been referred to in later papers. So, in researching how orgasm works, Sandy decided to look at the early stuff. The Heath, 1972 paper was useful, as was Gil-Vernet, 1994, which provided an amazingly detailed series of events that take place in the ejaculatory mechanisms accompanying orgasm (that include, for example, urethra, prostate, bladder neck, and so on), all via endorectal ultrasonography. Incredible work!

Interestingly, epilepsy has been very recently reported to be associated with activation of the TRPV1 receptor (Naziroglu, 2015), for which capsaicin (component of hot pepper) is an agonist. Anti-epileptic medications which reduce the sensitivity of the TRPV1 receptor to its agonists, tend to increase the difficulty of reaching orgasm. The TRPV1 receptor can also cause pain and itch and, it may not be coincidental that orgasm in some individuals can be enhanced by pain. “It is well known that neurogenic inflammation is associated with the activation of nociceptors [pain receptors] sensitive to capsaicin …” (Origoni, 2014, pg. 5).

The NIACIN FLUSH and the TRPV1 “Capsaicin” receptor—the connection to better orgasms

Durk has commented that he finds that experiencing the niacin flush while having an orgasm produces a stronger orgasm. (Sandy has noticed that, too.) Recently, niacin has been discovered to activate the TRPV1 receptor (Linlin, 2014) and this is thought by the researchers who made that discovery to be a part of the niacin flush of itching and increased cutaneous (skin) blood flow with the sensation of warmth. Incidentally, we find here the return of the inflammatory prostaglandin PGE2 and its counteractive antiinflammatory prostaglandin PGD2 in the pain activation at the irritant receptor TRPA1 (related to and interactive with TRPV1). The TRPA1 receptor is activated by pungent, warming spices, such as mustard, garlic, and cinnamon (Materazzi, 2008). As explained in Sandy Shaw’s paper on the niacin flush (see Life Enhancement website for August, September, and October 2015), the pulsatile release of PGD2 by immediate release (not extended release) niacin is the cause of the niacin flush. Niacin has been shown to activate, as part of the niacin flush, the TRPV1 receptor (as does capsaicin) (Linlin, 2014) and perhaps, like capsaicin, this activation could desensitize the TRPV1 receptors.

These anecdotal observations and very recent scientific discoveries are consistent with TRPV1 activation being part of orgasm.

It is known that, “Sexual experience promotes adult neurogenesis in the hippocampus despite an initial elevation in stress hormones,” as it says in the title of a paper by Leuner, Glasper, Gould, PLoS ONE July 2010. This is consistent with the increased neuronal excitation required for neurogenesis and, thus, neurogenesis and orgasm may be cousins in terms of electrical pathways. Now if only we could figure out how to generate orgasms at will and perhaps lengthen them (much too short, like life itself, don’t ya think?)

It may be that a simple way to increase the strength and/or length of orgasms is to activate the TRPV1 receptors at the time that you want to experience an orgasm. Hence, eating hot pepper, cinnamon, ginger, mustard, garlic, or other “hot” foods and spices just before you want to “come” might be just the ticket. In fact, “hot” foods and spices have long been thought to be aphrodisiac and the TRPV1 receptor activation may be a large part of why they appear to have sex enhancing effects. Hot Indian spices are indeed used in Tantric yoga sex ceremonies as we found when we were guinea pigs in studies of tantric sex by doctors Hartman and Fithian in the 1970s.

IN FACT, HOT FOODS AND SPICES
MAY HELP YOU LIVE LONGER

TRPV1 Regulates Longevity and Metabolic Health in Mice

Indeed, TRPV1 does a lot more than regulate pain and itch and (perhaps) orgasms. It has recently been found that TRPV1 knockout mice (mice that have no TRPV1 receptors, with the result looking as if their TRPV1 receptors are entirely desensitized) are exceptionally long-lived, “displaying a youthful metabolic profile at old age.” “These data suggest that ablation of select pain sensory receptors or the inhibition of CGRP [calcitonin gene-related peptide, which promotes neurogenic inflammation or antagonizes insulin release] are associated with increased metabolic health and control longevity” (Riera, 2014). This suggests that the niacin flush and the consumption of “hot” foods and spices may be beneficial to one’s health and longevity.

TRPA1: a Gatekeeper for Inflammation

TRPA1 has been described as a “gatekeeper of chronic inflammatory disorders of the skin, airways, and gastrointestinal tract” (Bautista, 2013).

It has been linked to diseases that include asthma, cough, inflammatory bowel disease, colitis, and many others (Bautista, 2013). Hence, consuming hot foods and spices that activate the TRPA1 receptor—including mustard, garlic, cinnamon, etc.—is a way to desensitize the TRPA1 receptor, which studies show to decrease inflammation in the skin, airways, and GI tract, and possibly to extend life and induce stronger orgasms. WOW! What more could you ask?

TRPV1 Desensitization Also Improves Cognitive Function

You might add to the list of potential benefits of TRPV1 desensitization that, “TRPV1 inactivation [via desensitization] also improves cognitive functions” (Steculorum, 2014). TRPV1 has been reported to be highly expressed in brain areas important in cognitive function including the cortex and hippocampus and to modulate hippocampal synaptic plasticity including long term potentiation (Mezey, 2000). A more recent paper reported that, in mouse brain slices, capsaicin-induced changes in long term potentiation (LTP, a learning/memory process) in the lateral amygdala were mediated by TRPV1 (Zschenderlein, 2011).

Sandy (and Durk) have both noticed a REALLY remarkable improvement in Sandy’s visuo-spatial capabilities since using TRPV1 desensitization agonists as adjunct treatments for her temporal lobe epilepsy. This is an anecdotal report, not PROOF that TRPV1 activation followed by desensitization can improve visuo-spatial capabilities. Incidentally, the downside of this improved cognition via TRPV1 was, for Sandy, a concurrent increase in irritability, as well as impatience, so if you are prone to outbursts of irritability, be careful, and if you aren’t but your best friend using these supplements is, you might also be careful. Depending on how sensitive an individual is to the TRP system, changes in dietary constituents that affect TRP channels could have a noticeable effect on personality. The effect might be considered desirable by friends, but also might be undesirable—depending on how you use the supplements.

CAUTIONARY NOTES FOR THE USE OF SUPPLEMENTS THAT ACTIVATE OR DESENSITIZE TRP CHANNELS:

1. 1. In using natural substances (spices and herbs) that activate the TRPV1 and/or TRPA1 receptors (which are part of a family of 28 different Transient Receptor Potential channels), you have to be very cautious as some individuals are much more sensitive to activation than others. Highly activated, TRPV1 (for example) can produce states of irritability and even rage that go beyond the energy-increasing levels that most people would find comfortable. Just consider how much variation there is in how sensitive people are to capsaicin (hot pepper) to give you an idea of what could happen to some that you might want to avoid. A minor example: Durk gets a bellyache when he takes capsaicin capsules on an empty stomach, whereas Sandy doesn’t.
   2. Some animals used in research (principally rodents, but also dogs and others) respond to TRPV1 and TRPA1 activation very differently than humans do. Hence, when you read a scientific paper that lists purported “agonists” for the TRP receptors, be aware that whether the agonists in the list are really agonists in humans depends critically on what animals were used in the research and DO NOT assume that humans will have a similar response. A good example is peppermint (a TRPA1 agonist); people like it, rodents hate it and stay away from it (making peppermint a useful rodent repellant). The animals may not like the sensations in their mouth or throat or possibly even how it makes them feel.
   3. It may be that what is called an “agonist” could be an “antagonist” and that the dosage is what makes the difference, so that anything called an “agonist” might be an “antagonist” depending on dose and you can’t necessarily expect the substance to be committed to being an “agonist” or “antagonist” because a research paper found it to be so under certain conditions.
   4. Indeed, whether a substance is an agonist or antagonist depends not only on the species in which the substance is tested, not only on the dosage used, but also on the time of the day, the stresses the animal (or human) is under at the time, and other factors that make it far from a simple proposition to determine what effect you are going to get. The tried and true careful self-experimentation, recording the conditions under which the experiment was conducted, is really the best we have at present for personal use. Simple noninvasive tests would be very helpful.

References

• Naziroglu. TRPV1 channel: a potential drug target for treating epilepsy. Curr Neuropharmacol. 13:239-47 (2015).
• Linlin, Lee, Mao, et al. Nicotinic acid activates the capsaicin receptor TRPV1—a potential mechanism for cutaneous flushing. Arterioscler Thromb Vasc Biol. 34(6):1272-80 (2014).
• Origino, Maggiore, et al. Neurobiological mechanisms of pelvic pain. Biomed Res Int. 903848. doi: 10.1155/2014/903848. (2014).
• Materazzi, Nassini, Andre, et al. COX-dependent fatty acid metabolites cause pain through activation of the irritant receptor TRPA1. Proc Natl Acad Sci U S A. 105(33):12045-50 (2008).
• Riera, Huising, Follett, et al “TRPV1 pain receptors regulate longevity and metabolism by neuropeptide signaling. Cell. 157:1023-36 (2014).
• Bautista, et al. TRPA1: a gatekeeper for inflammation. Annu Rev Physiol.75:181-200 (2013).
• Mezey, Toth, Cortright, et al. Distribution of mRNA for vanilloid receptor subtype 1 (VR1), and VR1-like immunoreactivity, in the central nervous system of the rat and human. Proc Natl Acad Sci U S A. 97:3655-60 (2000).
• Steculorum and Bruning. Die another day: a painless path to longevity. Cell. 157:1004-6 (2014).
• Gil-Vernet JM, et al. Ejaculation in men: a dynamic endorectal ultrasonographical study. Br J Urology. 73:442-8 (1994).
• Heath. Pleasure and brain activity in man. Deep and surface electroencephalograms during orgasm. J Nerv Ment Dis. 154(1):3-18 (1972).
• Zschenderlein et al. Capsaicin-induced changes in LTP in the lateral amygdala are mediated by TRPV1. PLoS ONE. 6(1):e16116 (2011).

 

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TRPV1 Sensitization May Be Part of Opiate (or Sex?) Withdrawal 
by Sandy Shaw

There is a scientific literature describing connection between opioids and TRPV1 receptors (Hakimizadeh, 2014). In this particular paper, it was reported that in rats, morphine reduced the expression of TRPV1 receptors in the amygdala but not in the hippocampus. The amygdala is an important brain center involved with, among other things, the emotion of fear. The researchers (Hakimizadeh, 2014) found that in morphine-dependent rats, there was a significant decrease in TRPV1 gene expression in the amygdala and that this suggests that, “TRPV1 receptors may be involved in morphine-induced dependence.”

Sex addiction might be an example of what happens when endogenous (or exogenous) opioids interact with TRPV1 receptors, but it is quite complex because, for one thing, there are 28 different known Transient Receptor Potential (TRP) channels, and these may interact with each other, with feedback effects and compensatory activity that complicates the interpretation of these interactions (Kaneko, 2014).

For those with deficient interest in sex (the so-called “hypoactive sexual desire disorder”), TRPV1 activators (capsaicin and ginger, for example) may be useful in jazzing up sexual interest. Perhaps that is a reason that ginger beer (real beer, not a soft drink) is so popular. Actually, the soft drink would work, too, but small amounts of alcohol boost the TRPV1 effect of the ginger.

References

• Hakimizadeh, et al. Morphine reduces expression of TRPV1 receptors in the amygdala but not in the hippocampus of male rats. Iran J Med Sci. 39(3):261-7 (2014).
• Kaneko and Szallasi. REVIEW: Transient receptor potential (TRP) channels: a clinical perspective. Br J Pharmacol. 171:2474-2507 (2014).

 

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COMING UP: perhaps in next Durk & Sandy newsletter:

TRPV1 And Drugs, Sex, (And Rock & Roll?)

Hmmmm. I wouldn’t be surprised if TRPV1 plays a role in rock & roll by being part of the system that, particularly in young men (but also some young women) puts the energy and the sexual drive into rock & roll that you don’t see too much in aging rock performers. Does this mean that old rock performers can be “rejuvenated” by TRPV1 agonists??? A fun thought for the future of rock & roll.

Also, as noted above (see section on TRPV1 improvement of cognition), this receptor may be involved with visuo-spatial abilities (only a hypothesis), as Sandy and Durk have noted in Sandy, who has sensitivity to TRPV1 receptors. If so, then here is another way that TRPV1 agonists might be beneficial to aging musicians.

RECIPE
SCINTILLIA’S HOLIDAY CHEESECAKE

Yummy and SO easy to make. Other than shopping for the ingredients, prep time is only about 10 minutes.

Nutritional benefits: 1. sweetened with erythritol, 2. the whipped topping is made of low fat, low sugar content chocolate mousse yogurt with live cultures. Erythritol is not only free of sucrose or sweeteners, both natural and synthetic, with various adverse effects, but it is a scavenger of damaging hydroxyl radicals. 3. Vanilla is a mild agonist to the TRPV1 receptor, while nutmeg in the quantities used for the cheesecake will give you, in a serving, a mild agonist dose to the TRPA1 receptor. Ever think of eating as a virtual chemistry book of ingredients and their effects? These days, it can seem a lot like that. Your taste buds won’t know the difference, though. It will all just taste wonderful to them.

Ingredients you’ll need:

• Canned pineapple slices in pineapple juice, six or seven slices

• 1 prepared graham cracker pie crust

• 1 pkg (8 oz) of cream cheese, softened

• Two or three 6 oz. servings of Yoplait whipped chocolate

• Mousse yogurt

• 2 teaspoons vanilla extract

• Powdered nutmeg

• 1⁄3 cup erythritol

TIP: You don’t need to bake the prepared pie crust, though the package wrapper is likely to suggest it if you want a “golden” crust. The flavor difference is not very much whether “golden” or not.

1. Use a hand mixer or whip to blend the softened cream cheese and vanilla in a small bowl.

2. Line the pie crust with the drained slices of pineapple.

3. Pour the cream cheese and vanilla mixture evenly over the pineapple slices.

4. Sprinkle nutmeg over the cream cheese/vanilla layer to your taste.

5. Gently spoon out the chocolate mousse yogurt over the cream cheese/vanilla until even, without pressing down on it (so as to avoid squeezing out the air whipped into the mousse).

6. That’s it! You cover your pie shell containing its fillings with the plastic cover that generally comes with the prepared pie crust and refrigerate for three hours. Then ENJOY!!