Mineral Taste Testing: The Science Behind It

When Professor Kenneth Glander, of Duke University’s Primate Center, keeps an eye on his horde of lemurs, he is hardly concerned that the animals could poison themselves on the myriad food choices available so distant from their native habitat.  He holds that the lemurs are smart enough to know what to eat and what to avoid.  After all, living in the wild offers a minefield of the good, the bad, and the bitter. Wild things are pretty good at picking their way through the maze of foods and poisons, and even at choosing a dose of something curative for what ails them.  Dr. Glander is one of the few primatologists to publish on the intricacies of animal food choices, noting that humans are no different in using the nose to discern what we need and how much.  To test the lemurs, he offered them ten kinds of local leaves: five that were considered highly digestible and five that inhibited digestion, none being toxic.  The animals’ final choices gave them the highest nutrient values and the lowest tannin content. This discernment he attributed to the keen perception of taste and smell, physiologically partnered by the Jacobson’s organs that connect the mouth and nasal passages.  This vomeronasal (VNO) organ is part of the accessory olfactory system and contains sensory neurons excited by chemical stimuli, offering a kind of instant chemical analysis. Common to many vertebrates, the VNO in some mammals contracts to pump and to draw in the scents.  This can be seen when a cat, for example, tilts its head after finding an odorant and curls its upper lip while wrinkling its nose.

About one percent of gene sequencing in humans is devoted to smell and taste, the least understood of the senses.

Of mineral deficiencies in particular, that of zinc is more widespread than appreciated.  Its depletion is associated with disorders that include diabetes, food sensitivities and allergies, delayed wound healing and recurrent infections, among others. Fingernail ridges are an overt sign, and may be linked to infertility, arthritis, hair loss, learning disorders or eczema.  An interesting way to determine zinc sufficiency is to perform the zinc taste test developed by chemistry professor Derek Bryce-Smith, who was among the first scientists to describe the dangers of tetraethyl lead, the anti-knock gasoline additive. But it was his examination of N-P-K fertilizers that found an association with zinc deficiency.  His test requires placing a small amount of zinc sulfate in the mouth and determining if you can taste it. If you can’t, you are zinc deficient (Bryce-Smith, 1986). A study of pregnant women given 200 mg of ZnSO4daily until parturition assessed zinc status using the taste test, finding a sound correlation with serum zinc levels (Garg, 1993).  

At the University of Pennsylvania, rats were fed a calcium or sodium deficient diet for a few weeks, other nutrients being normal.  Later offered diets containing the mineral of which they were deprived, those missing calcium preferred calcium-laden comestibles and those missing sodium preferred that, both rejecting sugar-flavored anything (Coldwell, 1993).  These results provide evidence for the existence of innate mineral appetites as an expression of need.

Our sense of taste comes from the part of the brain called the parabrachial nucleus, located at the junction of the midbrain and pons, which transmits signals to the medulla oblongata, the spinal cord, the hypothalamus and the amygdala.  It was identified as a taste relay in the early 1970’s, and compartmentalized by subnuclei into dealing with different aspects of taste, visceral sensation, likes and dislikes. In rodents it is used in parallel processing of taste and hedonic information; in humans and other primates, serial processing precedes hedonics. Changing physiological conditions affect the neurons that influence feeding behavior in rodents, while in primates independent cognitive analysis directs food selection (Scott, 2009).

Parallel processing is the ability to carry out multiple operations or tasks simultaneously, while assessing stimuli of differing quality.  This becomes most valuable in vision, where the brain divides what it sees into four components—color, shape, motion and depth. Serial processing, on the other hand, applies memories to incoming presentations (one at a time) to make comparisons and then decisions.  If the serial processing is self-terminating, comparisons stop abruptly when the target is found, after which a response is generated. If the processing is exhaustive, comparisons continue until the entire set is compared; then the response is made.

There is also a behavioral component of acceptance versus rejection that helps humans to protect themselves against poisons.   Besides informing the individual about the external world, taste connects a perception with information about the internal environment.  Molecules act on specialized sensory cells in various regions of the mouth, thus triggering signals which, in turn, are relayed to those areas of the limbic system associated with the parabrachial nucleus.

Supplemental minerals are associated with different absorptive capacities, depending on physiological, biochemical and even hormonal characteristics of the user.   But a mineral’s bioavailability depends also on its valence, spin, mass, atomic number, isotopes and other properties. Being a chemical factory, the body has to take in the raw materials to manufacture the chemicals it needs to perform all its functions.  For a mineral to be usable, it has to be absorbed and find its way into the appropriate cells. Once there, it usually needs conversion to a utile form, after which it is eliminated if found unnecessary. Some toxic minerals are very easily absorbed and assimilated, even through the skin.  So, because potential mineral sources differ and because their deficiencies or excesses can cause concerns, their individual characters need to be evaluated.

When mineral stores are low, the intestine will upregulate the eagerness with which a nutrient is accepted.  With adequate or elevated levels, the opposite occurs. On a molecular basis, this regulation may be conveyed by intraluminal binding ligands, by cell surface receptors, by various carrier or storage proteins, or by the machinery of transmembrane transport. The bulk of mineral absorption occurs in the small intestine—in the duodenum—in some cases, such as with calcium, by more than one mechanism.  Active Ca absorption occurs only in duodenum when Ca intake is less than optimal. Here, Ca is imported into the enterocyte, is transported across the cell, and is exported to extracellular fluid and blood. Voltage-insensitive channels pump Ca out of the cell by way of calcium-ATPase. The carrier protein, calbindin, the synthesis of which depends on vitamin D, enhances transport across the epithelial cell.  Passive absorption of Ca occurs in the jejunum and ileum when dietary Ca levels are high. Here, ionized Ca diffuses through the tight junctions into the basolateral spaces of enterocytes, and then into the blood. The minerals in foods are normally present in low concentrations, so the body has devised active transport mechanisms to help guarantee absorption. Generally, there is an inverse relationship between mineral availability and absorption.  Therefore, the more you take, the less you absorb.

Small molecular weight ligands, such as amino acids and other organic acids, have the capacity to increase solubility and to facilitate absorption, but liquefied mineral supplements, being already dissolved, are immediately bioavailable.  Moreover, being acidified by design, they display increased availability (Vinson, 1988). The bottom line is that the minerals with the greatest solubility have the greatest bioavailability.

If the food supply were trustworthy, it might be possible to get a day’s worth of minerals from our diets.  But that also supposes a person will eat a healthy regimen without processed foods and rancid supermarket fats and oils.  It also means eliminating added sugars, avoiding aflatoxin-laden grains, and being faithful to grass-fed, hormone-free meats.  What’s the big deal about minerals? Alone, they are inactive chemical elements. In the body, however, they light up either as structural elements of teeth and bone, for example, or as functional partners in hormones or electrolytes.  Without them, there can be no muscle responses, no transmission of messages through the nervous system, and poor maintenance of physiological pH and food metabolism. The body can’t make them, so they have to come from what we eat.

The macro-minerals are needed in amounts of 100 milligrams a day, generally listed as calcium, phosphorus, magnesium, sodium, chloride and potassium.  Even on a good day, their RDI’s may be hard to achieve from food. Dr. Donald Davis, at the University of Texas Biochemical Institute, tracked changes in food quality of forty-three garden crops over the past few decades and reported statistically reliable declines in nutritional value (Davis, 2004).  

Iron, selenium, zinc, chromium, copper, molybdenum, silicon, boron, cobalt, sulfur and a few others, like iodine, are cited as micro-minerals, needed in far lesser amounts.   Each mineral, macro and micro, has a job to do and none is more or less important than any other. In some instances, minerals work as a team. To contract a muscle cell, calcium tells sodium to do its magic.  To relax that cell, magnesium directs potassium to let go.

To learn more about mineral balance and its relation to optimal health, read the BodyBio Research: The Importance of Minerals, Liquid Minerals:


One unheralded and obscure truth about minerals is that they have an electrical character to their individual personalities. There exist natural electrical potentials, electrical conductivity and resistivity, and a dielectric constant. If push comes to shove, we may even mention magnetic permeability.  Of these traits, conductivity is deemed the most important.

In colloid chemistry you may hear of Zeta Potential, a.k.a. electrokinetic potential.  This may be seen when a solution of electrical resistivity and viscosity is forced through a porous medium.  Or you may hear of diffusion potential, a difference generated across a membrane because of a concentration difference of an ion, where the membrane is permeable to the ion.  Then, of course, there has to be equilibrium potential that exactly balances the tendency for diffusion caused by concentration difference. Not all minerals share these characteristics because not all are metals or metalloids, such as sulfur and phosphorus.  But the liquefied minerals available from BodyBio and other top shelf supplement manufacturers have these electrical properties:

1-Potassium1.4 x 1077 x 10-8conductor
2-Zinc1.7 x 1075.9 x 10-8conductor
3-Magnesium2.3 x 1074.4 x 10-8conductor
4-Copper5.9 x 1071.7 x 10-8conductor
5-Chromium7.9 x 1061.3 x 10-7conductor
6-Manganese6.2 x 1051.6 x 10-6conductor
7-Molybdenum2 x 1075 x 10-8conductor
8-Seleniumnot established12.0 (?) metalloidsemi-conductor
9-Iodine1 x 10-71 x 107insulator

Without a physiological sensorium with which to identify the display of such an electrical behavior, this chart would make little sense. However, there are receptors on oral surfaces—lingual, buccal, palatal and pharyngeal—that respond to the presence of each mineral and the intensity with which it announces itself by identifying an electrical attribute.  This does not necessarily mean that potassium tastes like potassium and selenium tastes like selenium. It means only that the probes of the body’s volt-ohm meter are identifying an open or a closed circuit. If, for example, the body is replete in magnesium, the receptors will be able to detect a corresponding conductivity-resistivity and gustatorily classify it as having a metallic taste or not, largely due to ion concentration. It’s as if the receptors were tiny straws filled to the top with electro-chemical complexes that respond immediately to the impingement of compatible mineral molecules.  

Diverse channels and G-protein-coupled receptors activate taste transduction in response to various compounds, changing neurotransmitter release via depolarization or other activity. Different sweeteners, for example, activate enzymes that open or close appropriately related channels, depending on their synthetic or natural composition.   Uniquely, several pathways for perception may occupy the same cell. We also need to understand that there are concentration thresholds for detecting a single taste response—the presence of a mineral in this case. The ongoing presence of a mineral may shut off its perception and that of other molecules that share a receptor. That offers a rationale for changing the stimulus in a timely manner, as is expected with the BodyBio Mineral Taste test.  

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We feel for you Coconut Oil

Coconut oil has had a rough year. Announced as “pure poison” by a public health expert in a lecture posted on YouTube, coconut oil suddenly became one of the worst foods you can eat. Coconut oil is a saturated fat and unfotuantely for our health, saturated fats have been completely misunderstood.

Earlier this year, Harvard professor Karin Michels picked up where the 1970’s left off, in a diatribe that parallels the American Heart Association’s stance against fats. Last year, the AHA sent an advisory to cardiologists, warning them that saturated fats are killers, coconut oil and butter among them. Their suggestion is to use margarine and the supermarket-staple, polyunsaturated vegetable oils, neither of which is fresh, wholesome or particularly healthful. Professor Michels also agrees that the human papilloma virus vaccine is suitable for all, including senior citizens. Levity aside, Dr. Michels’ espousal carries some weight because she works at Harvard University. But hers is only part of the story.

Myth: Fat is Evil

The “fat is evil” myth is deeply entrenched in our society. Counter arguments are on the horizon, especially one from a noted British cardiologist, Dr. Aseem Malhotra, who respectfully demands a public apology and a retraction on behalf of coconut oil from Dr. Michels. As a proponent of saturated fats and a foe of refined sugar, Dr. Malhotra censured the professor’s commentary as “unscientific nonsense,” warning that she is bringing Harvard into disrepute.

Arguably, not all coconut oil is not the same. Certified organic is preferred by some, but a few studies that looked for pesticide residues in coconut products have gone home empty handed (Brito, 2002). If organic designation is of no practical importance, what is? Even the refined vs. unrefined debate has lasted for a while. In the health world, unrefined anything is deemed better than refined everything. Although unrefined wins the debate, with coconut oil it might not make much difference.

MCT Oil — What is it exactly?

The answer lies all in the fat, namely in caprylic (C8:0) and lauric (C12:0) acids. The former, also known as octanoic acid, is an 8-carbon saturated fatty acid with anti-microbial properties that help to maintain gut integrity. As a medium-chain triglyceride (MCT), caprylic acid is not processed by the liver and requires no energy for absorption, use or storage. Lauric acid accounts for half the fatty acids in coconut oil. Known also as dodecanoic acid, this 12-carbon fat may be found in human breast milk. Lauric acid has been touted as having a positive effect on high-density lipoprotein levels, despite increasing total cholesterol (Mensink, 2003). Unlike other MCT’s, lauric acid metabolizes in the liver instead of getting immediately converted into energy.

The long-chain fatty acids in coconut oil include myristic (C14:0), palmitic (C16:0), stearic (C18:0), oleic (C18:1), and linoleic (C18:2) acids. The melting points of the saturated fats in coconut oil, from caprylic acid to stearic acid, range from 61° F to 158° F, quite a disparity, one that explains the most significant physical property of the oil — unlike most fats, both natural and hydrogenated, coconut oil does not exhibit a gradual softening with increasing temperatures, but passes abruptly from a somewhat brittle solid to a liquid.

Refined coconut oil is made from dried coconut meat, or copra. It is steamed and pressed, removing some of the flavor and aroma, but allowing a higher smoke point, which is good for cooking. The number of polyphenols and MCTs may be reduced by this method, also reducing the anti-oxidant and anti-inflammatory benefits. Where raw coconut is used instead of copra, a wet process emerges that presents an emulsion of water and oil, which may be separated by centrifuge, effecting a fifteen percent lower yield that incurs a greater expense. In cases where high melting point is desirable, as in warm climates, the oil is hydrogenated to bring the melting temperature to more than 100° F. Of course, trans fatty acids result (Foster, 2009). Raw, virgin, cold-pressed oil is preferred for its flavor and nutrient profile.

In their advisory, the AHA carefully picked and chose the studies to include, painstakingly omitting the Minnesota Coronary Survey, which found no difference between treatment and control groups and saturated fat intake (Frantz, 1989); exactingly skipping the Sydney Heart Study, which found no benefit in substituting linoleic acid for saturated fats (Ramsden, 2013); and assiduously ignoring the stellar Women’s Health Initiative, which concluded that, after 8 years’ attention, a dietary intervention that reduced total fat intake and increased intakes of vegetables, fruits and grains did not reduce the risk of CVD or stroke (Howard, 2006).

The AHA and its allies would replace saturated fats with rancid, oxidized,, supermarket vegetable oils that have been denatured in processing, storage and exposure to the high heat of the sauté pan. The resultant production of toxic aldehydes far exceeds what could be made from coconut oil (or butter or lard), which lacks the profusion of double bonds that are damaged in PUFAs.

But where is the negativity coming from?

Tom Brenna is a professor of nutrition at Cornell. His study of the reports on coconut oil have concluded that the oil’s bad reputation stems from a single factor…hydrogenation. Most of the negative findings were based on the use of partially-hydrogenated coconut oil, which was purposely used to raise the cholesterol of the study subjects and promote the preordained conclusions. Virgin coconut oil would not render the same data. Remember, lauric acid raises HDL.

A piece in the November 2014 edition of the journal, Postgraduate Medicine, allowed that virgin coconut oil (VCO) may have a place in cardioprotection (Babu, 2014). Norwegian researchers learned that VCO has a favorable effect upon the fibrinolytic system and Lp(a) concentrations when contrasted to a diet high in unsaturated fats (Muller, 2003). This position is bolstered by a Brazilian team that observed a reduction in waist circumference, HbA1C, and body mass index, and an increase in HDL (Cardoso, 2015).

The MCTs in coconut oil appear to be the most beneficial fractions, but lauric acid is not to be discounted. As a substitute for trans fats in some foods, it’s healthier. And that it can raise HDL is a plus. Yes, coconut oil is a saturated fat. And, yes, water can dilute electrolytes to the point of coma. And, yes, too much vitamin A can make your sclera yellow. Yet, moderate amounts of these commodities do no harm.

This analogy is used to help medical students better visualize the cellular membrane. Picture a circus tent. The masts that support the ceiling represent cholesterol, without which the tent (and the membrane) would collapse. The fabric of the tent is phosphatidylcholine, the absence of which would effect nihility. The poles that hold up the sides of the tent are saturated fats, lacking which there would be no stable structure. The flaps that allow ingress and egress are essential fatty acids, hence the free passage of energy into the cell and detritus out.

The suggested dietary limit for saturated fats is 20 grams a day. Coconut oil carries about 11.7 grams of saturated fat per tablespoon. Most people will use it sparingly and wisely. But oils are more than just fats. They carry anti-oxidants and other substances that disallow the prediction of overall health effects merely by changes in LDL and HDL. Even Harvard’s famed Walter C. Willett, M.D., agrees that “coconut oil’s special HDL-boosting effect may make it ‘less bad’ than the high saturated fat content would indicate…”


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American Sugar: The Untold Story.

There is a metabolic difference between simple and complex carbohydrates. The simple ones become glucose soon after they are eaten. The complex ones take longer to turn into sugar and are less apt to spike insulin and cause energy crashes down the line. But that isn’t the only difference between the two.

Almost forty years ago scientists had an interest in the relationship of diet to health, specifically of sugar intake to immunity. But their curiosity went past simple sugar to include carbohydrates other than glucose. The cells that are the backbone of the immune system are supposed to kill, swallow, and dispose of alien bodies, including bacteria, viruses and cancer cells. Scientists at Loma Linda University in California examined the activity of neutrophilic phagocytes (cells that dissolve the enemy) after subjects ingested glucose, fructose, sucrose, honey, or orange juice and found that “…all significantly decreased the capacity of neutrophils to engulf bacteria…” (Sanchez, Reeser, et al. 1973). Looking more closely, the researchers also discovered that the greatest effects occurred within the first two hours after eating, but “…the effects last for at least 5 hours.” (Ibid.) If there is any promise, it’s that the effects can be undone by fasting from added sugars for the next two or three days.

At the start of the twentieth century, Americans consumed only about five pounds of sugar a year. By the fifties, that had grown to almost 110 pounds a year, and to more than 152 by the year 2000. Corn sweeteners account for 85 of those pounds. America’s sweet tooth increased 39% between 1950 and 2000 as the use of corn sweetener octupled.

Although the statistics above are decades old, its message is contemporary. High-fructose corn syrup has become the bad boy of the anti-sugar crusade. HFCS began replacing sugar in soft drinks in the 1980’s, after it was portrayed by marketers as a healthful replacement for demon sugar. It didn’t hurt the industry that it cost less, either. The biological effects of sugar and HFCS are the same, however. Neither has any food value — no vitamins, protein, minerals, antioxidants, or fiber — but they do displace the more nutritious elements of one’s diet, and we tend to consume more than we need to maintain our weight, so we gain.

Even though the number of calories from the glucose in a slice of bread or other starch is the same as that from table sugar (half fructose and half glucose), they are metabolized differently and have different effects on the body. While fructose is metabolized by the liver, glucose is metabolized by every cell in the body. When fructose reaches the liver, especially in liquid form (as in soda), it overwhelms the organ and is almost immediately converted to fat. (Taubes. 2011)

Innate immunity is that which occurs as part of your natural makeup and defends you against infection by other organisms. Short-term hyperglycemia, which might come from a pint of vanilla, has been found to affect all the major components of the innate immune system and to impair its ability to combat infection. Reduced neutrophil activity, but not necessarily reduced neutrophil numbers, is one of several reactions to high sugar intake. (Turina. 2005) Way back in the early 1900’s, researchers noted a relationship between glucose levels and infection frequency among diabetes sufferers, but it wasn’t until the 1940’s that scientists found that diabetics’ white cells were sluggish. (Challem. 1997) More recent study has corroborated the diabetes-infection connection, agreeing that neutrophil phagocytosis is impaired when glucose control is less than adequate. (Lin. 2006) Impaired immune activity is not limited to those with diabetes. As soon as glucose goes up, immune function goes down.

Some people think they’re doing themselves a favor by using artificial sweeteners. Once the brain is fooled into thinking a sweet has been swallowed, it directs the pancreas to make insulin to carry the “sugar” to the cells for energy. After the insulin finds out it’s been cheated of real sugar, it tells the body to eat in order to get some, and that creates artificial hunger, which causes weight increase from overeating. Even environmental scientists have a concern with fake sweeteners in that they appear in the public’s drinking water after use. You can guess how that works. (Mawhinney. 2011)

Mineral deficiencies, especially prevalent in a fast-food world, contribute to immune dysfunction by inhibiting all aspects of the system, from immune cell adherence to antibody activity. Paramount among minerals is magnesium, which is part of both the innate and acquired immune responses. (Tam. 2003) Epidemiological studies have connected magnesium intake to decreased incidence of respiratory infections (PDR. 2000). But sugar pushes magnesium — and other minerals — out of the body. (Milne. 2000) This will compromise not only immune function, but also bone integrity. (Tjäderhane. 1998). Mix a sweet alcohol cocktail and find the whammy doubled. (Fuchs. 2002).

Zinc has been touted for its ability to shorten the duration of the common cold. Like magnesium, zinc levels decrease with age, and even tiny deficiencies can have a large effect on immune health, particularly in the function of the thymus gland, which makes the T-cells of the immune system. Zinc supplementation improves immune response in both the young and the old. (Haase. 2009) (Bogden. 2004) (Bondestam. 1985) All the microminerals, in fact, are needed in minute amounts for optimal growth and development…and physiology. Low intakes suppress immune function by affecting T-cell and antibody response. Thus begins a cycle whereby infection prevents uptake of the minerals that could prevent infection in the first place. Adequate intakes of selenium, zinc, copper, iron plus vitamins B6, folate, C, D, A, and E have been found to counteract potential damage by reactive oxygen species and to enhance immune function. (Wintergest. 2007)

Who would have viewed something as sweet as sugar as being so hostile to its host? It likes to let itself in, but has the nasty character of pushing everything else out.

Albert Sanchez, J. L. Reeser, H. S. Lau, P. Y. Yahiku, et al. Role of sugars in human neutrophilic phagocytosis. American Journal of Clinical Nutrition, Nov 1973; Vol 26, 1180–1184

Profiling Food Consumption in America. USDA http://www.usda.gov/factbook/chapter2.pdf

Taubes G. “Is Sugar Toxic?” in New York times Magazine, 13 April, 2011

Turina M, Fry DE, Polk HC Jr. Acute hyperglycemia and the innate immune system: clinical, cellular, and molecular aspects. Crit Care Med. 2005 Jul;33(7):1624–33.

Challem J and Heumer RP. The Natural health Guide to Beating the Supergerms. 1997. Simon and Schuster Inc. New York. Pp. 124–125

Lin JC, Siu LK, Fung CP, Tsou HH, Wang JJ, Chen CT, Wang SC, Chang FY. Impaired phagocytosis of capsular serotypes K1 or K2 Klebsiella pneumoniae in type 2 diabetes mellitus patients with poor glycemic control. J Clin Endocrinol Metab. 2006 Aug;91(8):3084–7.

Mawhinney DB, Young RB, Vanderford BJ, Borch T, Snyder SA. Artificial sweetener sucralose in U.S. drinking water systems. Environ Sci Technol. 2011 Oct 15;45(20):8716–22.

Tam M, Gómez S, González-Gross M, Marcos A. Possible roles of magnesium on the immune system. Eur J Clin Nutr. 2003 Oct;57(10):1193–7.

PDR: Physicians’ Desk reference for Herbal Medicines. Magnesium. 2nd edition. Mintvale NJ: Medical Economics Company; 2000: 5340540

Milne David B, PhD and Forrest H. Nielsen, PhD. The Interaction Between Dietary Fructose and Magnesium Adversely Affects Macromineral Homeostasis in Men. J Am Coll Nutr February 2000 vol. 19 no. 1 31–37

Tjäderhane Leo, and Markku Larmas. A High Sucrose Diet Decreases the Mechanical Strength of Bones in Growing Rats. J. Nutr. October 1, 1998 vol. 128 no. 10 1807–1810

Fuchs, Nan Kathryn Ph.D. Magnesium: A Key to Calcium Absorption. The Magnesium Web Site on November 22, 2002. http://www.mgwater.com/calmagab.shtml

Haase H, Rink L. The immune system and the impact of zinc during aging.. Immun Ageing. 2009 Jun 12;6:9.

Bogden JD.. Influence of zinc on immunity in the elderly.. J Nutr Health Aging. 2004;8(1):48–54.

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What is a Liposome?

(lĭp′ə-sōm′, lī′pə-)

Not discernable with a light microscope, a nanoliposome can be seen under an electron microscope as a sphere. Just as a water balloon has a thin outer layer with a water-filled interior, a liposome likewise has a thin outer wall — similar to a membrane — made of a phospholipid bilayer and an interior containing a water-soluble material. First identified in the early 1960’s, liposomes have undergone extensive research, the aim being the optimization of encapsulation, stability, circulation time and targeted delivery of its cargo, which may be a drug or a nutrient to a specific site of action. Until recently, the use of liposomes as a carrier of nutriments was limited, the delivery of drugs being more the focus. Their versatility is now being realized in other domains.

A few companies are pioneering the benefits of this unique science. It has long been the case that absorption and bioavailability rates of oral dietary and nutritional tablets and capsules is low and unreliable. Now, the natural encapsulation of lipophilic and hydrophilic nutrients within a liposome has created an effective method of bypassing the destructive elements of the digestive system, allowing the encapsulated nutrient to be delivered directly to cells and tissues.

To make a suitable microscope image, the liposomes are frozen and then sliced into ridiculously thin layers. This “freeze fracturing” will open some, but not all, and you will be able to distinguish the intact spheres from the concave surfaces of the incised liposomes. If this arrangement fails to emerge, you most likely do not have liposomes. But most clinics and manufacturers do not own electron microscopes. So, how do you determine that you have liposomes? Mix your material with water. Solid globs of amorphous matter are not carrying anything inside them and are not liposomes. If this happens, the phosphatidylcholine (PC) content is either too low, of poor quality, or is non-existent. If what you think is a liposome appears to be floating in foam, you are stuck with a mere emulsion, not a liposome. The liquid around a liposome should be clear.

Liposomes do not form spontaneously, typically needing energy applied to a dispersion of PC in a polar solvent, such as water. Heat, agitation and the aqueous province of the human body afford the right conditions. Sonication of phospholipids in water does the same thing, but likely will form layers like those of an onion, with progressively smaller liposomes. The inclusion of ancillary lipids facilitates the preparation. Microscopic vesicles — nanoliposomes — of PC can trap desirable payloads and provide controlled release of various bioactive agents at the right place at the right time. Here, otherwise volatile, reactive or sensitive additives become stabilized. Liposomes are bioresponsive because they and cell membranes share a common constituent — the lipid bilayer. As liposomes and cell membranes sidle near each other, they become conjugated and meld into each other, allowing the liposomal cargo to be deposited in the cellular cytosol, where its ameliorative destiny can be fulfilled. Liposomes with target specificity offer the prospect of safe and effective therapy for challenging clinical uses.