Sponsored by

PuffItUp Dynavap VGoodiez 420EDC
  • Welcome to VaporAsylum! Please take a moment to read our RULES and introduce yourself here.
  • Need help navigating the forum? Find out how to use our features here.
  • Did you know we have lots of smilies for you to use?

Tips Lecithin

momofthegoons

Vapor Accessory Addict
Staff member
How Adding Lecithin Affects Your Cannabis Edibles

Many patients make their own edibles these days for a few reasons. It is much more cost effective for those on a tight budget as it makes your medicine go further. Many vape their cannabis bud and then use the by product in edibles. While the second use is not as potent, it can still provide medicinal benefits. Another reason to make your own edibles is to have control over what ingredients they contain. The majority of packaged edibles are sweet. For those who prefer a savory edible or are diabetic and need to monitor their sugar intake, making your own edible is your best option. Lastly, you can choose the strain, dosage of cannabis and delivery method to create your unique edible. You know exactly how much cannabis you are using and you can gauge the portion size that works best for your needs. This brings us to the focus of this article;

How Adding Lecithin Affects Your Cannabis Edibles

What is lecithin? It is an emulsifier, a substance that helps ingredients bind together. But it is also a phospholipid emulsifier. A phospholid is a fat molecule which makes up cell membranes. Its function is to act as a barrier so that the emulsified product stays stable for a long time. The reason that lecithin makes such a good emulsifier is that it is suited to combining oil in water AND water in oil. Water and fats typically repel each other. Lecithin helps keep them consistently dispersed and bound together so that it facilitates a more even distribution of cannabis in your edible product. This will increase the likelihood that each portion contains about the same dosage of cannabis.

More importantly, lecithin improves bioavailability which is the degree and rate that the body can absorb and process the cannabinoids. You receive more medicinal benefits from the cannabinoids without increasing the amount of cannabis you use. Lecithin minimizes the long acting effect edibles have by allowing a faster absorption. More THC will be metabolized by the body, making the psychotropic effects more intense. If you are interested in a more prolonged and gradual experience, do not use lecithin.

Sources of Lecithin…the good and the not so good

Let’s start with the lecithin that is very common but is NOT recommended; soy lecithin. It is considered lower quality and is highly processed, using the extraction process of hexane or acetone solvents. Another reason to avoid it is that soy can be pro-inflammatory and mimic estrogen.

The recommended sources are sunflower lecithin, egg yolks (unless you are vegan) and chocolate

Sunflower lecithin is highly recommended. It is cold pressed, similar to olive oil in its processing, raw and chemical-free of harsh solvents. You can purchase it in liquid, granule or powdered form.
Eggs yolks are a good emulsifier. They do an adequate job of keeping fats and water based ingredients together.
Most chocolate contains lecithin, but not as much as eggs or sunflower lecithin. This explains why chocolate cannabis brownies have been a mainstay of edibles for so many decades.
Both eggs and sunflower lecithin contain choline, a vitamin-like, water soluble essential nutrient. It is very important for liver function, normal brain development, nerve function, muscle movement, supporting energy levels and maintaining a healthy metabolism. Many Americans are not getting enough choline in their diets. Who knew? So, not only does lecithin make your edible more potent and beneficial, it also provides an essential nutrient that you were probably lacking.

All you need is one teaspoon of lecithin per cup to increase the binding of THC-infused coconut oil to your water based brownie batter. Make sure that all liquids are warm enough to stay liquid. This is particularly important when mixing infused cannabis oil with eggs and water when baking. Once you add your dry goods, mix with a “fold and press” motion. Then, mix again. You can also use a blender at high-speed in order to increase its emulsion properties. Lecithin also increases the shelf life of your edibles by preventing the separation of fats and water. There is less chance of the development of molds and mildews if you keep your edibles for any length of time. Anyone for Alice B. Toklas brownies?
 

Shredder

Dogs like me
How Adding Lecithin Affects Your Cannabis Edibles

Many patients make their own edibles these days for a few reasons. It is much more cost effective for those on a tight budget as it makes your medicine go further. Many vape their cannabis bud and then use the by product in edibles. While the second use is not as potent, it can still provide medicinal benefits. Another reason to make your own edibles is to have control over what ingredients they contain. The majority of packaged edibles are sweet. For those who prefer a savory edible or are diabetic and need to monitor their sugar intake, making your own edible is your best option. Lastly, you can choose the strain, dosage of cannabis and delivery method to create your unique edible. You know exactly how much cannabis you are using and you can gauge the portion size that works best for your needs. This brings us to the focus of this article;

How Adding Lecithin Affects Your Cannabis Edibles

What is lecithin? It is an emulsifier, a substance that helps ingredients bind together. But it is also a phospholipid emulsifier. A phospholid is a fat molecule which makes up cell membranes. Its function is to act as a barrier so that the emulsified product stays stable for a long time. The reason that lecithin makes such a good emulsifier is that it is suited to combining oil in water AND water in oil. Water and fats typically repel each other. Lecithin helps keep them consistently dispersed and bound together so that it facilitates a more even distribution of cannabis in your edible product. This will increase the likelihood that each portion contains about the same dosage of cannabis.

More importantly, lecithin improves bioavailability which is the degree and rate that the body can absorb and process the cannabinoids. You receive more medicinal benefits from the cannabinoids without increasing the amount of cannabis you use. Lecithin minimizes the long acting effect edibles have by allowing a faster absorption. More THC will be metabolized by the body, making the psychotropic effects more intense. If you are interested in a more prolonged and gradual experience, do not use lecithin.

Sources of Lecithin…the good and the not so good

Let’s start with the lecithin that is very common but is NOT recommended; soy lecithin. It is considered lower quality and is highly processed, using the extraction process of hexane or acetone solvents. Another reason to avoid it is that soy can be pro-inflammatory and mimic estrogen.

The recommended sources are sunflower lecithin, egg yolks (unless you are vegan) and chocolate

Sunflower lecithin is highly recommended. It is cold pressed, similar to olive oil in its processing, raw and chemical-free of harsh solvents. You can purchase it in liquid, granule or powdered form.
Eggs yolks are a good emulsifier. They do an adequate job of keeping fats and water based ingredients together.
Most chocolate contains lecithin, but not as much as eggs or sunflower lecithin. This explains why chocolate cannabis brownies have been a mainstay of edibles for so many decades.
Both eggs and sunflower lecithin contain choline, a vitamin-like, water soluble essential nutrient. It is very important for liver function, normal brain development, nerve function, muscle movement, supporting energy levels and maintaining a healthy metabolism. Many Americans are not getting enough choline in their diets. Who knew? So, not only does lecithin make your edible more potent and beneficial, it also provides an essential nutrient that you were probably lacking.

All you need is one teaspoon of lecithin per cup to increase the binding of THC-infused coconut oil to your water based brownie batter. Make sure that all liquids are warm enough to stay liquid. This is particularly important when mixing infused cannabis oil with eggs and water when baking. Once you add your dry goods, mix with a “fold and press” motion. Then, mix again. You can also use a blender at high-speed in order to increase its emulsion properties. Lecithin also increases the shelf life of your edibles by preventing the separation of fats and water. There is less chance of the development of molds and mildews if you keep your edibles for any length of time. Anyone for Alice B. Toklas brownies?

Thanks for posting this. I never knew sunflower lecithin was better than soy lecithin. I've been using soy lecithin for years, but ordered powdered sunflower lecithin today.

For anyone who never used lecithin, it really does make a difference.

I use it at 1/2 tsp per fluid oz of coconut oil for cannacaps. A little more than the article suggested. (1tsp per cup)

I melt it in the coconut oil until the oil is clear. Then when I add concentrates they mix better than without. After concentrates are added I stir again on a coffee warmer untill it's clear.
 

momofthegoons

Vapor Accessory Addict
Staff member
They've touted the benefits of using lecithin in edibles over at the Magical Butter United Facebook group for years. And that's where I found out about sunflower lecithin being better for you than soy.

I've also noticed a difference when it's added to an edible recipe. You'll still see benefits if you don't use it, but the addition does increase potency a bit.

Never thought of putting it in cannacaps before. Thanks back for that. :biggrin:
 

momofthegoons

Vapor Accessory Addict
Staff member
If you are on the fence about using lecithin in your edibles, here's some information that might dissuade you...

The Dark Side of Lecithin Supplements

There is no credible evidence to support the myriad claims of benefit of lecithin supplements, but finding lecithin metabolites in the blood of heart attack and stroke patients raises a safety concern.


Lecithin supplements have been heavily promoted as a panacea for:

  • Cardiovascular health
  • Liver and cell function
  • Fat transport and fat metabolism
  • Reproduction and child development
  • Physical performance and muscle function
  • Cell communication
  • Improvement in memory, learning, and reaction time
  • Relief of arthritis
  • Healthy hair and skin
  • Treatment for gallstones
I have always been suspicious of promotions that promise to cure all human ailments. But recently, I came across a paper that prompted me to examine the evidence behind those claims. I’ll save you an excruciatingly detailed account—none of the claims have any credible evidence to back it up. There is one possible exception. Lecithin is a natural emulsifier, so claims that it dissolves gallstones may be credible, except that I haven’t come across a good study documenting it. WebMD gives lecithin treatment of gallstones an unenthusiastic “recommendation” of possibly ineffective.



What is lecithin?
Chemically, lecithin is called phosphatidylcholine. It is found in egg yolk, meats, soy, and vegetables. Most commercial lecithin is made from soy. So, you’d assume that when you take lecithin supplements, you get phosphatidylcholine. In fact, as is the case with many nutritional supplements, commercial preparations vary widely (between 20% to 90%) in the amount the substance is actually in their product.


Why such variability? Because the suppliers of supplements were exempted by Congress from adhering to any standards of manufacture, purity, or claims of benefits. How this came about is emblematic of our broken political system, but don’t get me going on this.

Anyway, if only a fraction of commercial lecithin is made up of the real thing—phosphatidylcholine—then what makes up the rest? The answer: fatty acids! Not exactly the stuff to help in weight reduction, cardiovascular health, or liver function. In fact, it may work against all those potentially wonderful benefits.



What’s the downside of lecithin supplements?
If they don’t cause any harm, why not give it the benefit of the doubt? A future study may prove its benefit.


In a paper in Nature, Wang et al. of the Cleveland Clinic studied the metabolic fate of lecithin. But first, by way of explanation, let me introduce a new term. We are all familiar with the concept of genomics, meaning the study of the genome, or the total genetic content and its effect on health and disease. Similarly, the total of chemicals, substrates, and metabolites in the body is called the metabolome, and the study of those substances in health and disease is called metabolomics. The advantage of such an all-inclusive approach is that it is unbiased.

The classical scientific approach is to study a specific gene or molecule, essentially ignoring everything else. This is akin to peeping through a keyhole; you see only what the hole allows you to see. On the other hand, studying the whole genome or the whole metabolome gives a complete picture of everything that is involved in the process being studied.

For instance, for many years, type 2 diabetes was thought to involve only one or two genes. Why? Because these were the only genes that “made sense” as targets for study. The advent of whole-genome studies demonstrated the involvement of dozens of genes in the disease, which was a complete surprise.

Back to the paper. Wang and his collaborators used the metabolomic approach to look for circulating small molecules associated with coronary heart disease. They screened blood from patients who had experienced a heart attack or stroke and compared the results with those from the blood of people who had not. They found major differences in choline, betaine, and trimethylamine (TMA). It turns out that these metabolites are produced from lecithin by gut bacteria and converted to trimethylamine-N-oxide (TMAO). This terminal metabolite, TMAO, is a known atherogenic (involved in atherosclerotic plaque formation).

Indeed, when the gut flora was wiped out with an antibiotic, none of the metabolites appeared in the blood. Could it be that the gut flora in people with cardiovascular disease is different in some way from that of healthy people? We don’t know, but we do know that the physiological state of a person can determine the gut flora. For instance, the gut flora of obese people is markedly different from that of the non-obese.


Based on this study alone, we still can’t tell if these lecithin metabolites are causative factors, or whether they are just markers of the disease. Correlative studies can show only correlations, not cause and effect.



Wait, wait, there’s more
Is lecithin the only culprit that produces TMAO? Red meat contains another triethylamine, similar to choline and lecithin, called L-Carnitine, which should be metabolized by the gut flora into MAO and then converted to TMAO in the circulation. So the same Cleveland Clinic group examined the production of TMAO by omnivores, vegans, and vegetarians following ingestion of L-carnitine. Indeed, the omnivorous humans had higher levels of circulating TMAO. The reason? Meat eaters have gut bacterial flora different than vegetarians and vegans. It contains species that feast on triethylamines: choline, lecithin, and carnitine.

Now let’s look at an interesting study published in the prestigious New England Journal of Medicine by Tang and colleague. It was conducted in two phases. In the first phase, the investigators gave healthy participants a phosphatidylcholine challenge using a stable isotope-labeled form of the phospholipid. They then used mass spectrometry to monitor choline metabolites before and after the suppression of gut microbiota with broad-spectrum antibiotics.

They found that the phosphatidylcholine challenge increased all choline metabolites but that antibiotics suppressed the generation of TMAO, which reappeared when antibiotics were withdrawn. In the second phase, they examined the relationship between fasting plasma TMAO levels and incident cardiovascular events over a 3-year period in more than 4,000 participants undergoing elective coronary angiography. They found an independent, dose-dependent relationship between the metabolite and the risk of a cardiovascular event on the basis of the TMAO quartile: The highest quartile had 2.54 times the risk over the lowest quartile.



The bottom line
Here is what we know about lecithin:

  • The phospholipid phosphatidylcholine (lecithin) is the major dietary source of choline, a semi-essential nutrient that is part of the B-complex vitamin family. Choline has various metabolic roles, ranging from its essential involvement in lipid metabolism and cell-membrane structure to its role as a precursor for the synthesis of the neurotransmitter acetylcholine.
  • Red meat, processed meat, pork, and egg yolk contain high levels of lecithin.
  • Phosphatidylcholine (lecithin) is metabolized by gut flora into three metabolites that show up at high concentrations in people who have had a heart attack or a stroke. We metabolize those bacterial metabolites into TMAO, a known atherogenic.
  • A large 4,000-patient study over 3 years showed a significant correlation between TMAO levels and cardiac events and stroke.
Still, although highly suggestive, none of these studies have demonstrated a direct effect of lecithin, or its metabolite TMAO, as a cause of atherosclerosis.



So, how does one make a decision whether to take lecithin supplements?
Since the lecithin metabolite, TMAO, is a known atherogenic, I believe that until we better understand whether it actually causes atherosclerosis, the prudent approach would call for moderation and limiting your intake of these foodstuffs with high levels of lecithin. Further, since there is no credible evidence supporting claims of health benefits, there is no reason to take high doses of lecithin in the form of nutritional supplements. If you do choose to take them, you could be increasing your risk of a heart attack or stroke in exchange for no known benefit.


And this question; posted to consumerlab.com:

Question:
Is there a danger in taking lecithin or phosphatidylcholine? I heard that they may increase the risk of heart attacks.

Answer:
Although a direct link to heart attack has not been made, researchers recently showed that intake of phosphatidylcholine, a major component of lecithin, temporarily raises blood levels of the compound TMAO. This is of concern because a 3-year study by the same researchers showed that people with the highest blood plasma levels of TMAO -- above 6 µM (micromoles) -- were 2.5 times as likely as those with the lowest levels (under 2.5 µM) to suffer a heart attack or other major adverse cardiovascular event (Tang, New Eng J Med 2013). TMAO is produced from the choline in phosphatidylcholine by the actions of microbes in the gut and enzymes in the liver. TMAO appears to advance atherosclerosis (hardening of the arteries) by reducing the normal clearing of cholesterol.
The researchers showed that eating two hard-boiled eggs (which contain about 500 mg of total choline) temporarily raised TMAO blood plasma levels, on average, from about 4 µM (micromoles) to close to 8 µM.

The data suggest that excessive routine consumption of dietary phosphatidylcholine and choline should be avoided. This may be advisable anyhow, as foods rich in these compounds (egg yolk, liver, beef, and pork) are also typically high in fat and cholesterol. The researchers note that a vegetarian or high-fiber diet can reduce total choline intake. Unless medically necessary, it may also be prudent to avoid long-term supplementation with high doses of lecithin, phosphatidylcholine, and/or choline.

(A similar connection with TMAO and cardiovascular disease risk was recently made by the same researchers for L-carnitine from red meat and, possibly, from supplements with L-carnitine, including acetyl-L-carnitine -- see the Concerns and Cautions section of the Acetyl-L-Carnitine Supplements Review>>).

 

Shredder

Dogs like me
If you are on the fence about using lecithin in your edibles, here's some information that might dissuade you...

The Dark Side of Lecithin Supplements

There is no credible evidence to support the myriad claims of benefit of lecithin supplements, but finding lecithin metabolites in the blood of heart attack and stroke patients raises a safety concern.


Lecithin supplements have been heavily promoted as a panacea for:




    • Cardiovascular health
    • Liver and cell function
    • Fat transport and fat metabolism
    • Reproduction and child development
    • Physical performance and muscle function
    • Cell communication
    • Improvement in memory, learning, and reaction time
    • Relief of arthritis
    • Healthy hair and skin
    • Treatment for gallstones
I have always been suspicious of promotions that promise to cure all human ailments. But recently, I came across a paper that prompted me to examine the evidence behind those claims. I’ll save you an excruciatingly detailed account—none of the claims have any credible evidence to back it up. There is one possible exception. Lecithin is a natural emulsifier, so claims that it dissolves gallstones may be credible, except that I haven’t come across a good study documenting it. WebMD gives lecithin treatment of gallstones an unenthusiastic “recommendation” of possibly ineffective.



What is lecithin?
Chemically, lecithin is called phosphatidylcholine. It is found in egg yolk, meats, soy, and vegetables. Most commercial lecithin is made from soy. So, you’d assume that when you take lecithin supplements, you get phosphatidylcholine. In fact, as is the case with many nutritional supplements, commercial preparations vary widely (between 20% to 90%) in the amount the substance is actually in their product.


Why such variability? Because the suppliers of supplements were exempted by Congress from adhering to any standards of manufacture, purity, or claims of benefits. How this came about is emblematic of our broken political system, but don’t get me going on this.

Anyway, if only a fraction of commercial lecithin is made up of the real thing—phosphatidylcholine—then what makes up the rest? The answer: fatty acids! Not exactly the stuff to help in weight reduction, cardiovascular health, or liver function. In fact, it may work against all those potentially wonderful benefits.



What’s the downside of lecithin supplements?
If they don’t cause any harm, why not give it the benefit of the doubt? A future study may prove its benefit.


In a paper in Nature, Wang et al. of the Cleveland Clinic studied the metabolic fate of lecithin. But first, by way of explanation, let me introduce a new term. We are all familiar with the concept of genomics, meaning the study of the genome, or the total genetic content and its effect on health and disease. Similarly, the total of chemicals, substrates, and metabolites in the body is called the metabolome, and the study of those substances in health and disease is called metabolomics. The advantage of such an all-inclusive approach is that it is unbiased.

The classical scientific approach is to study a specific gene or molecule, essentially ignoring everything else. This is akin to peeping through a keyhole; you see only what the hole allows you to see. On the other hand, studying the whole genome or the whole metabolome gives a complete picture of everything that is involved in the process being studied.

For instance, for many years, type 2 diabetes was thought to involve only one or two genes. Why? Because these were the only genes that “made sense” as targets for study. The advent of whole-genome studies demonstrated the involvement of dozens of genes in the disease, which was a complete surprise.

Back to the paper. Wang and his collaborators used the metabolomic approach to look for circulating small molecules associated with coronary heart disease. They screened blood from patients who had experienced a heart attack or stroke and compared the results with those from the blood of people who had not. They found major differences in choline, betaine, and trimethylamine (TMA). It turns out that these metabolites are produced from lecithin by gut bacteria and converted to trimethylamine-N-oxide (TMAO). This terminal metabolite, TMAO, is a known atherogenic (involved in atherosclerotic plaque formation).

Indeed, when the gut flora was wiped out with an antibiotic, none of the metabolites appeared in the blood. Could it be that the gut flora in people with cardiovascular disease is different in some way from that of healthy people? We don’t know, but we do know that the physiological state of a person can determine the gut flora. For instance, the gut flora of obese people is markedly different from that of the non-obese.


Based on this study alone, we still can’t tell if these lecithin metabolites are causative factors, or whether they are just markers of the disease. Correlative studies can show only correlations, not cause and effect.



Wait, wait, there’s more
Is lecithin the only culprit that produces TMAO? Red meat contains another triethylamine, similar to choline and lecithin, called L-Carnitine, which should be metabolized by the gut flora into MAO and then converted to TMAO in the circulation. So the same Cleveland Clinic group examined the production of TMAO by omnivores, vegans, and vegetarians following ingestion of L-carnitine. Indeed, the omnivorous humans had higher levels of circulating TMAO. The reason? Meat eaters have gut bacterial flora different than vegetarians and vegans. It contains species that feast on triethylamines: choline, lecithin, and carnitine.

Now let’s look at an interesting study published in the prestigious New England Journal of Medicine by Tang and colleague. It was conducted in two phases. In the first phase, the investigators gave healthy participants a phosphatidylcholine challenge using a stable isotope-labeled form of the phospholipid. They then used mass spectrometry to monitor choline metabolites before and after the suppression of gut microbiota with broad-spectrum antibiotics.

They found that the phosphatidylcholine challenge increased all choline metabolites but that antibiotics suppressed the generation of TMAO, which reappeared when antibiotics were withdrawn. In the second phase, they examined the relationship between fasting plasma TMAO levels and incident cardiovascular events over a 3-year period in more than 4,000 participants undergoing elective coronary angiography. They found an independent, dose-dependent relationship between the metabolite and the risk of a cardiovascular event on the basis of the TMAO quartile: The highest quartile had 2.54 times the risk over the lowest quartile.



The bottom line
Here is what we know about lecithin:




    • The phospholipid phosphatidylcholine (lecithin) is the major dietary source of choline, a semi-essential nutrient that is part of the B-complex vitamin family. Choline has various metabolic roles, ranging from its essential involvement in lipid metabolism and cell-membrane structure to its role as a precursor for the synthesis of the neurotransmitter acetylcholine.
    • Red meat, processed meat, pork, and egg yolk contain high levels of lecithin.
    • Phosphatidylcholine (lecithin) is metabolized by gut flora into three metabolites that show up at high concentrations in people who have had a heart attack or a stroke. We metabolize those bacterial metabolites into TMAO, a known atherogenic.
    • A large 4,000-patient study over 3 years showed a significant correlation between TMAO levels and cardiac events and stroke.
Still, although highly suggestive, none of these studies have demonstrated a direct effect of lecithin, or its metabolite TMAO, as a cause of atherosclerosis.



So, how does one make a decision whether to take lecithin supplements?
Since the lecithin metabolite, TMAO, is a known atherogenic, I believe that until we better understand whether it actually causes atherosclerosis, the prudent approach would call for moderation and limiting your intake of these foodstuffs with high levels of lecithin. Further, since there is no credible evidence supporting claims of health benefits, there is no reason to take high doses of lecithin in the form of nutritional supplements. If you do choose to take them, you could be increasing your risk of a heart attack or stroke in exchange for no known benefit.


And this question; posted to consumerlab.com:

Question:
Is there a danger in taking lecithin or phosphatidylcholine? I heard that they may increase the risk of heart attacks.

Answer:
Although a direct link to heart attack has not been made, researchers recently showed that intake of phosphatidylcholine, a major component of lecithin, temporarily raises blood levels of the compound TMAO. This is of concern because a 3-year study by the same researchers showed that people with the highest blood plasma levels of TMAO -- above 6 µM (micromoles) -- were 2.5 times as likely as those with the lowest levels (under 2.5 µM) to suffer a heart attack or other major adverse cardiovascular event (Tang, New Eng J Med 2013). TMAO is produced from the choline in phosphatidylcholine by the actions of microbes in the gut and enzymes in the liver. TMAO appears to advance atherosclerosis (hardening of the arteries) by reducing the normal clearing of cholesterol.
The researchers showed that eating two hard-boiled eggs (which contain about 500 mg of total choline) temporarily raised TMAO blood plasma levels, on average, from about 4 µM (micromoles) to close to 8 µM.

The data suggest that excessive routine consumption of dietary phosphatidylcholine and choline should be avoided. This may be advisable anyhow, as foods rich in these compounds (egg yolk, liver, beef, and pork) are also typically high in fat and cholesterol. The researchers note that a vegetarian or high-fiber diet can reduce total choline intake. Unless medically necessary, it may also be prudent to avoid long-term supplementation with high doses of lecithin, phosphatidylcholine, and/or choline.

(A similar connection with TMAO and cardiovascular disease risk was recently made by the same researchers for L-carnitine from red meat and, possibly, from supplements with L-carnitine, including acetyl-L-carnitine -- see the Concerns and Cautions section of the Acetyl-L-Carnitine Supplements Review>>).

Two things, one our bodies make lecithin so the source of lecithin in heart attack victims is far from proven. Second, although not addressed in the article, we use fairly small amounts of both lecithin and coconut oil in medibles (cannacaps) . I dont know anyone taking it as a supplement in larger amounts. And I think adding mj cannabinoids would be a significant factor as well.
 

Killick

Well-Known Member
  • Diets that contain processed foods and those that limit consumption of high-cholesterol foods, including eggs and meats, may not contain sufficient amounts of the essential nutrients that support cognitive function and membrane structure.
  • A growing body of research suggests that mild cognitive decline is preventable and sometimes reversible through the use of such supplements as phosphatidylcholine and GPC, which are known to support the optimal structure and function of brain cells.
  • After the age of 30, we become increasingly vulnerable to brain aging and its consequences, including impaired memory and progressive loss of cognitive function that can lead to the development of Alzheimer’s disease and other forms of dementia.
  • Preventing cognitive decline throughout life requires early intervention decades before the onset of the symptoms of cognitive decline.
  • A proactive and preventive approach to preserving and enhancing cognitive function using phosphatidylserine and GPC may help protect against mild cognitive decline and may be effective in helping people with senile dementia, including Alzheimer’s disease.
  • Data from animal and human studies that have tested phosphatidylserine and GPC strongly suggest that these neuroprotective and neurotrophic compounds play an essential role in preventing and restoringloss of healthy brain functions as we age.
  • Studies show that GPC and phosphatidylserine enjoy a higher safety profile and superior benefit-to-risk profile than drugs currently prescribed to treat dementia.
  • Studies suggest that GPC and phosphatidylserine act on multiple levels and work synergistically to prevent cognitive decline and restore healthy brain function.
http://www.lifeextension.com/magazine/2011/1/feed-your-brain/page-01
 

Disrupt

Well-Known Member
Any ideas what do to with an emulsion? In a stoner moment, forgot that lecithin was added before attempting to wash oil. A foamy, 1:1 emulsion resulted which is reluctant to separate. (So miss access to a large centrifuge.)

This oil possesses powerful sedative effects. Enjoyed some on popcorn before washing. (The original plan, as this is the apex of culinary creativity.) It's made from spent material after two-wash QWET. Filled the MB2 with it (decarbolxylated, about six ounces starting material) and used a mix of MCT oil and coconut butter on-hand. Produced about a quart of very dark oil - hence the washing.
 

momofthegoons

Vapor Accessory Addict
Staff member
@Disrupt , please keep in mind that I am extremely stoned when I'm writing this.....

When you say you 'washed' it.. what do you mean? I think understand the result... but what did you do to create it?

And if I understand it correctly, your end result is a solution that has droplets that wont combine with the other ingredient? Or is it actually separating into layers? Or... is it like a froth?

I'm so confused. :thinker::lol:
 

momofthegoons

Vapor Accessory Addict
Staff member
It's a froth. To "create" it, added equal volume of water to the oil and shook. Intended to separate the oil and water layers and keep the oil, discarding water solubles for a cleaner oil.
Got it. I've had the same thing happen to me, only I put water into the MB during the processing (on the advice of someone in the MB FB community). Huge mistake.

Have you tried 'remelting' it in a double boiler? Perhaps if you did that the water would separate. You could try with a small amount to see if it works.
 

Disrupt

Well-Known Member
You could try freezing the mix, before it freezes solid, the oil will coagulate on the top, and you can scoop it up with a slotted spoon and pat dry.

Thanks - already put it in the refrigerator, where it solidified to the consistency butter without separating.
 

Killick

Well-Known Member
Hhmmm... Put a cup of your emulsified sleepy meds in a pan, with a cup of cocoa powder, 1 cup cocoa butter, 1/4 cup of honey or maple syrup. Melt, stir, pour into a greased pan, and chill. If you add a cup of peanut butter to the recipe it'll be fudgey :)
 

Disrupt

Well-Known Member
Hhmmm... Put a cup of your emulsified sleepy meds in a pan, with a cup of cocoa powder, 1 cup cocoa butter, 1/4 cup of honey or maple syrup. Melt, stir, pour into a greased pan, and chill. If you add a cup of peanut butter to the recipe it'll be fudgey :)

Sounds delicious, but might eat it all at once.

The effects are still lovely. Two tablespoons for a Reverend Jim face.

 

psychonaut

Florist
Company Rep
I eventually ditched a lb of butter that didn't remulsify after a wash. Shredders suggestion of using the freezer along with melting, re freezing, patting dry is about the best method if you're patient. I gave up after 4 attempts and glad I did because the resulting material just had too much water in it. I think the milk solids played a role and a part of me wants to try again with ghee next time as I don't think it would have the emulsion problems.

Now a days I'm decarbing rosin quickly in the oven (275F) Then adding it to candy melts (easy mode) or butter if for baking along with 1/2 tsp sunflower lecithin per gram of rosin.
 

Sponsored by

PuffItUp Dynavap VGoodiez 420EDC
Top