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Mighty Mitochondria… and Cardiolipin, Too

mitochondrion-cross-sectionMitochondria Are…

Suppose you were asked to name the most important part of your car?  Of course, without an engine you’re not going anywhere.  Without a transmission you’re not going anywhere, either.  So, which is it, the engine or the transmission?  Then, once you get moving, it’s nice to be able to stop.  Brakes, right?  Or perhaps you choose to steer around an obstacle.  Maybe there isn’t a most important part.  Ditto the cell, the unit of structure and function of living things, the smallest unit that can perform an essential life process.  Like your car, the cell has parts.  Considering that you have more than fifty trillion cells, the parts have to be tiny, really tiny.

Each cell is enclosed by a membrane that is made from proteins and a double layer of lipids.  The membrane is vital to the existence and function of the cell because it controls the flow of materials into and out of it, and it keeps the cell’s contents from spilling all over the place.  Not only does the cell have a membrane, but also do its components.  If we were to open and stretch out all the membranes of your body, they’d cover more than forty square miles.  But that’s nothing.  If we uncoiled all your strands of DNA and laid them end to end, they’d reach the sun and back more than once.  When the Psalmist said he was fearfully and wonderfully made, he didn’t realize how right he was.

A component of the cell that shares its architecture is the mitochondrion, sometimes referred to as the power plant of the cell because it makes most of the cell’s supply of adenosine triphosphate (ATP), used as a source of chemical energy.  Like the cell itself, the mitochondrion has an inner and an outer leaf to the membrane.  Mitochondria have other tasks besides making energy, including signaling, cell death, and control of the cell cycle. You already know that different cells have different jobs, each determined by what the nucleus says. Some cells do more work than others and require more energy.  Therefore, some have more mitochondria than others.  You would expect to find more mitochondria in a bicep than in the muscle that blinks an eye.  Each mitochondrion has an intermembrane space—found between the outer and inner membrane leaflets—that controls the movement of proteins. Small molecules have no problem crossing the outer membrane, but larger proteins need to be escorted by a specialized signaling sequence. (sorry about the alliteration)  A noted protein that is localized to the intermembrane area is called cytochrome c, the most abundant and stable cytochrome, principally involved in energy transfer.  Mitochondrial proteins vary depending on the tissue.  More than six hundred types have been identified in the human cardiac mitochondria, for example.  And, even though most of a cell’s DNA is in the nucleus, mitochondria have their own supply.

If there were no mitochondria, the higher animals could not exist.  Mitochondria perform aerobic respiration, requiring oxygen, which is the reason we breathe.  Without them we would have to rely on anaerobic respiration, without oxygen.  That process is too inefficient to support us.  Besides, the lack of mitochondria would reduce energy production by fifteen times, which is far too low to allow survival. A mitochondrion’s DNA reproduces independently of the cell in which it is found.  In humans, this DNA covers more than sixteen thousand base pairs, not very many compared to the whole organism.  Mitochondrial DNA holds thirty-seven genes, all of which are needed for normal function.  Thirteen of these supply information for making enzymes involved in oxidative phosphorylation, which is how ATP is made by using oxygen and simple sugars.  The other twenty-four genes help to make transfer RNA (tRNA) and ribosomal RNA (rRNA), which are chemically related to DNA.  These kinds of RNA are responsible for assembling amino acids into functioning proteins.

Mitochondria are passed on through maternal lineage.  Just as a car’s energy supply from gasoline is in the rear, so is a sperm’s mitochondrial energy—in the tail, which falls off after the sperm attaches to the egg.  This means that any problems, like mitochondrial diseases, necessarily come from the female.  Mitochondrial DNA (mtDNA) does not get shifted from generation to generation, while nuclear DNA does.  It is mtDNA that sends some diseases down the line.  mtDNA, though, is also subject to non-inherited mutations that cause diseases.  Fortunately, these are not passed on, but are accountable for various cancers, such as breast, colon, stomach and liver, diseases that have been attributed to reactive oxygen species.  mtDNA has limited capability to repair itself, so the inherited changes may cause problems with the body’s systems, where the mitochondria are unable to provide sufficient energy for cells to do their work.  The inherited consequences may present as muscle wasting, movement problems, diabetes, dementia, hearing loss, or a host of other maladies.

Some mitochondrial functions are performed only in specific cells.  In the liver, for example, they are able to detoxify ammonia, a job that need not be accomplished anywhere else in the body.  Other metabolic tasks of mitochondria include regulation of membrane potential, apoptosis, calcium signaling, steroid synthesis, and control of cellular metabolism.  You can see that mitochondria are vital to life, and their malfunction can change the rules.  In some mitochondrial dysfunctions there is an interaction of environmental and hereditary factors that causes disease.  Such may be the case with pesticides and the onset of Parkinson’s disease—cellular damage related to oxidative stress.  In other dysfunctions, there may be mutations of certain enzymes, such as coenzyme Q10 deficiency, or aberrations in the cardiolipin molecules that are found inside mitochondria, causative of Barth syndrome, which is often associated with cardiomyopathy.  Mitochondria-mediated oxidative stress may also play a role in Type 2 diabetes.  In cases where misconstrued fatty acid uptake by heart cells occurs, there is increased fatty acid oxidation, which upsets the electron transport chain, resulting in increased reactive oxygen species.  This deranges the mitochondria and elevates their oxygen consumption, resulting in augmentation of fatty acid oxidation.  Merely because oxygen consumption increases does not necessarily mean that more ATP will be manufactured, mostly because the mitochondria are uncoupled.  Less ATP ultimately causes energy deficit, accompanied by reduced cardiac efficiency.

Mitochondria can become involved in a vicious cycle of oxidative stress leading to mitochondrial DNA mutations, which leads to enzyme irregularities and more oxidative stress.  This may be a major factor in the aging process.

Rescue My Mitochondria, Please

The neurodegeneration of Parkinson’s disease is characterized by a loss of dopaminergic neurons and a deficit in mitochondrial respiration.  Exposure to some neurotoxins can present with both characteristics.  In a Parkinson’s model provoked by a drug that was produced to mimic the effects of morphine or meperidine (Demerol), but which interferes with oxidative phosphorylation in mitochondria instead, causing depletion of ATP and cell death, scientists at Columbia University’s Center for Neurobiology and Behavior found that the administration of ketone bodies akin to those used in the treatment of epilepsy were able to attenuate the dopaminergic neurodegeneration and motor deficits induced by the drug (Tieu, 2003).  From this and other studies it has been determined that ketones may play a therapeutic role in several forms of neurodegeneration related to mitochondrial dysfunction (Kashiwaya, 2000).

Moving across the mitochondrial membrane, phosphatidylcholine (PC) limits the phospholipid turnover in both the inner and outer leaflets that epitomizes the membrane defect identified in neurological diseases (Dolis, 1996), including Alzheimer’s, a disease in which impairment of mitochondrial function is part of the pathophysiology.  Substances that inhibit mitochondrial function also activate an enzyme called phospholipase A2 (PLA2) that degrades PC in the membrane (Farber, 2000), but reparation to mitochondria may be realized by administering PC liposomes, as evidenced by Russian studies performed in the early 1990s (Dobrynina, 1991).

Cardiolipin is an important component of the inner mitochondrial membrane, where it makes up about 20% of the lipid composition.  Its operational character is critical to the optimal function of numerous enzymes essential to mitochondrial energy metabolism.  Mitochondrial cardiolipin is distinguished from other phospholipids by the presence of linoleic acid derivatives (Schlame, 1990).  The formation of cardiolipin is dependent upon molecules donated by PC, but because it contains 18-carbon fatty alkyl chains with two unsaturated bonds, it bespeaks a linoleic acid heritage.   The need for linoleic acid, an omega-6 fat, was announced by the American Heart Association several years ago (Harris, 2009).

In the aforementioned Barth syndrome there exist cardiolipin abnormalities and resultant defects in the electron transport chain proteins and the architecture of the mitochondrion.   The electron transport chain (ETC) moves electrons from one cytochrome to another during the production of ATP, terminating at oxygen through a series of increasingly strong oxidative activities.  Those few electrons that fail to make it through the entire process leak and form superoxide, a substantially reactive molecule that contributes greatly to oxidative stress and aging.

Since the heart is rich in cardiolipin, it is more than appropriate to maintain its stores.  And linoleic acid is just the thing to do that.  Dutch researchers found that linoleic acid, readily available from sunflower, hemp, grape seed and other oils, restores and even increases cardiolipin levels (Valianpour, 2003).   Chronic over-consumption of omega-3 fats, such as those from fish oils, creates a deficit of omega-6 fats that interferes with the rate of oxygen use by mitochondria, with consequent decrease of cardiolipin (Yamaoka, 1999) (Hauff, 2006).

Coronary heart disease is a major health issue that may be addressed by supporting cardiolipin integrity, but other conditions likewise respond to such support.  Besides maintaining membrane potential and architecture, cardiolipin provides sustainment to several proteins involved in mitochondrial energy production.  If cardiolipin activity is interrupted or deranged, either through oxidative stress or alterations in acyl chain composition, we may anticipate contending with other pathological conditions, such as ischemia and hypothyroidism, and accelerated aging (Chicco, 2007).  These concerns can be allayed by attending to the status of the tafazzin protein that partly underlies cardiolipin metabolism (Xu, 2006).  Superheroes have long been associated with a sidekick, occasionally with role reversal for the nonce.  Working with linoleic acid to bolster cardiolipin is phosphatidylcholine (PC), which assists protein reconstitution by its ability to transfer acyl groups (Xu, 2003) (Schlame, 1991) and enhance protein signaling.  PC exists in every cell of the body, occupying the outer leaflet of the membrane.  Throughout the course of life, PC levels become depleted and may drop as low as 10% of the membrane in elderly people.  Being so, supplementation is warranted, not only to maintain cardiolipin levels and mitochondrial stability body-wide, but also to retard senescence and to improve brain function and memory capacity.

References

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Administration of phosphatidylcholine increases brain acetylcholine concentration and improves memory in mice with dementia.
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Danièle Dolis, Anton I. P. M. de Kroon and Ben de Kruijff
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John R. Dyer, Carol E. Greenwood
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STEVEN A. FARBER, BARBARA E. SLACK and JAN KRZYSZTOF BLUSZTAJN
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F. B. Jungalwala, R. M. C. Dawson
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José L. Quiles, Estrella Martínez, Susana Ibáñez, Julio J. Ochoa, Yolanda Martín, Magdalena López-Frías, Jesús R. Huertas and José Mataix
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Schlame M, Beyer K, Hayer-Hartl M, Klingenberg M.
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Sparagna GC, Lesnefsky EJ.
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Arie B. Vaandrager
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Kim Tieu, Celine Perier, Casper Caspersen, Peter Teismann, Du-Chu Wu, Shi-Du Yan, Ali Naini, Miquel Vil, Vernice Jackson-Lewis, Ravichandran Ramasamy and Serge Przedborski
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*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.

The Skinny On Skin: Zap The Zits and More

fighting-pimplesIt seems to happen just when the prom is a week away, or on the day before your date with the most popular gal or guy in school.   You get a pimple big enough to get its own name, like Everest or Matterhorn.  What can you do about it?  Could it have been prevented?  If you’re a teenager reading this, and suffer from acne, read closely as there may be an answer to your dilemma. If you’re a parent, maybe you could pass this on.

Acne has a bunch of names, but we bet you could add your own.  Basically, it’s an inflammation of the sebaceous glands, those that make sebum, the stuff that acts as a lubricant for the hair and skin and offers some protection against attackers like bacteria.  The “stuff” consists of fat, keratin, and cellular material that ooze from the follicle, the hair tube to which the sebaceous gland is attached.  As skin cells lining the follicle die off, they are pushed out by a growing hair.  Sometimes too much keratin interrupts this process and the dead skin cells stick together, clogging up the works.  This is how acne starts.  That thing we call a zit or blackhead is known as a comedone.  This word has nothing to do with comedy—there’s nothing funny about it, especially if it’s yours.

Acne is considered a normal response to abnormal levels of the male hormone testosterone.  Women may experience moderate acne due to hormonal changes associated with female health issues that include pregnancy, the use of birth control pills, and menstruation.   Not that this will make you feel any better, but four out of five people between ages twelve and twenty-four will get acne at least once.  As with most horrendous teenage afflictions, there are risk factors for acne, including some you can control and some you can’t.  You might be able to control bacterial growth by frequent and careful washing and rinsing.   You most assuredly can avoid using steroids to bulk up for a sport, and you can avoid skin irritation from scratching or the constant contact of a telephone against your face.  Genes and overproduction of sebum and hormone activity are not under your direct control.  Stress may or may not be, depending on whether or not you share living space with the Wicked Witch or the kindly Wiz.

Treatment for acne is generally based on reducing skin oil production, hastening skin cell turnover, fighting bacterial infection, or all three at the same time.  Topical treatments can do that, sometimes over-the-counter, sometimes by prescription.  Antibiotics, either rub-on or by-mouth, require an Rx.  For acne that fails to respond to other treatment, there’s an oral drug called Accutane, which is the atomic bomb of acne treatments, with a list of precautions, interactions and side effects long enough to choke a giraffe.  Recently, a slightly less offensive medication, a topical formulation called clindamycin phosphate, was matched head-to-head with an all-natural preparation made from vitamin B3 (as nicotinamide) and phosphatidylcholine (PC).

Remember, previously where we said keratin can clog up the works?  That’s termed hyperkeratinization.  That unwelcome activity was found to be reversed and normalized by using topical linoleic-acid-rich PC combined with nicotinamide’s anti-inflammatory character.  Contrasted to clindamycin in a 12-week, double-blind, randomized study, the PC/B3 compound was better tolerated and slightly superior in outcome (Morganti, 2011).

For more than a few years science has been concerned that bacteria are learning to become resistant to medicine’s barrage of chemical agents.  Concurrently, it’s been accepted that natural villains do not generally grow immune to natural heroes.  In the matter of acne, this was realized about nicotinamide more than a decade ago.  The emergence of resistant pathogens led researchers to look in a direction away from systemic and topical synthetic antimicrobials in the treatment of this condition.  Topical nicotinamide as a 4% gel was discovered to be a potent anti-inflammatory agent without the risk of bacterial resistance and, in fact, showed an 82% symptom improvement rate over clindamycin’s 68% (Shalita, 1995).  But wait, there’s a whole lot more to this.  In order for topical treatments to be effective, they have to get through the skin’s horny layer, the stratum corneum, without causing damage to tissue.  What natural substance can do this without unwanted side effects?  Phosphatidylcholine!

The prime phospholipid from which we are made, phosphatidylcholine renders cell membranes vibrant and alive, an activity lacking which we’d all succumb.  But it’s not only a stanchion; it’s also an escort.  PC helps desirable materials to permeate the skin’s stratum corneum and deliver healing, whether all natural or man-made, the former being preferred.  The higher the concentration of PC, the higher the efficacy of the escorted material (Kim, 2002).  While this holds true for nicotinamide, it also holds for drugs.  Indomethacin is an Rx non-steroidal anti-inflammatory drug (NSAID) used to address the discomfort of arthritis, tendinitis, and bursitis and like conditions.  It’s usually taken orally, but an Indomethacin topical gel made with liquid paraffin and mixed with PC was found to be considerably more effective at crossing the skin’s horny layer than the product that omitted the PC (Fujii, 2001).  Compared to conventional petroleum-based carriers of topical interventions, PC-based carriers improve the effectiveness of drugs used for skin cancer, as well (Romagosa, 2000).

PC as an oral supplement has long been known to attenuate serum cholesterol. In combination with niacin therapy for elevated cholesterol, PC is astounding.  No one ever dreamed that it could pass through the skin and have a similar effect.  The University of Miami’s School of Medicine looked at PC through a creative eye, and applied it topically to the shaved backs of rabbits that were bred to develop hypercholesterolemia and atherosclerotic lesions.  After two weeks’ treatment, investigators noted reduced levels of serum cholesterol and LDL, accompanied by less severe signs of atherosclerosis in the aorta (Hsia, 1996).

The incredible characteristics of real phosphatidylcholine—the kind that forms a liposome—are easier to realize than you might think.  Check out www.bodybio.com for more PC facts.

References

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Downing DT, Stewart ME, Wertz PW, Strauss JS.
Essential fatty acids and acne.
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Fujii M, Shiozawa K, Watanabe Y, Matsumoto M.
Effect of phosphatidylcholine on skin permeation of indomethacin from gel prepared with liquid paraffin and hydrogenated phospholipid.
Int J Pharm. 2001 Jul 3;222(1):57-64.

Godin AM, Ferreira WC, Rocha LT, Seniuk JG, Paiva AL, Merlo LA, Nascimento EB Jr, Bastos LF, Coelho MM.
Antinociceptive and anti-inflammatory activities of nicotinamide and its isomers in different experimental models.
Pharmacol Biochem Behav. 2011 Oct;99(4):782-8. Epub 2011 Jul 8.

Makiko Fujii, Kumi Shiozawa, Yoichi Watanabe, Mitsuo Matsumoto
Effect of phosphatidylcholine on skin permeation of indomethacin from gel prepared with liquid paraffin and hydrogenated phospholipid
International Journal of Pharmaceutics.  Vol 222, Iss 1, 3 July 2001, Pages 57–64

Hsia SL, He JL, Nie Y, Fong K, Milikowski C.
The hypocholesterolemic and antiatherogenic effects of topically applied phosphatidylcholine in rabbits with heritable hypercholesterolemia.
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Kanmaz T, Karakayali H, Sakallioglu AE, Ozdemir BH, Haberal M.
Polyunsaturated phosphatidylcholine protects against wound contraction in experimental skin burn injury.
J Invest Surg. 2004 Jan-Feb;17(1):15-22.

Kim C, Shim J, Han S, Chang I.
The skin-permeation-enhancing effect of phosphatidylcholine: caffeine as a model active ingredient.
J Cosmet Sci. 2002 Nov-Dec;53(6):363-74.

McCusker MM, Grant-Kels JM.
Healing fats of the skin: the structural and immunologic roles of the omega-6 and omega-3 fatty acids.
Clin Dermatol. 2010 Jul-Aug;28(4):440-51

Morganti P, Berardesca E, Guarneri B, Guarneri F, Fabrizi G, Palombo P, Palombo M.
Topical clindamycin 1% vs. linoleic acid-rich phosphatidylcholine and
nicotinamide 4% in the treatment of acne: a multicentre-randomized trial.

Int J Cosmet Sci. 2011 Oct;33(5):467-76.

Romagosa R, Saap L, Givens M, Salvarrey A, He JL, Hsia SL, Taylor JR.
A pilot study to evaluate the treatment of basal cell carcinoma with 5-fluorouracil using phosphatidyl choline as a transepidermal carrier.
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Shalita AR, Smith JG, Parish LC, Sofman MS, Chalker DK.
Topical nicotinamide compared with clindamycin gel in the treatment of inflammatory acne vulgaris.
Int J Dermatol. 1995 Jun;34(6):434-7.

*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.

Phosphatidylcholine And Memory: Aw, Forget It. Oh, You Already Did.

Forgetful-manIn his 1932 inaugural address, FDR told the world that we have nothing to fear but fear itself. If you ask people today what they fear, the list will likely include more specific things, like public speaking, ostracism, blindness, death, poverty, failure, memory loss, disease and a host of other states, conditions or activities. Some fears can be overcome with counseling, such as acrophobia; some can be prevented by being active instead of passive, such as poverty and failure; and some might require nutritional or medical intervention, such as certain diseases. Getting and using education, which doesn’t necessarily entail sitting in a classroom, might possibly attend to these needs. A modern-day fear is that of Alzheimer’s disease (AD), one that people associate with memory dysfunction, disorientation, and eventual loss of function. It’s a matter of not knowing that you don’t know. And it’s frightening.

The loss of cognitive ability takes a while to manifest, maybe ten to fifteen years, and is associated with the development of abnormal tissues and protein deposits in the brain’s cerebral cortex, which is the outermost layer of gray matter responsible for higher brain functions, such as sensation, voluntary muscle movement, thought, reasoning and memory. The primary neurotransmitter involved with the latter three of these cerebral obligations is acetylcholine, which is released at the ends of nerve fibers to send nerve impulses from one cell to another. Other jobs of this neurotransmitter involve decreasing heart rate and contraction strength, dilating blood vessels, increasing peristalsis, and raising elimination pressure during urination.

The dementia we fear results in deterioration of mental faculties, causing apathy, confusion and occasional stupor. A couple centuries ago it was synonymous with insanity, and was termed dementia praecox, now known as schizophrenia. Of its several forms, senile dementia is the one most commonly recognized, usually occurring after age 65, though it can happen earlier.

Natural deficits of acetylcholine accompany the aging process, causing those sporadic lapses in short-term memory that many individuals experience from time to time. Called benign forgetfulness, this non-debilitating memory decline is not to be confused with Alzheimer’s disease. It’s the degeneration of neurons in the cerebral cortex that leads to difficulties with language and judgment in AD. From the cortex, degeneration proceeds to the hippocampus, which is the part of the limbic system that deals with memory and spatial navigation. The hippocampus helps us to retain facts that pertain to specific events so they can be regurgitated if needed, but it also helps to order the chronology of one’s lifetime events. All this is what we typically call recollection. Memory tasks usually excite considerable hippocampus engagement, but that response is substantially weakened by advancing age, particularly in the absence of nutrients that feed the process. In transient global amnesia, a state induced by statin drugs’ cholesterol reduction and subsequent interference with the body’s manufacture and use of co-enzyme Q10, hippocampus activity is seriously constrained, though reversible by judicious supplementation of the enzyme.

Late in the last century, scientists demonstrated interest in the enhancement of memory in lab animals by introducing the phospholipid called phosphatidylcholine (PC) to their diets. “Demented” mice showed very low levels of choline and acetylcholine. After adding PC to the rations of the experimental group, the examiners saw an expected reversal in choline and acetylcholine levels, and an improvement in memory (Chung, 1995). Yes, mice are not the same as people, but they share a commonality in cerebral function, providing a good model for this scrutiny of memory acquisition and retention (Moriyama, 1996).

PC not only increases neurotransmitter efficiency, but also improves the supportive nature of polyunsaturated fatty acids (PUFA’s) in the revival of cell membrane fluidity. Since PC is the major structural and functional component of the cell membrane, this is not small news. Its reinstatement to a place of high stature in membrane architecture helps to sequester renegade substances that inhibit the membrane’s full capabilities in directing the machinery of life (Hiratsuke, 2009) (Gong, 2004).

After it was found that Alzheimer’s disease is related to abnormal metabolism of membrane phospholipids, researchers began to examine faulty homeostasis for discovery of diagnostic biomarkers. Alterations in phosphatidylcholine and phosphatidylethanolamine values were seen as indicative of membrane breakdown that could lead to fatty acid and phospholipid-related disorders that include dementias (Gonzalez-Dominguez, 2014). This is of particular interest because the pathophysiological changes associated with AD begin decades before clinical symptoms appear (Trushina,2013) (Whiley, 2014).

Since the brain is about sixty percent fat, it seems logical to ensure its repletion. Fatty acids and phospholipids (PL’s) are the most crucial molecules to occupy the space. It’s not very likely that seniors can get sufficient phospholipids from their diets because of diminished sense of taste for food, living and eating alone, being food insecure, and being broke. We realize this doesn’t describe all people in the group, but it probably covers someone you know. Egg yolks, liver, wheat germ and peanuts have some of the precursors to PL’s, but frequency of ingestion and concentration are often insufficient. Neither are many older folks amply hydrated to allow the PL’s to become organized into carriers of helpful molecules. The administration of PL’s, notably PC, can do much to restore function—and structure—of the membranes that make life more enjoyably livable.

References

Chang CY, Ke DS, Chen JY.
Essential fatty acids and human brain.
Acta Neurol Taiwan. 2009 Dec;18(4):231-41.

Chung SY, Moriyama T, Uezu E, Uezu K, Hirata R, Yohena N, Masuda Y, Kokubu T, Yamamoto S.
Administration of phosphatidylcholine increases brain acetylcholine concentration and improves memory in mice with dementia.
J Nutr. 1995 Jun;125(6):1484-9.

Conquer JA, Tierney MC, Zecevic J, Bettger WJ, Fisher RH.
Fatty acid analysis of blood plasma of patients with Alzheimer’s disease, other types of dementia, and cognitive impairment.
Lipids. 2000 Dec;35(12):1305-12.

Gong J, Shi F, Shao L, Zheng X.
Effects of soybean phospholipids on learning and memory ability and contents of lipids in mice’s brain.
Wei Sheng Yan Jiu. 2004 May;33(3):324-7.

González-Domínguez R, García-Barrera T2, Gómez-Ariza JL3.
Combination of metabolomic and phospholipid-profiling approaches for the study of Alzheimer’s disease.
J Proteomics. 2014 Jan 25. pii: S1874-3919(14)00026-8.

Hiratsuka S, Koizumi K, Ooba T, Yokogoshi H.
Effects of dietary docosahexaenoic acid connecting phospholipids on the learning ability and fatty acid composition of the brain.
J Nutr Sci Vitaminol (Tokyo). 2009 Aug;55(4):374-80.

Ladd SL, Sommer SA, LaBerge S, Toscano W.
Effect of phosphatidylcholine on explicit memory.
Clin Neuropharmacol. 1993 Dec;16(6):540-9.

Moriyama T, Uezu K, Matsumoto Y, Chung SY, Uezu E, Miyagi S, Uza M, Masuda Y, Kokubu T, Tanaka T, Yamamoto S.
Effects of dietary phosphatidylcholine on memory in memory deficient mice with low brain acetylcholine concentration.
Life Sci. 1996;58(6):PL111-8.

Nagata T, Yaguchi T, Nishizaki T.
DL- and PO-phosphatidylcholines as a promising learning and memory enhancer.
Lipids Health Dis. 2011 Jan 28;10:25.

J. Peter Slotte, Bodil Ramstedt
The functional role of sphingomyelin in cell membranes
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Trushina E, Mielke MM.
Recent advances in the application of metabolomics to Alzheimer’s Disease.
Biochim Biophys Acta. 2013 Jun 29. pii: S0925-4439(13)00223-8.

Whiley L, Sen A, Heaton J, Proitsi P, García-Gómez D, Leung R, Smith N, Thambisetty M, Kloszewska I, Mecocci P, Soininen H, Tsolaki M, Vellas B, Lovestone S, Legido-Quigley C; AddNeuroMed Consortium.
Neurobiol Aging. 2014 Feb;35(2):271-8.
Evidence of altered phosphatidylcholine metabolism in Alzheimer’s disease.

*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.

Phosphatidylcholine and Vision: Will The Real PC Please Stand Up?

pc-vision-testA disquieting commentary about a globally progressive mentality is that even the most highly educated among us can be misled into believing a falsehood, a misrepresentation often based on linguistic nuance. It’s all in the spin enunciated by those with a systematic plan to pull the undereducated into their fold. The point in this case is the semantic concerning phosphatidylcholine (PC), the phospholipid purposely and ignorantly confused with lecithin, a material that contains PC as its main constituent, but itself is not PC.

Lecithin is an extracted and purified product made from soybeans, eggs, sunflower, or canola seeds, the last being genetically modified to make it what it is from rapeseeds. Lecithin is a natural emulsifier, keeping mayonnaise from separating, for example, but it contains triglycerides, sterols, fatty acids and carbohydrates that cause it to be digested in the gut before the phospholipid fraction can do its work in the cell membrane. True PC, the actual phospholipid, is an amphiphilic molecule, meaning that is has a polar, water-soluble group attached to a non-polar water insoluble hydrocarbon chain. It’s the primary component of the cell membrane and acts as a reservoir of choline for the obligatory manufacture of acetylcholine, the neurotransmitter in charge of nerve impulse transmission that enables muscle contraction, vasodilation, peristalsis and mood changes. Convention has permitted triple strength lecithin, which now is thirty-six percent phosphatidylcholine, to be called PC because of the chief constituent, adding to the confusion. Phosphatidylcholine is the largest fraction of the phospholipids that make the cell membrane. It’s accompanied by three others, however, including phosphatidylethanolamine (PE), phosphatidylserine (PS), and phosphatidylinositol (PI). Each of these fractions has its own character.

PC is a famous molecule in its own right but, as an ancillary agent to the function of fat-soluble nutrients, it displays the loyalty of a favorite sidekick. Lutein is one of the major players in eye health and has been the focus of considerable study as a therapeutic and preventative agent in the treatment of the retinal diseases. Found in green leafy vegetables such as spinach and kale, lutein is a yellow carotenoid pigment that modulates light energy to serve as a photoprotector by absorbing blue light and inhibiting the consequent free radicals from exposure to it. The increases in pigmentation of the retina afforded by lutein protect the eye against macular degeneration and the formation of cataracts (Richer, 1999, 2004) (AREDS Study Group, 2001, 2007) (Barker, 2010). Should the retina be scourged by inflammation, lutein can serve as a rescue molecule (Sasaki, 2009) and help to prevent damage to the functional proteins rhodopsin and synaptophysin (Ozawa, 2012). Some pharmaceuticals and nutraceuticals need a supporting cast to enhance their performances. Such is phosphatidylcholine, an adjuvant that increases the bioavailability and efficacy of more than only a few therapeutic materials.

Curcumin, the active ingredient of turmeric, is an anti-inflammatory agent with a substantial fan club. Combined with PC, curcumin enjoys increased respect in the clinical world, particularly in the treatment of uveitis, which is inflammation of the uvea, the part of the eye that includes the choroid, the ciliary body and the iris. Dry eye, maculopathy, glaucoma and diabetic retinopathy are other conditions addressed by using PC-enriched curcumin (Allegri, 2010).

The retina is one of the vertebrate tissues with the greatest concentrations of polyunsaturated fats. Unlike most organs, though, the lens is another story, having a lipid composition that varies from species to species and with age. The sphingolipids and PC concentrations of the lens have been used to predict life span in some species, where humans have so adapted that their lens membranes have greater sphingolipids content to confer protection against oxidation, allowing the lens to remain clear longer than in other species (Borchman, 2004). Since the fibers of the human lens rely on phospholipids for their integrity, reductions in phospholipids may be predictive of cataracts, while simultaneously implying to clinicians that phospholipid intake will prevent, or at least slow, their progression (Siddique, 2010) (Deeley, 2010). As much as contemporary science would like to deem this a modern position on the architecture of the eye, the idea of ocular phospholipid degradation over time has been studied since the 1960’s, and perhaps earlier, when it was found that PC and PE do not exhibit phosphate turnover as readily as the other phospholipids, phosphatidic acid and PI, once more indicating a position of respect for PC (Broekhuyse, 1969).

Behind the cornea and before the lens is the aqueous humor, the transparent gelatinous fluid made mostly of water plus a little bit of amino acid, electrolytes and vitamin C. It helps to maintain intraocular pressure, to protect the cornea against the environment and to refract light. In a normal eye, all four phospholipid fractions are present, but not in a glaucomatous one. Supplemental PC, then, has the potential to resolve such an issue, while maintaining the structure and function of the framework that scaffolds the anterior members of the eyeball (Edwards, 2014) (Abindi, 2013).

There are mechanisms in the body that can make PC either from the methylation of PE or through the enlistment of a substance called citicoline, which directs the manufacture of PC from choline. Decreases in members of this cascade can change the phospholipid makeup of every cell, affecting every neuron of the central nervous system, of which vision is vital. To address this concern, PC is a desirable option, and both citicoline and exogenous PC have produced favorable results (Grieb, 2002) (Zigman, 1984).

Whether we look for enhanced lutein (Lakshminarayana, 2006), a sophisticated phospholipid complex (Baskaran, 2003), or supercharged curcumin (Belcaro, 2010), we can rely on phosphatidylcholine to vitalize the cell membrane and all that it does for the eyes… and for all our other parts.

References

Acar N, Berdeaux O, Grégoire S, Cabaret S, Martine L, Gain P, Thuret G, Creuzot-Garcher CP, Bron AM, Bretillon L.
Lipid composition of the human eye: are red blood cells a good mirror of retinal and optic nerve fatty acids?
PLoS One. 2012;7(4):e35102.

Age-Related Eye Disease Study Research Group.
A randomized, placebo-controlled, clinical trial of high-dose supplementation with vitamins C and E, beta carotene, and zinc for age-related macular degeneration and vision loss: AREDS report no. 8.
Arch Ophthalmol. 2001 Oct;119(10):1417-36.

Age-Related Eye Disease Study Research Group, SanGiovanni JP, Chew EY, Clemons TE, Ferris FL 3rd, Gensler G, Lindblad AS, Milton RC, Seddon JM, Sperduto RD.
The relationship of dietary carotenoid and vitamin A, E, and C intake with age-related macular degeneration in a case-control study: AREDS Report No. 22.
Arch Ophthalmol. 2007 Sep;125(9):1225-32.

Allegri P, Mastromarino A, Neri P.
Management of chronic anterior uveitis relapses: efficacy of oral phospholipidic curcumin treatment. Long-term follow-up.
Clin Ophthalmol. 2010 Oct 21;4:1201-6.

Anderson RE, Maude MB, Kelleher PA, Maida TM, Basinger SF.
Metabolism of phosphatidylcholine in the frog retina.
Biochim Biophys Acta. 1980 Nov 7;620(2):212-26.

Aribindi K, Guerra Y, Lee RK, Bhattacharya SK.
Comparative phospholipid profiles of control and glaucomatous human trabecular meshwork.
Invest Ophthalmol Vis Sci. 2013 Apr 30;54(4):3037-44.

Barker FM 2nd.
Dietary supplementation: effects on visual performance and occurrence of AMD and cataracts.
Curr Med Res Opin. 2010 Aug;26(8):2011-23.

Baskaran V, Sugawara T, Nagao A.
Phospholipids affect the intestinal absorption of carotenoids in mice.
Lipids. 2003 Jul;38(7):705-11.

Berdeaux O, Juaneda P, Martine L, Cabaret S, Bretillon L, Acar N.
Identification and quantification of phosphatidylcholines containing very-long-chain polyunsaturated fatty acid in bovine and human retina using liquid chromatography/tandem mass spectrometry.
J Chromatogr A. 2010 Dec 3;1217(49):7738-48.

Belcaro G, Cesarone MR, Dugall M, Pellegrini L, Ledda A, Grossi MG, Togni S, Appendino G.
Efficacy and safety of Meriva®, a curcumin-phosphatidylcholine complex, during extended administration in osteoarthritis patients.
Altern Med Rev. 2010 Dec;15(4):337-44.

R.M. Broekhuyse
Phospholipids in tissues of the eye: III. Composition and metabolism of phospholipids in human lens in relation to age and cataract formation
Biochim Biophys Acta. 1969 Oct 28;187(3):354-65.

Deeley JM, Hankin JA, Friedrich MG, Murphy RC, Truscott RJ, Mitchell TW, Blanksby SJ.
Sphingolipid distribution changes with age in the human lens.
J Lipid Res. 2010 Sep;51(9):2753-60.

Donoso LA, Edwards AO, Frost A, Vrabec T, Stone EM, Hageman GS, Perski T.
Autosomal dominant Stargardt-like macular dystrophy.
Surv Ophthalmol. 2001 Sep-Oct;46(2):149-63.

Edwards G, Aribindi K, Guerra Y, Lee RK, Bhattacharya SK.
Phospholipid Profiles of Control and Glaucomatous Human Aqueous Humor.
Biochimie. 2014 Feb 20. pii: S0300-9084(14)00052-2.

Frederik J. G. M. van Kuijk and Paul Duck
Fatty Acid Composition of the Human Macula and Peripheral Retina
Investigative Ophthalmology & Visual Science. Dec 1992; 33(13): 3493-6

Frederik J. G. M. van Kuijk and Paul Duck
Fatty Acid Composition of the Human Macula and Peripheral Retina
Investigative Ophthalmology & Visual Science. Dec 1992; 33(13): 3493-6

Grieb P, Rejdak R.
Pharmacodynamics of citicoline relevant to the treatment of glaucoma.
J Neurosci Res. 2002 Jan 15;67(2):143-8.

Lakshminarayana R, Raju M, Krishnakantha TP, Baskaran V.
Enhanced lutein bioavailability by lyso-phosphatidylcholine in rats.
Mol Cell Biochem. 2006 Jan;281(1-2):103-10.

Li LK, So L, Spector A.
Membrane cholesterol and phospholipid in consecutive concentric sections of human lenses.
J Lipid Res. 1985 May;26(5):600-9.

Marisiddaiah R, Baskaran V.
Bioefficacy of beta-carotene is improved in rats after solubilized as equimolar dose of beta-carotene and lutein in phospholipid-mixed micelles.
Nutr Res. 2009 Aug;29(8):588-95.

Nagy K, Brahmbhatt VV, Berdeaux O, Bretillon L, Destaillats F, Acar N.
Comparative study of serine-plasmalogens in human retina and optic nerve: identification of atypical species with odd carbon chains.
J Lipid Res. 2012 Apr;53(4):776-83.

Oresic M, Seppänen-Laakso T, Yetukuri L, Bäckhed F, Hänninen V.
Gut microbiota affects lens and retinal lipid composition.
Exp Eye Res. 2009 Nov;89(5):604-7.

Yoko Ozawa, Mariko Sasaki, Noriko Takahashi, Mamoru Kamoshita, Seiji Miyake, and Kazuo Tsubota
Neuroprotective Effects of Lutein in the Retina
Curr Pharm Des. Jan 2012; 18(1): 51–56.

The Rigaku Journal. Vol. 17/ number 1/ 2000
Determination of human eye lens membrane structure by x-ray diffraction analysis
ROBERT F. JACOB, RICHARD J. CENEDELLAH, AND R. PRESTON MASON

Richer S.
ARMD–pilot (case series) environmental intervention data.
J Am Optom Assoc. 1999 Jan;70(1):24-36.

Richer S, Stiles W, Statkute L, Pulido J, Frankowski J, Rudy D, Pei K, Tsipursky M, Nyland J.
Double-masked, placebo-controlled, randomized trial of lutein and antioxidant supplementation in the intervention of atrophic age-related macular degeneration: the Veterans LAST study
(Lutein Antioxidant Supplementation Trial).
Optometry. 2004 Apr;75(4):216-30

Sasaki M, Ozawa Y, Kurihara T, Noda K, Imamura Y, Kobayashi S, Ishida S, Tsubota K.
Neuroprotective effect of an antioxidant, lutein, during retinal inflammation.
Invest Ophthalmol Vis Sci. 2009 Mar;50(3):1433-9.

M A Siddique, B K Tiwary and S B Paul
Phospholipid and protein contents of lens proteolipids in human senile cataract
Eye (2010) 24, 720–727

Zigman S, Paxhia T, Marinetti G, Girsch S.
Lipids of human lens fiber cell membranes.
Curr Eye Res. 1984 Jul;3(7):887-96.

*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.

Thanks For The Memories

memoriesThe pestering head of occasional forgetfulness rears itself just about the time we reach middle age. That happens because the brain has more than one location in which to store information. Even after we have become creatures of routine things go awry. Taking things for granted and performing certain actions day after day breeds mindlessness. We fail to notice this until we can’t find the car keys or the cell phone. But, fortunately, this is only a passing inconvenience.

The National Institute of Health, in its subsidiary, FamilyDoctor.org, makes it clear that there is little need to be overly concerned about periodic memory lapses. Trying to find the one word that will finish a sentence with flourish can be frustrating, but is not a matter of grave concern. Just as the body changes with time, so does the mind. Memory problems from mood, family and work can aggravate, and also the bad guys, medications, drinking, and injuries can contribute. Most of the time there is nothing to worry about. Let it be known, though, that serious problems are not part of normal aging. Forgetting the names of people you’ve known for years because you meet them by chance in a strange venue does not indicate a memory reversal, but merely a surprise that interrupts the status quo. Serious problems are those that affect daily living, such as forgetting things you have done many times over the years, or suddenly being unable to do things that require steps, such as assembling an object.

Remote and short-term memories are not usually affected by aging. The more important to you a piece of information is, the more likely you are to remember it longer. Depending on its significance, you’ll be able to retrieve that information sooner or later, even if it takes a few seconds longer than you like. Short-term memories are stored by transient patterns of neuron communication unless you purposely deem them significant enough to recall later on. This is controlled by regions of the brain called the frontal and parietal lobes. If this data is to be stored for a long time, the hippocampus consolidates the short-term into long-term, even though it isn’t the storage location itself.

Besides practicing sound dietary habits, it’s worthwhile to pay attention to the finer points of what we do, and to organize oneself. The method and intensity of processing makes a difference in memory. Using more than one sense to store information helps to shuttle it into neat and tidy storage. Instead of just looking at the number in the phone book, say it aloud so that hearing is combined with vision. Copying it onto a piece of paper entails the tactile sense.

Yes, the threat of Alzheimer’s disease is alarming, but transient memory snags are qualitatively different from those associated with Alzheimer’s. In this disease, recent memories are not stored and, therefore, cannot be recalled, although the distant past might be quite lucid. Over time, all facets of memory become affected.

What about diet? Since the brain is mostly fat, it makes sense to add in more fats and oils in the diet, but not just the fat at the edge of that sirloin. The essential fatty acids are needed for brain growth and development. In fact, the lipids of the central nervous system contain high proportions of arachidonic (n-6 AA) and docosahexaenoic (n-3 DHA) fatty acids. However, Freund-Levi 2006, found that administration of omega-3 fatty acids (he is referring to fish oil n-3 HUFAs) in patients with mild to moderate Alzheimers did not delay the rate of cognitive decline. Also, Devore 2009, reports that “These findings suggest that lower intakes of saturated and trans fat and higher intake of polyunsaturated fat relative to saturated fat may reduce cognitive decline in individuals with type 2 diabetes”.

A large percentage of us that are health conscious are leaning on the omega 3 fish oils, EPA and DHA for improved health, however research does not seem to support the omega 3 HUFAs for better brain performance. That does not make sense.

DHA is the reason we are smarter than the grazing animals, what gives? Solfrizzi, 2006, found that eating a high MUFA and PUFA diet were significantly associated with better cognitive performance. MUFAs are Mono-Unsaturated (think olive) and PUFAs, Poly-Unsaturated, are the first step for the omega 6s and 3s (sunflower and flax, not fish oil). Lauretani, 2007, also corroborated it by discovering that lower plasma PUFA, omega-6 and omega 3 fatty acids, linoleic and linolenic fatty acids, significantly predicted a steeper decline in nerve function parameters.

It seems that everybody on the planet is taking fish oils and getting nowhere trying to stay sharp. The answer may be obscure, but our research and clinical experience also corroborates the Italian researchers, Solfrizzi and Lauretani and others. At BodyBio we have focused on teaching our doctor friends on the necessity of getting an RBCFA blood test (Red Blood Cell Fatty Acid) for all their compromised patients.

One of the most consistent weaknesses we find in their test results is a low fatty acid content. What do you do with that reading? What you can’t do is take fish oil (HUFAs) or olive oil (MUFAs). You need the base 6s and 3s, PUFAs, and the only safe way is to stay with a 4:1 ratio, 80% 6s and 20% 3s, as in the BodyBio Balanced Oil.

At BodyBio all oils go to a lab for analysis to enable the correct mixture before blending. The absolute here is that there is no other safe way to raise fluidity – and fluidity — is everything. There is another essential – we need gobs of the stuff to avoid Alzheimers and all of the neurological disorders.

Take a look at this piece fromwww.FamilyDoctor.org to get the American Academy of Family Physician’s take on memory. Here is the link: http://familydoctor.org/online/famdocen/home/seniors/common-older/124.printerview.html

References

  • Freund-Levi Y, Eriksdotter-Jönhagen M, Cederholm T, Basun H, Faxén-Irving G, Garlind A, et al. Omega-3 fatty acid treatment in 174 patients with mild to moderate Alzheimer disease: OmegAD study: a randomized double-blind trial. Arch Neurol. 2006 Oct;63(10):1402-8.

    van Gelder BM, Tijhuis M, Kalmijn S, Kromhout D. Fish consumption, n-3 fatty acids, and subsequent 5-y cognitive decline in elderly men: the Zutphen Elderly Study. Am J Clin Nutr. 2007 Apr;85(4):1142-7.

    Solfrizzi V, Colacicco AM, D’Introno A, Capurso C, Torres F, Rizzo C, Capurso A, Panza F. Dietary intake of unsaturated fatty acids and age-related cognitive decline: a 8.5-year follow-up of the Italian Longitudinal Study on Aging. Neurobiol Aging. 2006 Nov;27(11):1694-704.

    Lauretani F, Bandinelli S, Bartali B, Cherubini A, Iorio AD, Blè A, Giacomini V, Corsi AM, Guralnik JM, Ferrucci L. Omega-6 and omega-3 fatty acids predict accelerated decline of peripheral nerve function in older persons. Eur J Neurol. 2007 Jul;14(7):801-8.

    Devore EE, Stampfer MJ, Breteler MM, Rosner B, Hee Kang J, et al. Dietary fat intake and cognitive decline in women with type 2 diabetes. Diabetes Care. 2009 Apr;32(4):635-40.

    Am J Clin Nutr. 2007 Apr;85(4):1142-7.
    Fish consumption, n-3 fatty acids, and subsequent 5-y cognitive decline in
    elderly men: the Zutphen Elderly Study.
    van Gelder BM, Tijhuis M, Kalmijn S, Kromhout D.
    Centre for Prevention and Health Services Research, National Institute for Public Health and the Environment, Bilthoven, Netherlands. [email protected]

    BACKGROUND
    Indications have been seen of a protective effect of fish consumption and the intake of n-3 fatty acids on cognitive decline. However, studies are scarce and results inconsistent.

    OBJECTIVE
    The objective of the study was to examine the associations between fish consumption, the intake of the n-3 fatty acids eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) from fish and other foods, and subsequent 5-y cognitive decline.

    DESIGN
    Data on fish consumption of 210 participants in the Zutphen Elderly Study, who were aged 70-89 y in 1990, and data on cognitive functioning collected in 1990 and 1995 were used in the study. The intake of EPA and DHA (EPA+DHA) was calculated for each participant. Multivariate linear regression analysis with multiple adjustments was used to assess associations.

    RESULTS
    Fish consumers had significantly (P = 0.01) less 5-y subsequent cognitive decline than did nonconsumers. A linear trend was observed for the relation between the intake of EPA+DHA and cognitive decline (P = 0.01). An average difference of approximately 380 mg/d in EPA+DHA intake was associated with a 1.1-point difference in cognitive decline (P = 0.01).

    CONCLUSIONS
    A moderate intake of EPA+DHA may postpone cognitive decline in elderly men. Results from other studies are needed before definite conclusions about this association can be drawn.

    Arch Neurol. 2006 Oct;63(10):1402-8.
    Omega-3 fatty acid treatment in 174 patients with mild to moderate Alzheimer disease: OmegAD study: a randomized double-blind trial.
    Freund-Levi Y, Eriksdotter-Jönhagen M, Cederholm T, Basun H, Faxén-Irving G, Garlind A, Vedin I, Vessby B, Wahlund LO, Palmblad J.
    Department of Neurobiology, Caring Sciences and Society, Section of Clinical Geriatrics, Karolinska University Hospital Huddinge, Stockholm.

    BACKGROUND
    Epidemiologic and animal studies have suggested that dietary fish or fish oil rich in omega-3 fatty acids, for example, docosahexaenoic acid and eicosapentaenoic acid, may prevent Alzheimer disease (AD).

    OBJECTIVE
    To determine effects of dietary omega-3 fatty acid supplementation on cognitive functions in patients with mild to moderate AD.

    DESIGN
    Randomized, double-blind, placebo-controlled clinical trial.

    PARTICIPANTS
    Two hundred four patients with AD (age range [mean +/- SD], 74 +/- 9 years) whose conditions were stable while receiving acetylcholine esterase inhibitor treatment and who had a Mini-Mental State Examination (MMSE) score of 15 points or more were randomized to daily intake of 1.7 g of docosahexaenoic acid and 0.6 g of eicosapentaenoic acid (omega-3 fatty acid-treated group) or placebo for 6 months, after which all received omega-3 fatty acid supplementation for 6 months more.

    MAIN OUTCOME MEASURES
    The primary outcome was cognition measured with the MMSE and the cognitive portion of the Alzheimer Disease Assessment Scale. The secondary outcome was global function as assessed with the Clinical Dementia Rating Scale; safety and tolerability of omega-3 fatty acid supplementation; and blood pressure determinations.

    RESULTS
    One hundred seventy-four patients fulfilled the trial. At baseline, mean values for the Clinical Dementia Rating Scale, MMSE, and cognitive portion of the Alzheimer Disease Assessment Scale in the 2 randomized groups were similar. At 6 months, the decline in cognitive functions as assessed by the latter 2 scales did not differ between the groups. However, in a subgroup (n = 32) with very mild cognitive dysfunction (MMSE >27 points), a significant (P<.05) reduction in MMSE decline rate was observed in the omega-3 fatty acid-treated group compared with the placebo group. A similar arrest in decline rate was observed between 6 and 12 months in this placebo subgroup when receiving omega-3 fatty acid supplementation. The omega-3 fatty acid treatment was safe and well tolerated.

    CONCLUSIONS
    Administration of omega-3 fatty acid in patients with mild to moderate AD did not delay the rate of cognitive decline according to the MMSE or the cognitive portion of the Alzheimer Disease Assessment Scale. However, positive effects were observed in a small group of patients with very mild AD (MMSE >27 points).

    Neurobiol Aging. 2006 Nov;27(11):1694-704.
    Dietary intake of unsaturated fatty acids and age-related cognitive decline: a 8.5-year follow-up of the Italian Longitudinal Study on Aging.
    Solfrizzi V, Colacicco AM, D’Introno A, Capurso C, Torres F, Rizzo C, Capurso A, Panza F.
    Department of Geriatrics, Center for Aging Brain, Memory Unit, University of Bari, Policlinico, Piazza G. Cesare 11, 70124 Bari, Italy. [email protected]

    Abstract
    There is evidence from a population-based study of an inverse relationship between monounsaturated fatty acids (MUFA) energy intake and age-related cognitive decline (ARCD), while high polyunsaturated fatty acids (PUFA) intake was positively associated with cognitive impairment in elderly subjects. We investigated the possible role of MUFA and PUFA on age-related cognitive changes. A population-based, prospective study was carried out on 278, 186, and 95 nondemented elderly subjects (65-84 years) evaluated for global cognitive functions (Mini-Mental State Examination, MMSE) at the first (1992-1993), second (1995-1996), and third survey (2000-2001), respectively, from the randomized cohort of Casamassima, Bari, Italy (n=704), one of the eight centers of the Italian Longitudinal Study on Aging (ILSA). MUFA and PUFA intakes were assessed at baseline with a semi-quantitative food frequency questionnaire. High MUFA and PUFA energy intakes and total energy intake were significantly associated with a better cognitive performance in a 8.5-year follow-up. In this prospective population-based study on older nondemented subjects with a typical Mediterranean diet, high MUFA and PUFA intakes appeared to be protective against ARCD.

    Am J Clin Nutr. 2007 Nov;86(5):1479-85.
    n 3 fatty acid proportions in plasma and cognitive performance in older adults.
    Dullemeijer C, Durga J, Brouwer IA, van de Rest O, Kok FJ, Brummer RJ, van Boxtel MP, Verhoef P.
    Wageningen Centre for Food Sciences, Wageningen, Netherlands. [email protected]

    BACKGROUND
    Very-long-chain n-3 polyunsaturated fatty acids (n-3 PUFAs) are suggested to be related to cognitive performance in older adults. However, limited data exist on the association between n-3 PUFAs and performance in specific cognitive domains.

    OBJECTIVE
    We evaluated the association between plasma n-3 PUFA proportions and cognitive performance in 5 cognitive domains and determined whether plasma n-3 PUFA proportions predict cognitive change over 3 y.

    DESIGN
    We used data from the FACIT trial, in which participants received folic acid or placebo capsules for 3 y. Fatty acid proportions in plasma cholesteryl esters at baseline were measured in 807 men and women aged 50-70 y. Cognitive performance for memory, sensorimotor speed, complex speed, information-processing speed, and word fluency was assessed at baseline and after 3 y. The cross-sectional analyses were based on all 807 participants; the longitudinal analyses were based only on 404 participants in the placebo group.
    RESULTS: Higher plasma n-3 PUFA proportions predicted less decline in sensorimotor speed (multiple linear regression coefficient, z score = 0.31; 95% CI: 0.06, 0.57) and complex speed (0.40; 95% CI: 0.10, 0.70) over 3 y. Plasma n-3 PUFA proportions did not predict 3-y changes in memory, information-processing speed, or word fluency. The cross-sectional analyses showed no association between plasma n-3 PUFA proportions and performance in any of the 5 cognitive domains.

    CONCLUSIONS
    In this population, plasma n-3 PUFA proportions were associated with less decline in the speed-related cognitive domains over 3 y. These results need to be confirmed in randomized controlled trials

    Eur J Neurol. 2007 Jul;14(7):801-8.
    Omega-6 and omega-3 fatty acids predict accelerated decline of peripheral nerve function in older persons.
    Lauretani F, Bandinelli S, Bartali B, Cherubini A, Iorio AD, Blè A, Giacomini V, Corsi AM, Guralnik JM, Ferrucci L.
    Tuscany Regional Health Agency, Florence, Italy.

    Abstract
    Pre-clinical studies suggest that both omega-6 and omega-3 fatty acids have beneficial effects on peripheral nerve function. Rats feed a diet rich in polyunsaturated fatty acids (PUFAs) showed modification of phospholipid fatty acid composition in nerve membranes and improvement of sciatic nerve conduction velocity (NCV). We tested the hypothesis that baseline plasma omega-6 and omega-3 fatty acids levels predict accelerated decline of peripheral nerve function. Changes between baseline and the 3-year follow-up in peripheral nerve function was assessed by standard surface ENG of the right peroneal nerve in 384 male and 443 female participants of the InCHIANTI study (age range: 24-97 years). Plasma concentrations of selected fatty acids assessed at baseline by gas chromatography. Independent of confounders, plasma omega-6 fatty acids and linoleic acid were significantly correlated with peroneal NCV at enrollment. Lower plasma PUFA, omega-6 fatty acids, linoleic acid, ratio omega-6/omega-3, arachidonic acid and docosahexanoic acid levels were significantly predicted a steeper decline in nerve function parameters over the 3-year follow-up. Low plasma omega-6 and omega-3 fatty acids levels were associated with accelerated decline of peripheral nerve function with aging.

    Diabetes Care. 2009 Apr;32(4):635-40.
    Dietary fat intake and cognitive decline in women with type 2 diabetes.
    Devore EE, Stampfer MJ, Breteler MM, Rosner B, Hee Kang J, Okereke O, Hu FB, Grodstein F.
    Channing Laboratory, Department of Medicine, Brigham and Women’s Hospital, Boston, Massachusetts, USA.

    OBJECTIVE
    Individuals with type 2 diabetes have high risk of late-life cognitive impairment, yet little is known about strategies to modify risk. Targeting insulin resistance and vascular complications-both associated with cognitive decline-may be a productive approach. We investigated whether dietary fat, which modulates glucose and lipid metabolism, might influence cognitive decline in older adults with diabetes.

    RESEARCH DESIGN AND METHODS
    Beginning in 1995-1999, we evaluated cognitive function in 1,486 Nurses’ Health Study participants, aged >or=70 years, with type 2 diabetes; second evaluations were conducted 2 years later. Dietary fat intake was assessed regularly beginning in 1980; we considered average intake from 1980 (at midlife) through initial cognitive interview and also after diabetes diagnosis. We used multivariate-adjusted linear regression models to obtain mean differences in cognitive decline across tertiles of fat intake.

    RESULTS
    Higher intakes of saturated and trans fat since midlife, and lower polyunsaturated to saturated fat ratio, were each highly associated with worse cognitive decline in these women. On a global score averaging all six cognitive tests, mean decline among women in the highest trans fat tertile was 0.15 standard units worse than that among women in the lowest tertile (95% CI -0.24 to -0.06, P = 0.002); this mean difference was comparable with the difference we find in women 7 years apart in age. Results were similar when we analyzed diet after diabetes diagnosis.

    CONCLUSIONS
    These findings suggest that lower intakes of saturated and trans fat and higher intake of polyunsaturated fat relative to saturated fat may reduce cognitive decline in individuals with type 2 diabetes.

The information contained in this web site is for educational purposes only and is not intended or implied to be a substitute for professional medical advice. Inclusion here does not imply any endorsement or recommendation.  Always seek the advice of your physician or other qualified medical provider for all medical problems prior to starting any new regiment.

These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.


The information contained in this web site is for educational purposes only and is not intended or implied to be a substitute for professional medical advice. Inclusion here does not imply any endorsement or recommendation. Always seek the advice of your physician or other qualified medical provider for all medical problems prior to starting any new regiment.

These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.

Life On The Membrane

Life-On-The-Membrane-1The membrane of the cell and the organelles are composed of two fatty acid tails facing each other. The bilipid layer is minute in comparison to its vital role as cell protector with a thickness of 3 to 4.5 nm. It would take 10,000 membranes layered on top of each other to make up the thickness of a piece of paper. The dynamics that occur inside this tiny organic sliver is a microcosm of supportive cytoskeleton microtubules complete with internal roadways and has fostered many hypotheses, one of the most interesting from Stuart Hameroff (Hameroff et ai, 2002). Joining with Roger Penrose, Hameroff orchestrated an objective reduction model suggesting a cognitive role conveyed on the inside, the hole in the center of microtubule structures, which is -10 nm and which acts as a quantum wave carrier of cellular information. Hameroff, an anesthesiologist and professor at the University of Arizona at Tucson, describes dynamic activities within every cell which are regulated by the cell cytoskeleton, particularly microtubules, which are cylindrical lattice polymers of the protein tubulin. Recent evidence indicates signaling, communication and conductivity in microtubules. There is a marriage between the soft flexible membrane and the structural rigidity of the microtubules. Not so within the body of the cell but significantly as the cell tries to extend its reach out into the outside world seeking nourishment in the gut using cilia, seeking oxygen in the trachea and lungs with micro-villi, and signaling in the brain with a vast array of dendrites. All are similarly constructed principally of membrane and microtubules.

Assessing the cell membrane through the examination of red cell lipids can lead the clinician into a deeper level of understanding of metabolic strategies to influence treatment outcome in a wide range of degenerative disorders. Essential (EFAs) and non-essential lipids are incorporated into the bilipid layer of the membrane of every cell in the body and brain. There is virtually no system of the body that does not require attenuation of specific fatty acid substrates and coenzymes to maintain health and repair of bodily tissues. The human cell membrane must be continually fed with the correct lipid substrates to enable the organism to function ideally, yet fatty acid metabolism has been poorly delineated in treatment protocols. Exploration of lipid metabolism brings a striking new intervention that unlocks the systemic nature of disorders as well as an exquisite capacity to impact the brain architecture.

The membrane of every cell and organelle is a lipid envelope that encases and protects the internal working cellular components. The bilipid layer is far more than isolation and protection, for linked and interlocked within the membrane are literally thousands of proteins (peptides) that are the windows and doors of the cell. They form the gates for ingress and egress; the multitudinous array of receptors and ion channels that perform the vast metabolic functions of life. In addition, select lipids, the Eicosanoids, after set free from the membrane, metabolize up to an intercellular communication and information system through their prostaglandin regulatory activity. Prostaglandins, thromboxanes, and leukotrienes may have evolved to be the basic information broadcasting and control mechanism that permitted metazoa, the grouping of cells, which we are, to advance to our present level. The mere thought of multi-cellular activity, and especially the evolution of humankind is, at our present level of knowledge, not possible without essential fatty acids (EFAs), which are the precursors to the regulatory prostaglandins, which provide cell to cell communication and basic molecular initiation. Before one can advance beyond protozoa, or a single cell organism, into multi-cell metazoa, there must be both communication and a means of regulation. This is the world of the prostaglandins (PGs), the “local hormones” that control the interactions without which there is no complex life form.

Life-On-The-Membrane-3This powerful role that lipids play is of prime importance for the clinician to understand metabolism. One of the greatest biochemical advances came about with the understanding of the energy cycle for plants and animals. Looking at oxidative energy through a lipid lens can help to adjust our view of their importance. Peter Mitchell’s earlier research on membrane transport led him towards a construct that explained oxidative phosphorylation (Mitchell 1961). Mitchell realized that the bilipid membrane would have to be a key factor in any hypothesis to explain that substances (hydrogen ions) were moved from one side of a membrane to the other to accumulate potential energy.

In his chemiosmosis theory, Mitchell proposed that the movement of electrons down the chain of oxidation chemistry results in the translocation (shifting) of protons (H-ions) from one side of the membrane to the other, (Mitchell 1963). In essence, the hydrogen atom is separated with the electron moving down the chain on the inside of the membrane while the H-ion is shuttled to the outside using the membrane as an insulator for a momentary separation. In his hypothesis, Mitchell stressed the importance of the spatial arrangement of the various carriers within the energy-transducing membrane. Spatial arrangement refers to the positioning of the molecules involved that sit on and span the membrane and carry out the chemistry. He suggested that those carriers that bind both electrons and protons must be facing on the inside of the membrane, while the carriers facing the outside would only accept electrons, leaving the protons to accumulate resulting in an electrochemical gradient. The accumulation of ions (hydrogen protons) is then the motive force required to link substrate oxidation to phosphorylation and drive the ATP energy cycle.

After 15 years of controversy and experimentation, mostly designed to prove him wrong, Mitchell’s hypothesis coupling oxidation to phosphorylation earned him a Nobel Prize. The awarding of this Nobel Prize was probably the most significant in Nobel history since the hypothesis, now universally accepted, explains the creation of energy for life in plants and animals.

The details of oxidation chemistry is not a prerequisite for clinicians. Every cell biology text covers the subject of oxaloacetate to citric acid to C02 and H20 with the ultimate end product of phosphorylation of ADP to ATP, (Karp 1999). The Krebs or TCA (citric acid) cycle is an example of cellular beauty in the creation of energy for the biochemistry of life. The elegance however, lies in the lipid membrane that embraces the enzymes, manipulating them to their most optimal position to allow it all to occur. The preciseness of the various peptides and lipids and their relation to one another is critical for the chemistry to play out.

The significant role of the membrane and the lipids is hidden in the details of the chemistry. The high energy phosphate heads and their lipid tails provide the structure for the trans-membrane peptides (carriers), which are positioned in that lipid membrane sea in correct juxtaposition to carry out the energy production, most of which is little understood. The membrane is one of the most elegant structures in the universe. The lipids themselves are one of the smallest molecules in biochemistry, which may contribute to their mystery, and possibly the reason for their late prominence in biochemistry. In comparison, proteins and nucleic acids are much larger and more photographable, which often provides important clues as to their function. The most famous example is when Watson snuck a look at Rosalind Franklin’s photographs which led to the discovery of DNA. Not the most honorable event but certainly an important one. Lipids however are too small with frequencies too high to capture. Their performance lies in their enormous numbers and their resonance for communication and metabolic influence which moves us into the world of Quantum Mechanics.

Without the view of the lipid membrane as the insulator that permitted charge separation and the transfer of ions to the opposite side of the membrane from the site of the actual oxidation, Mitchell, or anyone else, could not have developed the TCA cycle hypothesis. All of the TCA cycle chemistry, as well as much of metabolism in both plants and animals, occurs on one or both sides of the membrane, be it in the cell, the mitochondria, the ER, the golgi, the nuclear membrane, or the vast neuronal network of the body and the brain. All thought, all sensory transmission, and all motion, involves the lipid membrane which carries the signals and information.

Mitochondria are tiny energy organelles often described as miniature power plants for the TCA energy producing cycle. There are -200-500 per cell, with 10,000 or more in a heart myocyte. The citric acid chemistry occurs on the inside of the second bilipid membrane (there are 2); with the space between the first and second layer (intermembrane space) the collection area of the hydrogen ions. Oxidation produces the separation of ions, which are accumulated and guided to ATP synthase, the enzyme responsible for phosphorylation of ATP. The hydrogen ions are passed back into the matrix by the ATP pump (ATP synthase) sitting on the inside membrane, after which they combine with oxygen (with H20 as a byproduct).

Life-On-The-Membrane-5

Both of the bilipid membranes of mitochondria are the typical “unit membrane” (railroad track) type in structure. Between the two membranes is the space where the H ions accumulate. Inside the 2nd membrane is the matrix, which appears moderately dense and one may find strands of DNA, ribosomes, or small granules. The outer and inner membranes have very different properties. The outer membrane is composed of approximately 50 percent lipid by weight. In contrast the inner membrane contains more than 100 different polypeptides and has a very high proteinllipid ratio, more than 3: 1 by weight, which corresponds to about one protein molecule for every 15 phospholipids, (Karp 1999). The outer membrane has porins, which permit / accommodate molecules up to – 5000 Daltons for the passage of ATP, NAD, and coenzyme A. The inner membrane however is highly impermeable; virtually all molecules and ions require special transporters situated in the inner membrane space to facilitate entrance through the inner membrane to the matrix, i.e. L-carnitine for the transport of long chain fatty acids.

Life-On-The-Membrane-6In addition there is a phospholipid peculiar to the inner leaflet of mitochondria that is found nowhere else in the body called cardiolipin (CL). As the drawing shows CL is a joining of the head groups of two phospholipids. It looks something like Siamese Twins — actually it is one. The two head groups are chemically linked together at the sides of the head groups. It has the compulsory two lipid tails on each PL and can be positioned comfortably in the membrane but now with the odd connection contains four lipid tails instead of two. CL is found only in the inner matrix of the mitochondria, nowhere else, and appears to have one specific function, that of hindering, slowing down the high activity level characteristic of all normal active membrane PLs.

Because of its bulky shape its activity level would be severely restricted. Active PLs are in constant motion including rotation. Placing a bulky CL strategically could restrict normal PL movement. Placed in the right spot with its inability to spin as most all PLs do — could, quite possibly — be the restricting agent that the inner mitochondrial membrane needs to fix the citric acid participants in juxtaposition and keep them steady as they perform the critical electron handoff. (PIC)

Normally, the accurate positioning of the necessary proteins within that crowded lipid sea involve a combination of phospholipids with a high concentration of double bonds (think high energy). The high frequency character of the double bonds guarantees the energy required to perform the accurate peptide positioning. There is also a wide assortment of many other proteins as well as the ones involved in the chemiosmotic production of energy. The precise arrangement of those proteins is not known, however, the requirement for a tight control and still maintaining fluidity is paramount and the main element lost with age and disease.

The membrane surrounds and protects every cell of every organ including the tissues of the heart and the neurons of the brain. It is a remarkably thin insulator, the protective outer skin, with a carbon copy duplicated over and over surrounding the tiny organelles inside each cell. Bruce Lipton puts the lipid cell membrane in perspective, in his book ‘The Biology of Belief’ when he compares the function of the membrane to the DNA, currently the darling of medical science. Dr. Lipton calls the DNA the gonads of the cell and compares it to the hard drive of a computer, while comparing the lipid membrane to the keyboard. He describes the DNA as a storehouse of information, a personal library housing a pattern (copy) of every protein molecule specific to each of us. The DNA of each cell contains a duplicate set of genetic instructions for the development and function of every organ of our body.

However, the concept we are led to believe is that we are controlled by our genes, by our hard drive, but this is inaccurate. The DNA, like a central processor, is a library of information. A cell can actually exist for a few weeks or even months without its DNA. Lipton performed this in his lab with cells in a petri dish. By surgically extracting the contents of the nucleolus, the DNA, and continuing to provide nourishment, the cell could last for several months. The same does not occur with a fractured membrane, the cell dies instantaneously without it’s outer coat. It’s a bit sacrilegious to call our libraries dumb, but they are certainly not smart. Some form of energy must exist to extract the information from the library and direct it to perform a necessary function. Even though the DNA holds the program for the production of all the intricate proteins we need, it acts exactly like a library. It holds all the intelligence, but initiates no activity.

The membrane is continuously collecting pertinent information from the outside world sending instructions inward to the cytosol and the DNA. In part, it is both in position to collect knowledge and equipped with the energy component within the essential fats to initiate and direct cellular activity, the details of which is yet unknown. Dr. Lipton says, as the keyboard, we should refer to it as our mem-Brain — and, since it is -70% fatty acids, our lipid membranes now take on a whole new level of importance.

Renowned lipid researcher Michael Crawford defines the dry weight of the human brain as 60% lipid, with the dendrites and synapses up to 80% composed predominantly of the Highly Unsaturated w6 and w3 Fatty Acids (HUFAs). Phospholipids, cholesterol, cerebrosides, gangliosides and sulfatides are the lipids residing within the bilayers in the brain (Bazan et aI., 1992). The phospholipids and their fatty acid tails provide second messengers and signal mediators (Schachter et aI., 1983). Those phospholipids play a vital role in the cell signaling systems in the neuron (Rapoport, 1999). The functional behavior of neuronal membranes depend largely on the ways in which individual phospholipids are aligned and interspersed with both cholesterol and the necessary functional proteins. Neurotransmitters are wrapped up in phospholipid vesicles waiting for the right moment of release. The release and uptake of the neurotransmitters is dependent upon the realignment of the phospholipid molecules containing a high concentration of n-3 DHA. The energetic nature of the phospholipids is a vital factor in determining how efficiently the neurotransmitters are delivered since the violent expUlsion at the synaptic cleft can only be accomplished efficiently with a ready supply of the highest energy lipid, DHA. Re-modeling of the phospholipids may be accomplished by supplying both oral and intravenous phosphatidylcholine with a balance of the w 6 and w 3 oils at the preferred ratio of 80% w 6 to 20% w 3 (Yehuda 1993).

One of the most important biochemical changes regarding aging is a change in membrane phospholipid composition. Phosphatidylcholine (PC), is the predominate head group PL in the outer leaflet of the membrane, which as discussed above, is composed of two phospholipid groups opposing each other. PC also tends to incorporate a predominance of HUFAs, especially arachidonic acid (AA) on the Sn2 position, thus the outer leaflet is composed of a grouping of higher energy lipids than the inner leaflet. This varies with the curvature demands of the membrane since the tighter the curve would necessitate the preference for a smaller head group i.e. PC over PE, since PC has a larger dimension. In mammalian plasma membranes, the main variation occurs in the relative composition of phosphatidylcholine (PC), and both sphingomyelin (SM) and cholesterol. PC decreases with age while SM and cholesterol increase with age (Schacter et aI., 1983). The impact of this shift in the outer membrane is difficult to envision. It involves every cell of the body. Every sensory neuron, touch, smell, taste, sight, hearing; skin, blood cells, brain neurons, endothelium, alveoli, immune cells, bone cells, etc. It involves the organelles within the cell such as the mitochondria the peroxisomes and the nuclear membrane. The concept of aging and PC decline is a dramatic shift in the body’s homeostatic ability.

The changes in the relative amounts of PC and SM are especially great in tissues, which have a low phospholipid turnover. For example, plasma membranes associated with the aorta and arterial wall show a 6-fold decrease in PC/SM ratio with aging. SM also increases in several diseases, including atherosclerosis. The SM content can be as high as 70-80% of the total phospholipids in advanced aortic lesion (Yechiel et al.,1985), (Yechiel and Barenholz, 1985), (Yechiel et al.,1986), (Yechiel and Barenholz, 1986; Barenholz 2004), (Cohen and Barenholz, 1984). Both sphingomyelin (SM) and cholesterol are structurally similar to saturated fats. They are rigid, with the concommitment decline in fluidity and lower metabolic performance. The loss of those dynamic double bonds of the high energy lipids could be the major cause of the aging disease.

In 1985 Yechiel and Barenholtz, from Hebrew University, authored a significant paper highlighting phosphatidylcholine and its relationship to aging and disease (Yechiel 1985a.b, 1986; Muscona-Amir 1986). Using rat myocytes (heart cells) in a 20 day in vitro study, they demonstrated the ability of PC to completely rejuvenate cells that were all but expired. Heart cells can be separated in a dish in vitro, but with proper feeding within a few days, they self agglomerate (gather together) and beat in unison at a rate of – 160 beats per minute.

To demonstrate the importance of PC, they fed one group of cultures (the A Groups) egg yolk PC and continued to do so for the life of the experiment (20 days), while two other groups (the Bs and Cs) were deprived of PC and later had it added back into their feed.

The Group A cultures are represented with a straight line (green) at the top of the chart. They had been given egg PC after day 6 and for the entire 20 days they maintained a constant beating rate of – 160 beats/ min. Group B (Red) cultures were not as fortunate and were denied PC until day 16. The chart shows the result for after 6 days the B groups started to weaken and by day 8 began a precipitous decline in beating rate until day 12 wherein some of the B groups were only beating at – 20 beats/min. and others not beating at all. The Group Cs (Blue) were given PC as the A groups, but only to day 11, after which PC was removed from their feed. As you can see on the chart, almost immediately the Cs started a decline in their beating rate and mirrored the decline of group B with a 5 day drop to – 20 beats/min. In addition both Band C groups suffered a variety of cellular distortions in size and production of protein.

On day 16 all cultures, including groups Band C were given PC, and within 24 hours, the Bs and Cs recovered their beating rate to – 160 beats/min and continued so until the study was concluded at day 20. In addition, they also recovered most of their distorted chemistry. This was a remarkable demonstration of the power of phosphatidylcholine, or to be more precise, of the absolute necessity of it.

A medline search on ‘Phosphatidylcholine’ will reward you, or inundate you, with 37,471 citations. To review them would easily take a year or two, but it speaks volumes of the importance of PC. In all of our studies, we have yet to uncover a report as powerful as that of Yechiel and Barenholtz. However, there are two that are noteworthy. Tile review by Cui and Howeling, PC and Cell Death 2002, that focuses on the ability of PC to reverse a number of biochemical distortions and prevent cellular necrosis and / or apoptosis. Apoptosis is a controlled, regulated death, while necrosis is a rupture of membranes with the release of vital components into the surrounding blood stream. Cui et al presented their prior biochemical studies and many others demonstrating that perturbation of PC leads to cell death, and the subsequent replacement of PC reestablishes homeostasis.


The information contained in this web site is for educational purposes only and is not intended or implied to be a substitute for professional medical advice. Inclusion here does not imply any endorsement or recommendation. Always seek the advice of your physician or other qualified medical provider for all medical problems prior to starting any new regiment.

These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.

David Horrobin and Schizophrenia

MAD-bookDavid Horrobin MD, PhD, was one of the leading fatty acid researchers in the world. He had a life-time fascination with schizophrenia which culminated in his 2001 publication, “The Madness of Adam and Eve”. He believed that schizophrenia is a leading characteristic of mankind that makes us human. Not the debilitating versions of the disorder, but milder significant variations that contributed to a higher level of achievement in the realms of politics, religion, science, and the arts. The history of prominent world leaders who were schizophrenic or had a prevalence of the disorder in their families ranged from Da Vinci, Newton, Van Gogh, Einstein, even Churchill. What Horrobin firmly believes is that schizophrenia lies at the very foundation of human culture.

MAD-DavidHHorrobin was a brilliant Oxford student earning him two scholarships to Balliol resulting in a doctorate in neuroscience. He later became a Fellow of Magdalen College where he studied medicine. Shortly thereafter he received a prize fellowship to a chair in physiology at the Nairobi Medical School in Kenya and later a Professorship of Medicine at the University of Montreal. Unfortunately, we lost him to cancer in April 2003. He was only 64 but during his lifetime authored or participated in 939 publications, receiving a further 114 patents in which he is a named inventor, bringing the grand total to 1053. From his first publication in 1964 to his death, this equates to one publication every two weeks for 39 years – a prodigious achievement. He also developed fatty acid supplements that were revolutionary for their time, one of which was Kirunal which he formulated specifically for schizophrenia, and to a lesser degree, bipolar, which he describes in chapter 17 of “The Madness”. The book is currently out of print, however, used copies and an imported paperback are available on Amazon.

Dr. Horrobin describes his collaboration with Malcolm Peet and Krishna Vaddadi and others who worked with chronic, difficult to-treat schizophrenic patients. Vaddadi’s early work in the field found that fatty acid abnormalities, specifically low arachidonic acid (AA), when exposed to a fever, manifested an improved mental and physical states. Schizophrenics also demonstrate resistance to pain and arthritis which is indicative of low AA (Horrobin 1995, 1998). These symptoms were corroborated in the patients’ red blood cell fatty acid test scores which showed a deficiency in both omega 6 (AA) and omega 3 (DHA) (Peet 2008).

Vaddadi, a Professor of Psychiatry at Monash University in Melbourne, was first to use gamma-linolenic acid (GLA, an AA precursor) to modulate schizotypal symptoms. However, the results were modest and too insignificant to rely on as a treatment (Vaddadi 1989, 2006). About the same time Horrobin and Peet collected additional evidence that omega-3’s as well as omega-6 fatty acids were deficient in schizophrenic patients (Horrobin 1994, Peet 1995). Shortly thereafter they began a series of trials that included both EPA and DHA from fish oils, focusing first on a higher concentration of one and then the other. They were shocked to learn that higher DHA levels did not improve the symptoms, in fact, the outcome was slightly negative. It was EPA that was beneficial; hence the focus on Kirunal which is formulated with twice the EPA to DHA ratio at 3 to 1 instead of the standard fish oil ratio of 1-1/2 to 1.

Case Study

Jonathon was thirty-one years old and had had a schizophrenic breakdown at the age of nineteen which caused him to drop out of college. Earlier he had received a single dose of an anti-schizophrenic drug but experienced such a severe adverse reaction that he vowed “never again – no drugs for me”. For ten years he drifted around London, leading the all-too-typical life of an unemployed schizophrenic patient. Peet was approached by Jonathon’s doctors who wanted to try Kirunal. Jonathan took 8gr a day providing him with about 2gr a day of pure EPA.

After four weeks there was no effect on his psychiatric state. His delusions, his auditory hallucinations and his general apathy were unchanged. But Alex, Jonathon’s doctor, felt that there was some improvement but difficult to define. She felt that he looked healthier, and that his skin and hair condition had improved. By eight weeks, Jonathan and Alex realized that something important had happened. Jonathan was clearly better. His appearance was transformed. He was more alert; more interested in life and had experienced a dramatic reduction in his delusions and hallucinations.

MAD-cellmembraneOne of the reasons why Alex was so interested in Jonathan was that he was dyslexic as well. She noted that on her tests for dyslexia his performance was improving. It was now quite easy to persuade Jonathan to continue with Kirunal. Over the following twelve months Jonathan progressively improved with regard to all aspects of his condition. After twelve years of illness, his scores on the schizophrenia rating scales were somewhat above the normal mean but not by much. People meeting him for the first time thought him somewhat quirky and unusual but certainly not schizophrenic. His dyslexia also improved substantially and he began to contemplate the idea of going back to school. Now, three years after starting the higher EPA fish oil, he has returned to college. But perhaps the most exciting aspect of Jonathan’s Kirunal treatment from the point of view of Alex is that his brain changes, as seen on the MRI scans, had reversed. He regained some of the brain tissue, the loss of which everyone believed to be permanent.

Meanwhile Malcolm Peet and Ramchand, a scientist from India, working together at Sheffield together with The Schizophrenia Association of Great Britain, organized a larger trial using Kirunal with 63 patients in Wales. The results matched Jonathon’s exciting success, but, in various degrees. For more complete details pick up a copy of the “The Madness”.

BodyBio: BodyBio was drawn into the schizophrenic scene from their research and extensive studies into psychosis and neurologic disorders and especially after the purchase of the Kirunal product line from the estate of David Horrobin after his death. Although BodyBio is a manufacturer of nutrients, it is predominantly a scientifically based research company focusing on the nutritional aspects of Fatty Acids (FA) such as Kirunal and conducts a series of lectures to doctors’ on the subject worldwide. After years of medical counseling and tracking patient’s results, BodyBio has realized that there is no single drug or nutritional answers for healing. As Vaddadi and Peet have shown prior, deficiencies in fatty acids can be confirmed by a red cell fatty acid analysis, which BodyBio has been performing for doctors for ~15 years. The lab work is performed at Johns Hopkins that is the gold standard fatty acid laboratory in the world. Fatty acids are a complex subject which BodyBio attempts to unravel for physicians and health care professionals through a proprietary computerized analysis to help clinicians digest the complex results for their patients.

FO-KirunalBasically, Kirunal is not a drug, it’s a food supplement. It is an omega 3 combination of fish oil constituents. It should be administered with respect to the body’s need for dietary balance between the n-3 FAs (EPA and DHA) and the n-6 FAs (AA). There are ~100 billion neurons in our brains which have a high concentration of arachidonic acid (AA) and docosahexaenoic acid (DHA). Horrobin says that the dry weight of the brain is 60% FAs and the DHA and AA content is 20% of that total (“The Madness”).

article1-PC-moleculeWhile these constitute 80-90% of the essential polyunsaturated fatty acids in our neuronal tissues, there is a deficit of AA in schizophrenia (Kim 2010), which is best obtained from diet (eggs, dairy, meat, fish and shellfish). Glen in ’94, reported that while there is a disturbed fatty acid profile in both negative and positive schizophrenics, the different forms take an opposite FA pathway. Those with negative symptoms are high in saturated FAs and low in the poly-unsaturates, while the reverse occurs in those with positive symptoms. However, all schizophrenics are low in both AA and DHA which is caused by an over-expression of phospholipaseA2 (PLA2). PLA2 is a lipase which cleaves off the FA on the sn2 position (the middle of the phospholipid molecule) where AA and DHA normally reside. This is a normal function, which, in schizophrenics is over-expressed, and which prematurely frees up much of the bound AA and DHA, dumping them into the FA pool, and effectively wasting the two most vital FAs in the brain. EPA (high in Kirunal) has the ability to lower PLA2, which in effect, would tend to keep AA in the membrane ready and waiting to become the all-important eicosanoid/prostaglandin, and, at the same time, keeping DHA there as well where it can perform its high-wire act facilitating neurotransmitter release.

When treating schizophrenia, psychiatrists are accustomed to the idea that it is better to use a single drug rather than poly-pharmacy. The same approach is taken when investigating any new treatments. However, nutritional treatments are different. Nutrients are normally ingested in complex combinations with food, and in normal physiology they act synergistically. Either deficiency or excess of a particular nutrient can have harmful effects. In schizophrenia, there is evidence for benefits, not only from omega-3 PUFAs, which would include DHA, and the n-6 PUFA for AA, but also from other nutrients. These include the “homocysteine-lowering” vitamins folate, B6, and B12 (Levine 2006), and the antioxidant vitamins (Peet 2008).

MAD-tree-renderingEarlier, in private discussions between Dr. Horrobin and Patricia Kane, PhD, (BodyBio’s Chief Medical Advisor), he confirmed the importance of fatty acid balance, and specifically noted that with Jonathon, as well as with all studies involving Kirunal, patients were encouraged to add into their diet foods high in omega 6 PUFAs like AA, high in eggs, butter and cream. He also made a special effort to lower sugar intake; however, that was not always successful.

Of special interest in the two journals both authored by Peet, Glen, and Horrobin on Schizophrenia and the Biochemistry of Phospholipids, “Phospholipid Spectrum Disorder in Psychiatry, 1999” and 2003”, there is extensive discussion on phospholipid metabolism. However, both journals predominantly lean towards genetics and the consumate protein and peptide functions in signal transduction. There is, however, a total absence of the clinical use of phospholipids, specifically phosphatidylcholine (PC), which has had a long history of success in clinics worldwide for over 30 years as either an IV infusion or an oral supplement. Brian Ross reporting in chapter two of the first edition, “Numerous, though not all, investigators have observed that levels of the major membrane phospholipids, phosphatidylcholine and phosphatidylethanolamine, are decreased in erythrocytes, platelets, and skin fibroplasts of patients with schizophrenia.” However, the observation from Ross never made its way into Horrobin’s scientific exploration with psychosis and schizophrenia. This is the exact arena where BodyBio has had much success bringing both PC and PE directly into the clinic as either an IV or orally, and more importantly, introducing it directly to the doctors and their patients with psychosis. Unfortunately, David’s life struggle occurred about the same time that Dr. Kane was beginning her clinical success with PC.

There are two more important parts to the fatty acid / schizophrenic equation, which exists in a large part with all neurological disturbances and all metabolism as well, that is (1) the need for a more correct dietary intake of the base essential oils, n-6 Linoleic Acid, and n-3 Alpha Linolenic acid (Yehuda et al. 1993-2008), and (2) the loss of phospholipids as mentioned above by Ross, predominantly phosphatidylcholine (PC), as we age or become ill (Yechiel 1985, Hennis 1085). BodyBio has a long history of teaching clinicians on the science of balancing FAs (6s and 3s) and the use of both oral and i.v. administration of PC.

An interesting sequel in the effort of finding an answer for the “schizophrenia problem” is the clinical use of phospholipids, specifically phosphatidylcholine (PC). PC as Essentiale and Lipostabil has been available in Europe since the ‘70s. Both were 5 ml i.v. ampoules of PC used to rebuild the membrane phospholipids (think improved signal transmission). Essentiale (Aventis) focused on liver disease and Lipostabil (Rhone Poulanc) primarily addressed cardiovascular disorders. Both have a long history of success, especially in the former Eastern bloc countries where every doctor in that large part of the world used i.v. PC therapy to rehabilitate Russian livers from the over consumption of vodka, which either Essentiale or Lipostabil can effectively do, and which, as you might imagine, is a recurring event. We can only assume that Horrobin and his group of competent researchers who followed his lead were aware of some of the medical history of the medical use of PC.

The sequel really started with Dr. Patricia Kane of BodyBio who had researched those early years of success with IV PC and thought “why not apply it for neurological disorders”, which has since performed equally well for all the neurological disorders of our day, Parkinson’s, Alzheimer’s, MS, fibromyalgia, Autism, erythromelogia, etc. However, that was just about the time we lost David Horrobin to cancer and even though Dr. Kane and Dr. Horrobin were in communication, her success was beyond the timing for sharing her results. Since then Dr. Kane and Ed Kane have lectured in the US and Europe on the IV technology she developed for clinicians under the name of the “PK Protocol”. In addition to the IV PC, BodyBio has developed an oral equivalent (BodyBio PC) that has achieved therapeutic success as well and on certain occasions is more desirable since it incorporates PE as well as PC, and as a capsule, patient acceptance and compliance are more certain than the compulsory doctor administered IV

However, there’s another chapter, the fatty acid ratio. For some time FA researchers were left with two problems 1) too much linoleic (LA n-6) in the diet (much of it hydrogenated or from overeating as in fried foods), and 2) how to fill in the all important alpha linolenic (ALA n-3) which had had been fraught with difficulty since the mid 1950-60s. The early researchers had tried flax oil, which, at ~55% ALA, amply supplied the all important need for n-3 Linolenic. They soon discovered that it was only beneficial for a short time (Joanna Budwig and Donald Rudin, even Udo Erasmus), after which the individuals developed skin and neurological problems which self-corrected if they abstained. The solution came from Yehuda, Mostofsky, Carasso and Rabinovitz from Bar Ilan University in Israel. This exceptional team under the guidance of Professor Shlomo Yehuda cracked what is probably the most important nutritional answer of our time, the dietary ratio of the Omega 6 EFAs to the Omega 3s, Linoleic to Linlolenic. Before their 1993 study “Modulation of learning, pain thresholds, and thermoregulation in the rat etc”, there had been no way to know which or how much essential oils we needed. Yehuda effectively answered that question with his SR3 1:4 ratio, one part ALA to four parts LA (20% n-3 to 80% n-6) (Yehuda et. al. 1993, 94, 95, 962, 972, 983, 992, 20002, 02, 03, 04, 052, 07, 08,etc). The value of Yehuda’s work to the health of the world is of such huge import as to warrant a nomination for a Nobel Prize. For more on this important FA question please refer to the BodyBio Bulletin on the 4-1 ratio.

“Almost fifty years after the first anti-schizophrenic drug, chlorpromazine, was produced we have made virtually no further progress in controlling schizophrenic symptoms. Drugs, on average, still improve symptoms by only 15-25 per cent, leaving 75-85 per cent of symptoms unresolved. The side-effects of Parkinsonism, tardive dyskinesia (TD) and agranulocytosis have been drastically reduced, but new side-effects of weight gain, sedation, diabetes and cardiac problems are still there and may have even worsened” (Horrobin 2001). These comments were made a decade ago prior to the current BodyBio research and the development of the PK Protocol which has witnessed significant improvements in neurological and psychotic symptoms but have only been enjoyed by those in the integrative community. The relief of symptoms, however, can be monumental for those afflicted. We invite your inquiries at BodyBio – 888 320 8338.


The information contained in this web site is for educational purposes only and is not intended or implied to be a substitute for professional medical advice. Inclusion here does not imply any endorsement or recommendation.  Always seek the advice of your physician or other qualified medical provider for all medical problems prior to starting any new regiment.

These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.

The Nerve of That Signal

FO-powerlinesNerves carry signals throughout the body initiating activity in the body and brain. What has been slow to grasp is the role of the cell membrane in carrying those signals. The membrane is the covering and protection of our nerves. It also houses (embraces) the electrolyte enzymes in its thin encasing sliver. The enzymes set up the metabolic environment in the body to enable signaling to occur. Nerves can be viewed similarly to the wiring in our homes. Both deliver energy to do work. No wires no signal; no membrane, also no signal, but of course, no cell as well.

Signal propagation in the body is a bit different than sending power to our homes but a wiring is necessary for both. The nerve is a specialized cell but it has all the standard cellular components of all cells, however, it is made up of a vast network of axons and branches that carry the signals managing our thoughts and actions. The signals travel on those specialized limbs which are endowed with the same structural membrane that encase all our cells throughout the body and the brain. In the nerves the membrane is the roadway for the message.

Producing electricity for our homes involves huge rotating generators that wipe off electrons and chase them back and forth in the power grid which we then tap into to run our homes and offices. For our body we use a far more efficient system to build the electrical force – charge separation,

To maintain charge separation (potassium on the inside, sodium on the outside), we use a large amount of energy estimated to be ~half of all we produce. It’s quite a system. There are thousands of sodium-potassium pumps on the membrane of every cell with the role of collecting 3 sodium ions from the inside of the cell – dumping them out – picking up 2 potassium ions from the blood stream and taking them in. Each ion channel engineers that hundreds of times per micro second. The result is a high differential on either side of the membrane of every cell, potassium on the inside – sodium on the outside.

To initiate a signal a sodium ion channel (a gang of them all at once) opens and lets a flood of Na ions in. Like opening the flood gates because thousands of sodium ions rush in per microsecond through each one. The result is a change in polarity that starts the signal propagation down the nerve so we can wiggle our nose or blink an eye.

The juice to run our lights and TVs travels on a copper wire surrounded by a plastic cover for insulation. Not so in our bodies, our signals dance on our insulating membrane as the channels open and close in rapid sequence. Our signals do not move down the center of our nerves; they travel on the outside skin, the membrane. The actual signal may be a rapid change of ph but the signal actually occurs on the membrane.

Mitochondria are tiny energy generators in every cell that produce ATP, our tiny batteries. It’s a process called “electron chain transfer”. It’s also referred to as the “citric acid cycle”, or “Krebs cycle”, from Hans Kreb, 1937. The first one is more graphic since an electron is moved forward in a chain-like transfer. There are ~2-500 mitochondria in every cell, 20,000 or more in a heart cell. The chain transfer cycle occurs inside the mitochondrion with special molecules that sit (of course) on the membrane; they take an electron (-) from a hydrogen atom and keep it occupied while flipping the proton (+) on the other side of the membrane thereby separating the electron from the proton. The electrons (-) all remain on the inside, in the matrix of the mitochondria, while the protons (+) collect on the outside of the membrane. That separation of using the membrane as the insulator is our power grid in miniature. Accumulating the protons (+s) becomes the force to do work.

The end product is energy (ATP) and water. The mitochondria employ the membrane as the key player for the production of energy, which is a far more elegant electrical system than what we use.

FO-cellmembraneAll membranes are composed of molecules called phospholipids (PLs) with each having two fatty acid tails. It looks like a double sticked lollypop. The tails are strings of carbon some of which we can make and some come only from the diet. The double sticks, the fatty acid strings, are either saturated or unsaturated and come in a wide variety, but the really important ones are the poly-unsaturated, the omega 6 and omega 3 fatty acids. They are essential, meaning they must be in our diet. Those EFAs, the essential fatty acids, are the basic building blocks of the membrane and the beginning of life. The truth is finally out, we’re all made of fat.

article1-PC-moleculeWherever we look, the star of the show is the membrane, a thin sliver of fat surrounding every cell. It separates the inside of the cell, the cytosol, from the outside. Its size and shape is identical in all of life, including the cells of animals, plants, bacteria, nerves, etc. It’s composed mostly of fats and lipids that make it a perfect insulator, permitting the vital differential charge which the cell uses to either send a signal or to get out of here quick, there’s danger ahead. The membrane may be the skin on the perimeter of the cell but it is truly the center of life.

FO-poleclimberNeurologists are well aware of the electron chain transfer and the production of energy in the mitochondria. They also know that all signals are propelled down the nerve on the membrane for thought, pleasure and pain, basically for everything we think or do. Sending the signal on its way is only possible if the membrane enzyme complex has first done its job for charge separation. The cell membrane never sleeps – working continuously to be ready to propagate the next signal on command. Every doctor and especially every neurologist are well aware, or should be, of these basic characteristics.

If so — is it a correct proposition that the first order of the day would be to feed the right EFAs into our bodies — and if we did, would that enhance the health of the membranes of our neurons? YES – without question, they are constantly rebuilding. Would that in turn influence signal transmission? YES – of course. How about memory? YES again.
Then why isn’t the health of the membrane the first consideration, the first choice of treatment for all neurological disorders that plague society such as Parkinson’s, MS, Fibromyalgia, Alzheimer’s, epilepsy, palsy, etc.? Why indeed!


The information contained in this web site is for educational purposes only and is not intended or implied to be a substitute for professional medical advice. Inclusion here does not imply any endorsement or recommendation.  Always seek the advice of your physician or other qualified medical provider for all medical problems prior to starting any new regiment.

These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.

The Remarkable 4:1 Fatty Acid Ratio and The Brain

FA-gearbrainDelving into the subject of the Brain and Essential Fats is a difficult journey, primarily because of how important the topic is and how little we know about how we think. There are 100 billion neurons sitting on top of our shoulders with ~60% of that nerve material made up of fats, saturated and unsaturated fatty acids (PUFAs) (Connor 1990, Chang 2009). Every day some portion of our nibbling finds its way into the neurons of our brain and through some miraculous cellular metabolism directly affects how we think, play, sleep and dream.

All cells have fatty acid membranes protecting the cytosolic life that goes on busily inside our cells day after day. Nerves are no different. Neurons have the same protective membranes with the same fatty acid phospholipid composition, but nerve membranes have a special job, they are endowed with the task of carrying all the signals inside our head and transmitting them to regulate all thought and motion. We can’t blink or think without fatty acids, yet we rarely give a thought about what we throw down. Venturing into the kitchen for sustenance puts us in charge of what goes into our brain, or, we may simply transfer that to McDonald’s or Taco Bell, now they’re in charge. The potential for brain damage is awesome, especially if there are little ones waiting patiently at the table. Since our brains are mostly fatty acids (60%), and essential fats should be in most every bite of food we take, a primer on fats and oils is in order, but, caution, there’s a bit of cell chemistry involved, but only a little bit.

This article has 5 basic subjects 1) Shlomo Yehuda’s groundbreaking discovery of the preferred ratio of omega 6 and omega 3 Essential Fatty Acids (EFAs) 2) Yehuda’s 2005 paper on Test Anxiety with his preferred fatty acid ratio, 3) the over consumption of Fish Oils, 4) a primer on fatty acid technology, 5) Good oils, not-so-good oils and bad oil, which – you might want to read first.

There is extensive research on the topic of “diet” and “brain”. Type those two words into Medline, and you’ll get 15,577 “hits” or research reports. Medline is part of the NIH in Washington that organizes medical studies from universities around the world. However, you’ll draw a blank slate if you believe you will advance your knowledge on how to change your diet so you can think better. The subjects of either diet or brain are well researched, but putting them together doesn’t elevate you, in fact the literature appears to say “we don’t have a clue” (Joint WHO/FAO 2002, FAO Food 2008). We know that the membrane is composed of saturated and unsaturated fatty acids, including the omega 6 and the omega 3s, but until the research of Shlomo Yehuda from Israel in 1993, the medical community did not know, and for the most part, even today, refuses to acknowledge the magnitude of his contribution to the subject.

FA-yehudaThe Breakthrough 4:1 Fatty Acid Ratio
Prior to his ’93 paper, “Modulation of learning, pain thresholds, and thermoregulation in the rat by preparations of free purified a-linolenic and linoleic acids:”, Yehuda and others had proposed that diet had an effect on the fatty acid composition of nerve membranes and even stated that fatty acids could mediate some of the observed changes in learning and behavior (Yehuda 1987, Coscina & Yehuda 1986, Yehuda & Carasso 1987, Yehuda 1989). Even though they had observed “changes in learning” in those prior studies, Yehuda now is more definitive. He clearly states in this study that modulation of learning is achieved using a 4:1 ratio, four parts of omega 6 linoleic acid (LA) and one part of omega 3 a-linolenic acid(ALA). He called it Special Formula 3 (SR-3). ω6 linoleic LA is in most all seeds and nuts such as safflower, sunflower, corn, soybean, cottonseed, canola, etc., while ω3 a-linolenic ALA, is found in flax, hemp, chia, walnut, soybean, etc. The discovery of the optimal dietary ratio of the Essential Fatty Acids (EFAs) was highly significant, since, being essential signifies that we cannot produce them and they must be in our food supply.

Earlier Research leading up to the 4:1
Prior experiments using 14C-labeled fatty acids (for brain tracking) had shown a cellular preferential uptake of omega 3 ALA over ω6 LA in the brain as early as 1973 Dhopeshwarkar , 1973). (ω is the lower case Greek letter omega). Initially they attempted to explain it by focusing on the amount of PUFAs (multiple double bonds) in soybean oil. However, sunflower oil, which contains a higher amount of PUFAs than soybean oil, failed to produce the positive effects of soybean oil (Yehuda & Carasso 1987, Yehuda 1989). Since the oil from soybeans contains more ALA (8-9%) than sunflower (about 0.4%), the benefits for the brain must have come from the increased ω3 a-linolenic. If the higher quantity of EFAs were not the answer, it must be somewhere in the ratio of the 6s and the 3s, the ratio to each other that held the key.

It was earlier recognized that ω6 LA (linoleic Acid) was important for normal health and brain development (Dhopeshwarkar, 1983). ω3 ALA had also been determined to have significant biological effects, now both were classified as EFAs (essential). Also, earlier studies suggested that ALA may be quite different from LA and may even have a biochemically distinct function (Bernsohn 1973).

Although there were a few clinical reports of the deficiency of ALA (Holman 1982, Bjerve 1989, Uauy 1990), a number of experiments in monkeys and rats had shown visual and learning impairment after consuming diets that were deficient in ω3 a-linolenic acid (Neuringer 1988, Bourre 1991, Connor 1991). These studies prompted a surge of interest in the role of ω3 ALA in brain development including the eyes (Bazan 1980,1990, Bourre 1989, Clandenin 1991, Cook 1991, Crawford 1976, Cunnane 1991, Holman 1991, Scott 1989, Simopoulos 1991, Specter 1989, Wainwright 1992, Weigand 1991).

Since ω6 LA is more common in our food supply than ω3 ALA, and ALA is now deemed to be essential, even though ω3 ALA is high in grasses, which is not common in our food supply, the question is, how much of each do we need.

The aim of the Yehuda ‘93 study was to test the basic hypothesis; is the ratio of linoleic acid to a-linolenic acid the key factor in mediating the beneficial effects of PUFAs in the body and especially in the brain? This required a significant amount of research to challenge and record the learning characteristics of small animals in a stress condition.

FA-micetrialsThe Learning Apparatus
The Morris water tank, a circular tank ~43 inches in diameter (110 cm), was filled with water with powdered milk added to make it opaque so that rats swimming in the tank were unable to see the resting platform submerged below water level. Each animal was released facing the wall in one of four predetermined starting points each separated by 90° around the inner perimeter. While the animal was swimming in the tank, it was able to observe the contents of the room. Special care was given to keep things in the room in the same location. They could navigate in the tank only by external cues, by looking around while paddling. Each animal was tested 8 times per day in the tank. The order of the starting points was determined by random selection. To prevent possible effects of a magnetic field, each one was allowed 120 sec. to find the platform, with an interval time of 20 sec. between trials. The maximum duration of the test was 16 minutes. The rats were tested on 3 consecutive days. During this period, the platform was in the same location in the tank. For each of the 24 trials (eight trials x three days), the time to find the platform was recorded. A cutoff criterion, defined as the first successful trial, was used to calculate an index of learning ability (rate of learning).

The research team tested 9 groups of rats with 7 different ratios of LA and ALA –3:1, 3.5:1, 4:1, 4.5:1, 5:1, 5.5: 1, and 6:1. Temperature control (thermoregulation) as well as motor activity, and pain threshold, were tested, food intake and body weight were all recorded. The ratios between 3.5:1 to 5:1 showed significant performance, however, the best of all was the 4:1, (4 parts ω6 linoleic to one part ω3 a-linolenic, 80% LA to 20% ALA (note, there is no omega 3 EPA or DHA, only ω3 ALA). The achievement of identifying the optimum 4:1 ratio was of major significance, and has been repeated by the Yehuda team in additional studies and also by others (Clark 1992, Wainwright 1992, Ristić 2003).

FA-budwig-rudinBudwig and Rudin
Looking back on those early years is important to grasp the significance of Yehuda’s SR-3. At BodyBio we had recently completed a computer software analysis of a Johns Hopkins red blood cell fatty acid analysis (RBCFA) as an analytical service for physicians, which was central for our teaching program of fatty acids and the cell membrane. However, the basis of nutritional treatment was a dietary adjustment using the correct EFA oils according to each individual’s test. ALA had been determined by many others to be the key missing ingredient. Discovering Yehuda’s SR-3 was a major breakthrough, since prior dietary efforts to add in the missing a-linolenic acid (ALA) had been a hit or miss exercise. Both seed oils containing ω6 (LA) or ω3 (ALA) were readily available, however, we knew that focusing on either ALA or LA, by themselves, would not provide benefits primarily from the prior history of both Drs. Johanna Budwig and Donald Rudin. Between 1960 both (Budwig) and through 1980 (Rudin) experimented with flax oil, which has a high ALA content (~55%). For years both used flax oil and both recorded significant improvements for disorders such as Schizophrenia, gastrointestinal, drying skin diseases, mucous colitis (spastic colon, irritable bowel syndrome) and others, including cancer. They both reported remarkable healing results. Rudin, specifically wrote that it could last several months, but was always followed by a complete reversal, requiring stopping the flax oil. Then, several months later, he would try flax oil again on the same patient and it would work again, but only for a while and the on-again off-again cycle would return. One can only imagine their level of frustration. Both were brilliant scientists who had published extensively. Rudin was an MD and a Harvard professor, and Budwig had been nominated for a Nobel Prize seven times.

FA-balanceOil-productBoth had correctly identified ω3 a-linolenic as the missing nutritional ingredient for innumerable disorders that plagued society. The EFA ratio of flax oil is 1 to 3.5, completely opposite to Yehuda’s 4:1. They were using too much ALA. If only they had known of Yehuda’s work, the entire history of fatty acids would be rewritten. We know of this first hand since Donald Rudin was on our BodyBio Board of Advisors and shared his experience with us first hand. Unfortunately, he passed away in 2003. Before his death, Dr. Rudin wrote a letter to the editor of the Lancet, which was published, wherein he described the current fish oil ‘Omega 3 Overdose Syndrome.’

Ongoing Yehuda Research
After ’93, the Yehuda group continued their research with numerous studies using the SR-3 formula on both animals and humans, here are a few examples: 1994 on epileptic seizures with 84% reduction of seizures, 1996 on Alzheimer’s with improvements in mood, cooperation, appetite, sleep, ability to navigate in the home, and short term memory, 1996 on lowering cholesterol with improvements in fluidity, cognition, and neuro-pharmacological effects, 1997 with improved learning and improved neuronal communication, 1998 with in-depth analysis of learning, neuronal membrane composition and increases in brain essential fatty acid levels, 2000 on lowering cholesterol, stress, and improved learning, 2001 mediation of the nervous, endocrine, and immune systems, 2004 on control of induced anorexia and improved myelination, 2004 on seizure management, 2005 on student Test Anxiety (details below), 2007 on sleep deprivation, REM sleep, and cognitive impairment, 2011 on ADHD, currently poorly handled with drugs (check out “Anatomy of an Epidemic” by Robert Whitaker, 2010, a must read for anyone concerned about ADHD and all psychiatric disorders).

My wife, Dr. Patricia Kane, and I, have spent almost two decades teaching Yehuda’s brilliant work (the PK Protocol) to a growing group of doctors and their patients worldwide, which, even though subjective lacking documented research, have witnessed dramatic improvements for individuals especially with neurological disorders. In reviewing Yehuda’s studies for this article, we selected the 2005 paper on Test Anxiety with students, which epitomizes the uniqueness of the 4:1 ratio. Test anxiety can seriously impair academic performance, and the mere anticipation of a critical examination can hinder the ability to study for it. All of us, at one time or another, have experienced “Test Anxiety”. The anxiety experienced before an exam or an interview, or first standing before an audience, or a first date, or beginning an athletic event before a crowd of onlookers, all can induce apprehension and anxiety. It’s a universal malady; you could call it “butterflies”.

FA-anxietyManTest Anxiety 2005
As head professor of advanced psychology at Bar Ilan University, Israel, Yehuda had ample experience for this disorder. He first secured two trained psychologists who identified 126 male students as test anxiety sufferers. The Bar Ilan University Ethics Committee approved the study. Seventy other students from the same classes who did not suffer test anxiety, served as the control group. The study started one month before the examination. No food intake was allowed 30min before taking the sample. Each subject was instructed to take one capsule which contained 225 mg of pure linoleic acid and pure a-linolenic acid in a ratio of 4:1, twice daily in the morning and evening. Thirty-eight students received placebo (mineral oil) and 88 received the special FA mixture.

There’s no easy way to judge the EFA’s examination outcomes, however, there are a number of characteristics that illuminated their benefits. The subjects reported better appetite, improved mood, better ability to concentrate, less fatigue during the day, better sleep and the ability to organize themselves for the test was much improved. No improvement was observed among the placebo group. The non-anxiety group who also took the treatment likewise showed some improvement in ability to concentrate, less fatigue during day and improved quality of sleep. While test anxiety students showed an elevated morning cortisol level, the PUFA treatment reduced the elevated level to normal. It is interesting to note that the control group also showed a reduction in their cortisol level.

Improving cortisol levels (lowering) with the SR-3 mixture had also been reported earlier (Yehuda et al. 1999, Van Duinen et al. 2004). The Anxiety Study started one month before the examination. Morning salivary cortisol samples were collected at 8:00 AM, while the subjects were still at home. No food intake was allowed 30min before taking the sample. Briefly, samples were collected using cotton swabs chewed for 2 min and inserted into a plastic test tube, cooled and later measured by radio immunoassay. Seventy-eight out of the 88 test anxiety students reported that even after the conclusion of the study they no longer experience a state of anxiety.

FA-veggieKidEven though the Test Anxiety study demonstrates the importance of correcting body EFAs though diet, there is a subtle characteristic reviewing the results. The improved studying capability occurs without fanfare. There’s no spontaneous improvement, which suggests a subtle changed mental ability. It now becomes the norm. It’s not easy to wrap your mind around the implications of adding the correct EFAs to the diet. Just one teaspoon of 4:1 oil a day. How difficult is that? We readily add 3-4 times that much oil on our salads, which rarely provide the correct EFAs we need. It is generally something like olive oil, which has little beneficial value. What would that do for our youngsters, not just university students, going to school every day? The whole concept is life-changing, and the cost is literally peanuts. At BodyBio we currently use a mixture of sunflower and flax oils that we combine to deliver a 4:1 ratio. Some of our little ones take 5 – 6 tablespoons a day, and request it. Imagine – they request it. What do they know—or what is their brain telling them they need?

FA-mombabyThe Basic Fatty Acid Dilemna
Part of the difficulty of a better understanding of fats and oils stems from the word itself – fat. Some think instantly of excess weight or of someone they knew who was a bit dull “fathead”. The word “fat” has a bad image. In addition the recent media explosion regarding fish oils has managed to distort the entire fatty acid picture. Anyone interested in their health searching Google for the latest is inundated with the marvelous results of fish oil and omega 3 EPA and DHA. However, reviewing the research of brain benefits for fish oil the results are mixed, there are as many negative results as positive (Holness 2004, Arendash 2007, Church 2010, Rockett 2012), even though fish has long been regarded as brain-food.

The sheer volume of information on fish oil and omega 3 is overwhelming. As you would imagine much of the Googled information originates from producers touting their special fish oil. After so much media hype, the inevitable occurred sweeping everyone into taking fish oil. The general philosophy prevailed, “if one is good, 2 or more is better”. I don’t have to tell you that most go for the “MORE”. Yes – fish oils are important for our health, but, careful, too much of any nutrient can harm, remember Budwig and Rudin. At BodyBio we see the over-expression in their RBCFA test results from Hopkins. The over-expression of fish oil has become endemic. Almost everyone seeking to improve their health has taken too much. The RBCFA Report tells it like it is. Too much omega 3 fish oil suppresses the omega 6s. You now have too much 3s and too little 6s, all of which is correctable, if, you know that you have overindulged. Most don’t know. Most never get an RBCFA Report which could tell them. Should you now rush out and get a FA test? The answer is — not necessarily. That’s a medical decision. If you’ve taken more than one a day, our general suggestion is to stop the fish oils and go back to eating fish, or, stop for 3-6 months and then take just 2-4 capsules per week, which will allow the body’s metabolism time to readjust. However, if you are plagued with a difficult health problem an effort to balance your EFAs scientifically is highly recommended, but would require a consultation with your doctor.

Most everyone associates fish oil with the omega 3s, which they are, but – fatty acid technology needs a bit more explanation. To get “the rest of the story” please read the Two EFA Families.

The Two Essential FA Families and their two levels:
As reported there are two (2) EFA families, omega 6 (ω6) and omega 3 (ω3), with the lower FA level LA and ALA (1st floor) becoming the precursor for the upper FA levels (2nd floor) in both families. The lower ω6 level is linoleic acid (LA), found in most nuts and seeds and high in safflower, sunflower, corn, soybean, *cottonseed, *canola, etc. (*these last two are not recommended, canola is high in erucic acid which is toxic to the membrane, cottonseed is permitted higher pesticides since it is not classed as a food). The 2nd floor ω6s, which all animals can produce initially, however slight, is arachidonic acid (AA), which the media has been attacking for half a century, and which is also totally mistaken. There are also two additional 2nd floor ω6 EFAs, GLA from Primrose oil and DGLA from GLA, both are on the 2nd floor with AA. For this discussion we will disregard GLA and DGLA and confine the 2nd floor omega 6s to AA. The 1st floor ω3 FA is a-linolenic acid (ALA) found in flax, hemp, chia, walnuts, soybeans, canola, etc, which is the precursor for the 2nd floor ω3s, EPA (eicosapentaenoic acid) and DHA (docosapentaenoic acid). Viewing the precursors ALA and LA as living on the 1st floor and AA, EPA and DHA as living on the 2nd, we can begin to unravel the distortion of fish oils and the omega 3s.

Fish oil contains only the 2nd floor EPA and DHA, while eating fish provides all of the membrane FAs that the body needs including ω6 EFAs (Connor 1990). A reverse distortion is quite possible concerning omega 6s. Egg yolk contains a high concentration of AA. Imagine a concentrated capsule of egg yolk with a high AA content, which, I must add, we would welcome for individuals with a low test result of AA. Now picture the media taking off touting “Egg Yolk” and the health benefits of Arachidonic Acid (Payet 2004), which is critical for our health (eggs and animal proteins are a preferred source of AA). However, touting that singular nutrient “Egg Yolk AA”, even though important, would not work any better than it has for fish oil. The end result would be an overdose of AA. Balanced nutrition is the only way to go. The vast majority of the media has been woefully ignorant of the two levels of EFAs in their touting of fish oils, omega 3s, and their tirade against ω6s and inflammation, which, is significantly one sided and beyond the scope of this article*.

FA-fishoil-pillsThe Large Animal FA Dilemma
Humans have very limited ability to take the 1st floor EFAs, LA and ALA, and metabolize them up to the 2nd floor EFAs, DGLA, AA, EPA, and DHA (Singh 2005, Chang 2009). Our cellular production for all the vital 2nd floor fatty acids dramatically declines with age (Uauy 2006). All large animals, which we are, lose the ability to maintain adequate production of 2nd floor EFAs, either ω6 or ω3s. Little guys like mice and gerbils, etc., are capable in producing all the AA, EPA and DHA they need, and they do it from LA and ALA. Their metabolism is much higher and their life span much shorter. They can do it – we can’t. So, in a way, for us, all the FAs on the 2nd floor, of necessity, become Essential. We must add them into our diet (which has been our evolutionary history). As a consequence of the metabolic insufficiency, all large animals including the grazing animals, in ratio to their size, have smaller brains and weaker eyesight, except humans and dolphins (Crawford 1989, 2000). All predators get their 2nd floor EFAs – predominantly AA and DHA, from the internal organs and brains of the grass eaters which have accumulated them over their lifetimes. Predators enjoy the higher EFAs at almost every meal, which directly relates to their superior brains and eyesight. Where do we fit into that evolutionary picture (?), certainly not with the grazers.

As discussed, much of Yehuda’s research was with rats. To an extent, using efficient little animals has added to the confusion regarding our evolution. How come we are we so smart and endowed with a large brain if we are inefficient in metabolizing the important brain fatty acids that would make us smart? Michael Crawford, Imperial College, London, along with David Marsh, clears up the mystery in ‘The Driving Force’. They hypothesized, that we did not evolve on the plains of Africa, we were more aquatic and lived near oceans or lakes where we had access to shell fish, crustaceans, and fish oils, as we continue to do today with modern cooling technology.

Fatty Acid metabolism is generally not a table-talk discussion, even though it is a part of most meals and a vital detail for our health. The health value of the essential omega 6s does not correlate with the media hype of claiming that they are the sole source of inflammation in the body*, or that fish oil and the omega 3s are the panacea. However, fatty acid technical manuals cover the subject of fatty acids and membranes quite accurately, showing the beneficial role of the ω6 PUFAs. Also, the newly discovered 4:1 ratio brings the ω3 ALA PUFAs into a clearer focus.

Yehuda laid the foundation in ‘93 with his seminal paper regarding the ratio between the omegas’. His profound 4:1 ratio of omega 6 LA and omega 3 ALA has given us the basic Essential FA formula to enable us to raise fluidity (Yehuda 1996, 2012, Lu XF 2010) of our highly active membranes, which are endowed with that very task. Now, we are better equipped to send the right signals from the brain to run the entire system, and we can do it throughout our lives. In media vernacular, that’s “News”. Think of it – brain function for a lifetime. Take a walk through any psychiatrist office on the globe today and the mere thought of sending clear intelligent signals simply by changing your diet, takes on a whole new meaning.

Good oils, not-so-good oils and bad oils
However it evolved, the bad image of FATs is with us, even though fatty acids are vital for every cell of the body and brain. To add to the distortion, the medical media has descended on saturated fats as heart destructive, which it is not, yet reversing a 100 year negative concept is probably impossible; however, we may be able to dent it with facts.

  1. article1-LipidMembraneFats and oils come in just 2 varieties, either phospholipids with two fatty acid tails or triglycerides with three FA tails. Phospholipids make up the protective skin of the membranes of our cells, while triglycerides are simply put away for later. Phospholipids are tiny building blocks which automatically assemble into membranes and surround every cell and organelle. They are the beginning of all life on the planet, and they are 70% FAT.
  2. FA-moleculeFatty acids do not make you fat, carbs do. Carbohydrates (excess sugar) are converted into the 3 tailed FAs – triglycerides, which are stored for use later, an important asset to have in case we run out of food, which no one does any more, at least not the ones in our neighborhood. A triglyceride is a fat molecule with 3 (tri) fatty acid chains that finds their way around our middle and is the stored fat we regard as “bad”, however, on a baby it can be quite pleasant.
  3. We generally eat fats at most every meal, even if it’s in a salad with dressing. The EFAs are highly fluid, but the SFAs (saturated FAs) are rigid, they are not fluid. Real butter from a cow is a SFA. Our membranes need the SFAs for substance and form, however, we are able to produce SFAs, they are not essential. Most all seeds and nuts have fluid EFAs that are crushed into oils that go into food manufacturing, most of which are over-processed and become rancid and/or hydrogenated, which covers all supermarket oils on the shelf. The over-processing oils also include processed butter look-a-likes, margarines, butter-type spreads, including your favorite mayonnaise, Hellman’s, Mayo, etc. Vegenaise, in the refrigerated section, is a much better choice for mayonnaise.The runny, liquid oils (safflower, sunflower, soybean, corn, flax, etc.) contain the healthy EFAs and should be cold pressed and organic for your table oils. Suggest keeping them in the frig. SFAs are solid in the body (butter, lard, coconut (less so)) but are still vital for our health. They are plentiful in animal foods (beef, eggs, chicken, fish etc.). We need both, SFAs and EFAs.
  4. FA-oliveoil-bottleWhat we generally do not need are MUFAs, mono-unsaturated FAs. They are the omega 9s, predominantly olive oil. All plants and animals are able to produce ω9 MUFA, which provides some fluidity in the body, but, in reality, ω9s are inconsequential. We don’t need them which includes olive oil. It will not harm you if you use it, but will not be missed if you avoid it. Olive oil has an image of health – and respectability. Placing a bottle of olive oil on the table makes the chef look good, though, in essence, what olive oil actually does is provide an oil with less value when there are really better choices. Olive oil has a nice image, but the EFAs are where the action is for body function, especially the brain. If the EFAs are not on the table where you can eat them, you’re thinking machinery will just make do without — not a good idea. Put the olive oil back on the kitchen counter, you can heat it without concern so use it for cooking.
  5. FA-coconutCoconut oil – now there’s a winner. Coconut oil is fluid in the body, but it’s solid in any spot on the globe that happens to be cool. Coconut is a medium chain fat which is rapidly burned for energy in the mitochondria, which loves those shorter FA chains. They are more easily handled and absorbed. There is no better oil for French fries than coconut. In fact that should be a stable food in every house. Try it, their yummy.
  6. FA-frenchFriesThe bad guys on the block are the fast food fries, they’re everywhere in most every fast food chain. They all use vegetable oils, the EFAs, which should not be heated because of their multiple double bonds. They quickly become rancid, and are turned into hydrogenated fats, trans fats, the worse kind for our health. The Fast Food emporiums all heat the EFA oils over and over again, and, for the most part, this same disregard for oils goes on in every restaurant on the globe making it very difficult to dine out and make good food choices.
  7. Over the last century and continuing today, we have been plagued with disinformation about Fats and Oils and have been the recipients of bad manufacturing processes originating from the oil and food producers with mechanical hydrogenation of the EFAs. This is currently changing and becoming less in the Western countries with the increased knowledge of trans fats. However, this ugly mechanical distortion of oils has yet to reach most of the world.

The information contained in this web site is for educational purposes only and is not intended or implied to be a substitute for professional medical advice. Inclusion here does not imply any endorsement or recommendation.  Always seek the advice of your physician or other qualified medical provider for all medical problems prior to starting any new regiment.

These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.

Fat Facts on Omega 3 and Omega 6 Fatty Acids

Omega-3 fatty acids —EPA and DHA— are the BIG news in nutritional m medicine today — and for some very good reasons. The scientific evidence is now irrefutable that EPA and DHA are essential for good health and long life. They are such important nutrients that agencies and institutions historically hostile to nutrition have gone on record to support their use. The American Medical Association, the American Heart Association, the United States Department of Agriculture (USDA), even the good ol’ “Food and Drug Administration (FDA),” are all praising EPA and DHA.

While all of this is certainly a positive development, the rise in sales of omega 3 (n-3) fatty acid is in direct response to the high press coverage. It’s like everybody on the globe is jumping on the omega 3 fish oil bandwagon. The result of this excessive reporting in the media with relatively little knowledge of fatty acid chemistry, has lead to overindulgence (prescribing and taking too much). TThis overzealous use of omega-3 fish oils has occurred worldwide at a disturbing rate.

At BodyBio we have been observing these results through the in-depth examination of thousands of individual fatty acid tests, year after year. Analyzing red blood cell fatty acids (RBCFAs) is a principal part of what we do at BodyBio. The bioactive ingredients of fish oil, EPA and DHA, are generally found in a ratio of 3 to 2 (180 mg of EPA and 120 of DHA). They are both dynamic and powerful nutrients, with a wide range of functions that influence the brain, the sensory organs, synaptic and cardiac activity, and the modulation of arachidonic acid effects in inflammation. All membrane fatty acids are intimately involved in regulating all aspects of the body’s chemistry, including control of each others’ families, the 6s and the 3s. However, excess omega 3s will easily suppress the omega 6s, whereas the reverse does not seem to occur; 6s do not suppress the 3s.

If we follow the popular media mantra, we are led to believe that adding fish oil to the diet will improve our wellbeing by raising the omega 3s and avoiding / lowering the omega 6s. This should be a good thing, since any suppression of omega 6 arachidonic acid would tend to reduce inflammation and lead to a healthier state. However, based on our research and the testing of red cell lipids over the years, we have found the opposite to be true. Dr. Patricia Kane’s own findings concur.

To understand the fatty acid disturbance we see requires a shift in thinking about omega 6 fatty acids and inflammation. While inflammation can be disturbing, in itself it should not be regarded as bad. Aside from the correction that the body undertakes to alleviate the stress that results in inflamed tissues, it is predominantly sending a signal, a message that something is wrong. We certainly want to suppress the disturbance, but the last thing we should be doing is killing the messenger, which is exactly what fish oil does.

More than 80% of the BodyBio red cell fatty acid tests performed yearly* register high omega 3s and low omega 6s. There is a direct correlation with the amount of fish oil consumed and the elevation of EPA and DHA. Associated with the distorted fatty acid analysis is a wide array of disorders, such as fatigue, irritable bowel syndrome, nausea, eczema, headaches, visual disturbance, memory loss, etc.

While we are told that omega 6s are “bad guys,” there is really no such thing. If it is essential, as omega 6s are, and the body spends precious energy to create and maintain it, it is wrong to assume that the metabolic effort is misdirected. Maybe too little or too much — but certainly not bad. Currently, there is no way for humans to survive without omega 6 fatty acids. This includes arachidonic acid (AA), containing 4 double bonds and occupying as much as 14% of the red cell membrane.  Arachidonic acid also boasts the highest concentration of energy in the membrane as the lead regulator of all cellular signaling, and quite possibly of all regulation in the body. As we have recently seen and hereby report the suppression of AA in a large number of individuals by the over-consumption of fish oil has been directly responsible for an unusual increase in physical and mental distress.

Our approach is to remove fish oil from the diet for a time and to encourage a nutrient-dense diet that is low in carbohydrates and rich in omega 6 fats from foods that include egg yolks, evening primrose oil and a blend of cold-pressed safflower and flaxseed oils (BodyBio Balance Oil delivers a 4:1 ratio of linoleic acid to alpha-linolenic acid.).  Together with essential vitamins and minerals, these dietary inclusions help to elevate lower-order EFA saturation levels. The patients, after shifting their diet and supplementation, consistently report that they all improve. In the world of medicine one should never say all, however, we repeat, all patients tend to reverse their negative symptoms by bringing their omega 6s and their omega 3s back in balance.

It is, after all, about balance. Is fish oil bad for you?? Of course not! The error, either by self-medication or by being over prescribed, is an excessive expression of omega 3s which can occur with any drug or nutrient. Also required, and in part because the medical reliance on fatty acid nutrition is quite new, is a new-found respect for the metabolic power of the omega 3s, especially EPA. Without the valuable analysis from the world’s premier fatty acid laboratory, we would never have been able to make this analysis and relay to you how to readjust your patient’s essential fatty acid balance. We would have no reference to do so.

*The vast majority of BodyBio Red Cell tests were performed on individuals who had been seeking medical help for a period of time before consenting to do an Fatty Acid Analysis. Fish oils were commonly employed in their effort to find relief. The 80% referred to above is unusually high but is the result of 1) that narrow select group and 2) the individuals personal reporting of the use of fish oils often over several years. Would this have been the case 20 years ago? Probably not.

CASE HISTORY #1
Annette was determined that she would not follow in her family’s footsteps in regard to her health. To hold off aging and ill health she used 10 capsules daily of fish oil, restricted all meat, eggs and dairy in her diet and limited her intake of all oil except olive oil that she used in her salad and to cook with. After two years of high fish oil intake, Annette noticed that she was developing eczema. Her allergies got much worse and she felt tired all the time. Her moodiness was irritating to others but worst of all she had developed severe difficulties with her ability to think and perform at work. Annette visited a physician specializing in fatty acid therapy and longevity who tested her red cell lipids and found them to be alarmingly unbalanced. Her omega 3 EPA was 1500% high while her omega 6 Arachidonic Acid was 156 % low and her omega 6 Gamma Linolenic Acid was 94% low. Her doctor explained the importance of balance of her fatty acids and set up a targeted nutritional protocol for her. After two weeks of getting on the correct balance of fatty acids Annette felt much better. Her eczema started to clear, her mood stabilized, her energy and alertness returned and she found her work performance normalized. After 6 months of re-balancing Annette’s physician allowed her to begin fish oil with one capsule of Kirunal daily along with wild salmon and sardines, evening primrose, 4:1 omega 6 to omega 3 balanced oil, and eggs / butter in her diet.

CASE HISTORY #2
Jordan is a 3 year old boy with autism. His mother was told by his natural practitioner to give him 4 capsules of fi sh oil daily. After 4 months on fish oil Jordan’s behavior and attention had deteriorated. Testing Jordan’s red cell lipids revealed that he had a gross overdose of omega 3 as EPA and DHA with a deep suppression of the omega 6s. Jordan was then given primrose oil, eggs, butter and safflower oil for a few months and his behavior and attention improved dramatically. In keeping with balance, Jordan was then given 4:1 omega 6 to omega 3 balanced oil, primrose, eggs / butter and one capsule of Kirunal three times weekly to maintain a balance of his essential fatty acids.

CASE HISTORY #3
Adam is an 8 year old boy with Muscular Dystrophy. A health care practitioner prescribed 6 tablespoons of fish oil which he took over an 18 month period. Adam’s parents were deeply concerned with his deteriorating condition and a red cell lipid test was drawn June 2005. Adam’s EPA was grossly elevated (H) at 3888 %, his DHA was also (H) at 312 % and his Arachidonic was deeply suppressed (L) at 356 %. Adam’s EPA was the highest on record with Arachidonic Acid the lowest ever recorded. Adam presented with symptoms of nausea, poor appetite, hypotonia (low muscle tone), poor coordination, severely abnormal gait (walking), with stiff and very slow movement. Interesting to note that Adam’s brain function was good, even elevated, however he could not perform physically. As soon as the fi sh oil was stopped Adam’s appetite increased and his nausea disappeared. He was started on 10 capsules of high potency evening primrose oil daily along with 4 tablespoons of 4 to 1 omega 6 to omega 3 oil. Because of the severe distortion of Adam’s essential fatty acids it will be necessary to retest in 3 months to track the changes. Fatty Acids are normally tested yearly.

Adam’s hypotonia provides a clearer picture of the modulating effect of EPA on Arachidonic. the term modulate is insuffcient to describe the power of EPA considering excess intake. It takes an exaggerated overdose such as Adam’s to paint a vivid picture of the power of fatty acid function. Elevation of EPA can literally block function, not just modulate, thereby impacting all thought and motion. EPA’s effect is similar to the action of NSAIDS blocking Cox I and II, and could be an alternative therapy to those common drugs. A concept anathema to the drug world since the occasional use of EPA would have few negative concerns, however, deep over-expression could be — as with the above case histories. the mode of action of NSAIDS is to specifically block Arachidonic, which it effectively does. EPA accomplishes the same effect, which opens a new focus on EFA metabolism. It also brings the omega 3 fatty acids into sharper focus in relation to drugs and homeostasis, all of which is little understood or appreciated in today’s rush to endorse too much fish oil. A smaller fish oil capsule with a higher EPA content such as Kirunal could be a much better choice to fight inflammation. It’s natural (NSAIDs are drugs) and we all need fish oil, they’re essential – however, as stated above, use carefully.


Note: There is an innate ability to re-acquire a balanced state given a change in lifestyle. The variation in age, gender, and general health are so varied that to make an estimate as to time difficult. Physicians can order a BodyBio Fatty Acid Profile for accurate assessment to determine the right balance of fatty acids needed. (Information on the BodyBio Red Blood Cell FA test for Health Care Providers – please call BodyBio at 888 320 8338 or go to our website at bodybio.com).

The literature is replete with information on the value of omega 3, with little on the value of omega 6. It is much too deep and complicated a subject to address in brief; however, the omega 6 family is by far the predominant fatty acid family, having vast number of management functions throughout the body. The power of EPA, at ~ 0.46% of the red cell compared to ~14% of arachidonic acid, is relegated to modulate and down-regulate arachidonate, thereby refining function and raising performance to a higher level, which it effectively does. A look inside the retina provides an excellent example of the specialization of the two fatty acid families.

There are 100 million photoreceptor cells responsible for sight in each retina. To perform at a high level they require the optimal lipid energy available in the membranes of the outer segment of the cell. Predators such as cats, bears, birds of prey, all carnivorous life in the oceans, and especially primates have a high concentration of DHA, a 22 lipid carbon chain. DHA has the highest number of double bonds [6] within that chain. The more double bonds, the higher the energy value.

In primates, particularly humans, the membrane of the eye contains ~50-55% DHA (the highest in the body, the brain has ~17- 22%). Grazing animals have ample access to the lowest order of omega 3, alpha linolenic (ALA), which begins the n-3 family with 3 double bonds. ALA is high in green leafy vegetation, although the fatty acid content is low. However, grazing animals cannot efficiently metabolize ALA up to DHA. We are also inefficient in this process, however, we are a predator – we can eat fish and get all the DHA we need. Small mammals, such rats are 100% efficient in fatty acid metabolism. The big grass eaters use instead a 22 carbon omega 6, which they metabolize up to 5 double bonds, the maximum number for the n-6s.

There is a dramatic difference in the energy value of a 22 carbon n-6 with 5 double bonds contrasted to a 22 carbon n-3 DHA with 6 double bonds. That difference registers with a significant improvement in eyesight, which gives all predators a leg up in survival. The big cats can watch the herd close u,p whereas the antelopes have to raise their noses high in the air and sniff, hoping to get a sense of what’s out there. That’s a huge advantage. In addition, the higher concentration of DHA in our predator brains translates to higher intelligence since DHA is directly involved with synaptic activity and brain function. However, it does not correlate that an over-expression of DHA will increase brain power in adults, but if the mother does not take in sufficient omega 3 HUFAs (highly unsaturated fatty acids with DHA) during pregnancy or when nursing, the baby’s intellect may not fully develop. The pregnant mother needs generous intakes to nurture her fetus throughout pregnancy. Postpartum depression has in fact, been linked to omega-3 deficiency. The newborn needs it to build and mature all the organs. Older children need the omega-3s to help them function in school and avoid behavioral problems. Parents need them also, perhaps even more so.

The Right Stuff

Getting these vital fatty acids into the body has presented a challenge of purity, itself a concept that encompasses more than a single idea. Acquiring oil from fish is not as simple as getting juice from an orange, where a single earnest squeeze yields results. In juice, there is nothing that needs to be separated, unless pulp is an issue. With fish bodies, there are concerns with removing proteins, environmental insults like heavy metals and micro-organisms, and even ancillary fats that might impede EFA/DHA uptake.

Practically endless discussion has pitted the triglyceride (TG) form of fish oil against the ethyl-ester (EE) form in terms of bioavailability, safety and efficacy. Looking at myriad scientific reviews, we conclude that the differences are minor and inconsequential, unable to be judged as physiologically or clinically significant. So far, it seems that once a steady state of supplementation has been achieved, the biological outcomes are alike. In fact, most CVD-related trials have used the EE form and the National Eye Institute uses it in its AREDS 2 trials (West, 2016) (Ackman, 1992). Clouding the matter is that humans absorb these fats through different routes:  preduodenal, lymphatic via chylomicrons, and the route that uses the portal vein to the liver. Thus, it is difficult to compare results. It is the EE form that has been recommended for standardization (and has been used to manufacture a pharmaceutical fish oil).

BodyBio Kirunal is derived from fish bodies by a process that uses supercritical fluid extraction based on the very low temperatures of solid carbon dioxide. This process provides an oxygen-free media, therein preventing the oxidation and eventual rancidity common to most fish oil products on the market. It further allows extracting selectively low polar lipid compounds, thus avoiding the co-extraction of polar impurities that include inorganic substances, such as heavy metals.

If there be a limitation to supercritical CO2 extraction, it is the increased cost, not only because of the high-pressure equipment, but also because the raw material needs to be freeze dried in order to reduce moisture below 20% and to keep the n-3 fats, the delicate PUFA’s, unaltered. The high level of n-3 fats in supercritical CO2 extraction surpasses all other processes, largely due to low temperatures and a non-oxidant atmosphere. Rarely does the temperature reach 104° F (40 ° C).

There is no detriment to appearance of the oil liberated in this manner, since color, neutral lipid composition and fatty acids profiles are similar. Important are oil acidity, total oxidation value, inclusion of volatile compounds, sensory properties and heavy metals, all of these characters favoring the supercritical CO2 method. Here, fishy off-flavors are eliminated and the potential for a trimethylamine miasma removed.

To BodyBio’s delight, in spite of the high initial investment, refinement costs and downstream processing eventually make the process competitive in that it may likewise be used to make specialty oils, such as nut oils and seed oils.

EPA and DHA are large and spacious n-3 fats, unable to sit next to each other on a single glycerol molecule. Therefore, most fish oils do not contain more than about 30% EPA and DHA. To increase concentration, these fatty acids can be removed by converting them to ethyl esters. Once they are freed, their concentrations are enriched. Supercritical extraction is able to reduce or eliminate cholesterol and contaminants that include the typical environmental insults, such as dioxins, PCB’s, and heavy metals, offering an EPA/DHA content in excess of 60%. Extending the process to feature supercritical fluid chromatography, 90%+ concentrations may be realized.

Molecular distillation, long the darling of the fish oil trade, suffers as much as 350% higher thermal stress than supercritical fluid extraction, and a much lower capability to selectively extract the essential fats desired. Attaining 95% EPA and DHA gives BodyBio Kirunal a triple value in a single capsule.

Fat Facts: Separating Fat From Fiction

Our life blood is in the sources of fatty acids we ingest to nourish our bodies. The media circus makes it difficult to separate the factoidal wheat from the chaff. The internet would have us believe that fish oil is the answer to all of life’s aches, pains and decrepitudes, and that omega-6 (n-6) fatty acids, especially the linoleic acid that is common to seed oils, is the scourge of our well-being. Nothing could be further from the truth.

Here Are The Facts In A Nutshell:

All essential fatty acids are just that – essential. Removing an essential fatty acid from the diet will likely lead to serious medical conditions. The omega-6 fats in the food supply include linoleic, gamma-linolenic and arachidonic acids. Although health enthusiasts now agree that pasture-raised butter and free-range eggs are healthy, they draw the line at seed oils, labeling linoleic acid as especially detrimental to health. However, these purveyors of misinformation have no qualms about pushing the consumption of nuts, which are heavy in monounsaturated fats and shallow in the polyunsaturated omega-6s. The judgment that n-6 fats are unhealthy arose from their capacity to drive inflammation by converting to arachidonic acid (AA), a physiological process actually lacking in efficiency and reliable outcome. Nonetheless, indisputable is that Linoleic acid (LA) is a primary essential fatty acid vital to the mitochondria. Do you see the problem? No one checked the medical facts. Linoleic acid is crucial to health. To settle the dispute, not one medical paper, not even from the most respected lipid researchers, has found LA to be a threat to health at all.

So What Is Bad For The Body?

Toxic fatty acids from heated, overheated and continuously-heated oils are harmful. The greater is their unsaturation, the greater is their toxicity. While there is no doubt that trans-fats are vile, toxic fatty acids are worse. What they exact upon the brain and body is frightening.

Have you ever noticed a health food store chains with prepared food cook in canola oil? They actually fry chicken in canola oil! Canola is a genetically-modified, polyunsaturated oil that creates dangerous aldehydes when heated to cooking temperatures. These formaldehyde cousins eventually embed themselves into our lipid membranes, causing inflammatory responses and a menagerie of diverse problems. Is olive oil any better? A monounsaturated omega-9, it contains oleic acid, a fatty acid whose health benefits are heralded, but whose associated polyphenols display more salubrity by modulating the oxidation of blood lipids, this according to a 2011 report by the European Food Safety Authority. A monumental concern, made public recently, is that olive oil is being diluted as much as 70% with sunflower, canola, walnut and other polyunsaturated fatty acids (PUFAs).  These relatively tasteless adulterants contribute to aldehyde toxicity when heated. Even at two dollars an ounce, first-cold-pressed extra virgin olive oil may be a contaminated fraud. At its finest, (extra virgin) olive oil serves better as an enhancement than as a cooking oil, unless its temperature is carefully monitored, lest its phenolic promises be compromised. It is prudent to avoid cooking with any monounsaturated (avocado, olive) and especially with polyunsaturated oils (grape seed, sesame, canola, safflower, sunflower, corn) due to their PUFA content. It is advisable to cook at moderate temperatures, using coconut oil, animal fats, or butter/ghee. Get back to basics; guess what our grandmothers used?

To our disappointment, a majority of polyunsaturated fats have become hybridized without our knowledge, leaving us with altered products that fail to deliver the health benefits we once enjoyed. What is now high-oleic sunflower or safflower oil is not the same healthful fat we used to know. To compound matters, the food supply has become a nationwide, uncontrolled experiment in culinary and dietary manipulation, offering the spoils to the victorious industry and the spoiled results to the victims. Salad dressings, mayonnaises and assorted fat-related condiments have suffered a similar fate.

If people are destroyed for lack of knowledge, it is doubly so in the realm of fatty acids. To render false information is lying, but to hide information is also a lie. In this regard, we have been deprived of knowing the details of omega-6 pathways, having been told only that omega-6s present with inflammatory compounds as end-products. First, let’s be aware that pre-formed AA, provided by meat and its fat, and by butter and cream leads to the essential series 2 prostaglandins. Albeit pro-inflammatory, these prostaglandins are the lead eicosanoids in the body and are crucial to maintenance of our health. For example, without them there would be no healing of a cut, since white blood cells and platelets would not be beckoned to the scene. Linoleic acid, the mother n-6 fatty acid, is the premier support of cardiolipin and the mitochondria. LA is converted by enzyme activity to gamma-linolenic acid (GLA), dihomo-gamma linolenic acid (DGLA) and eventually to the anti-inflammatory series 1 prostaglandins. 

The second tidbit to which we need attend is the potentially virulent, toxic and inflammatory character of oils exposed to elevated temperatures. The problem does not come from linoleic acid or any other n-6 fat! We have seen microscope images of cell membranes that have been assaulted and battered by these debased and corrupted lipid entities, particularly in the membranes of individuals suffering autoimmune and neurological diseases, where aberrant, renegade lipids have become attached to their DNA, effectively altering gene expression from epigenetic insult. Removal of aldehyde-ridden supermarket oils from the diet is mandatory if optimal health is our goal. Though not top heavy with PUFAs, olive oil is likewise categorized.

Third in the list we find that essential fatty acids (EFAs) appear in echelons of physiological activity. The lower-echelon fats include linoleic acid (from sunflower seeds, high-linoleic safflower oil and high-linoleic acid sunflower oil) along the n-6 branch, and alpha-linolenic acid (from flaxseed oil, chia seeds and walnuts) along the n-3 branch. The higher-order fatty acids include arachidonic acid (from cream, egg yolks, cheeses and meat) along the n-6 branch, and EPA / DHA (from marine sources) along the n-3 branch.

The fourth item of interest tells us that monounsaturated fatty acids (MUFAs) and saturated fatty acids (SFAs) are not essential, meaning that the body can make them from the diet. These fats offer us only calories and gustatory satiety; they are not bioactive lipids. Avocados, olive oil and tree nuts provide MUFAs, while coconut oil and coconut butter, cocoa butter, meat fats, and dairy butter give us SFAs.

The quality of our Life is riveted in the lipids we ingest as they pivotal in the health of the cell membrane and as we have come to understand… the membrane is everything in optimizing our state of health.

Most Important To Avoid To Regain And Stabilize Health:

  • All fried food including French fries unless cooked at home in coconut oil
  • Fast foods, almost all contain heated, toxic oil
  • Commercial foods organic or not, almost all contain heated, toxic oil
  • Hydrogenated vegetable oil, margarine, processed oils
  • Canola oil -often in processed foods / dressing, contains very long chain fatty acids
  • Peanut butter, peanuts, peanut oil, contains very long chain fatty acids
  • Mustard- contains very long chain fatty acids
  • Commercial mayo or salad dressing, use homemade with high linoleic safflower instead
  • Most Olive oil, limited availability of the pure oil, difficult to tell which one is pure
  • Commercial oils, high-oleic hybrid oils, including those labeled organic

Lipids, Oils And Fats You May Be Included In The Diet, But Don’t Contain Bioactive Lipids:

  • Organic coconut oil, useful in cooking
  • Olive oil, caution – limited availability of the pure oil, does not contain bioactive lipids

Lipids, Oils And Fats That Contain EFAs To Include To Optimize Health:

  • Concentrated phospholipids as PC and PE from BodyBio
  • 4:1 omega-6 to omega-3 oil, SR-3, as BodyBio Balance oil
  • High Linoleic, organic, cold pressed Safflower oil (this is imported)
  • Nutiva® Organic Hempseed oil
  • Evening primrose oil, pure cold pressed (not sourced from China)
  • Wild caught, cold water fish
  • Caviar, Anchovies, Sardines from clean waters, not farmed
  • Free range, organic egg yolks
  • Raw, organic seeds-hemp, chia, sunflower, pumpkin, fenugreek, sesame
  • Homemade kefir (cow, goat, sheep, camel)
  • Limited amounts of grass-fed, free-range sources of dairy (cow, goat, sheep, camel) butter, ghee, cream

Alterations to the food supply explain the fifth entry. Where sunflower, safflower and soybean oils once were high in linoleic acid, they now are high in oleic acid, ostensibly making them candidates for the sauté pan, a place where they will still be denigrated and debased, yet a bad thing, although at a slower rate. The damage done to an oil that has been heated and reheated in a fast-food restaurant or local diner is mind-boggling. It’s little wonder that these oils are reclaimed to be used as biofuels in diesel engines. Using them in salad dressing or atop steamed vegetables is one thing, but cooking with them is quite another. No matter the molecular nature, a heated MUFA / PUFA oil is ultimately toxic.

Sixth in our hit parade is the contraindication of marine oils in the treatment of childhood seizure disorders, where administration of such has only exacerbated the condition. Here, the DHA fraction impinges upon the NMDA receptors and stimulates excitation, while the EPA moiety suppresses beta hydroxybutyrate, the primary ketone. Aggravating the matter is that most commercial fish oils are processed using elevated temperatures for extraction, leading to aldehyde formation and degradation of the fatty acids. Thus-damaged fish oils are toxic. On the other hand, wild fish, the ultimate source of marine oils, are not. Salmon, anchovies, sardines and caviar are preferred.

To realize that coconut oil, olive oil, and avocado oil, among a few others, are not essential fatty acids makes number seven in our list. Coconut oil and MCT oil produce ketones quickly, not needing bile to be digested and absorbed. Since coconut does not contain EFAs or MUFAs, it may be used for cooking.

Number eight is worthy of fanfare and flourish. Oils that carry very-long-chain fatty acids are a considerable challenge to the liver and the brain. Because of their size, they dangle outside the mitochondrial membrane, so need peroxisomes to be metabolized, to be burned or beta oxidized. Mustard oil, canola oil, peanut oil and peanut butter are sources.

Knowing the ninth entry introduces us to the bioactive oils that display EFAs and phospholipids crucial to optimal health. In this camp we find Specific-Ratio 3 or SR-3 oil as a prime source of a balanced 4:1 omega-6 / omega-3 ratio, featuring organic, cold-pressed, non-GMO safflower and flaxseed oils as the mother fatty acids. Related bioactive oils are high-linoleic safflower oil, raw organic seeds (sunflower, hemp, pumpkin, chia) and seed creams (soak overnight, blend), Canadian evening primrose oil, wild cold-water fish (especially caviar, anchovies, sardines), free-range eggs (the yolks).