Vitamin D & The Brain

Vitamin D DeficiencyVitamin D deficiency has hit an epidemic level. Not only are intakes devastatingly low, but also exposure to the sun has become increasingly limited for fear of contracting skin cancer. In his June 23, 1011, newsletter at Newsmax Health, Dr.Russell Blaylock educates his readers when he states that vitamin D3 is actually a hormone rather than a vitamin, and that a deficit of this compound may result in undesirable consequences in the brain, including depression.

Dr.Blaylock is a renowned neurosurgeon with a keen desire for people to take some control over their own health.  He implies that supplemental vitamin D3, “…lowers risk of infections, which would reduce the incidence of brain inflammation.”   He adds that research can place behavioral disorders in the lap of vitamin D deficiency, and  suggests that all of us get a vitamin D blood-level test to find out where we stand, noting that current accepted values are too low to be any benefit.   About the conditions, Dr. Blaylock says, “…depression, anxiety, panic attacks, obsessive-compulsive disorder, suicide risk, and even criminal behavior…can be traced to chronic brain inflammation.”  The good doctor would like to see blood vitamin D levels between 70 and 100 nanograms per milliliter.  That means that most of us need to take at least 2000 IU of vitamin D3 a day, with as much as 10,000 IU for severe deficiency.

The body needs cholesterol to make vitamin D from the sun’s ultra-violet radiation.  When the resulting chemical mix gets to the liver it becomes vitamin D3, the active form of the hormone, which the body uses to help maintain bone integrity, to increase neuromuscular function, and to modulate the immune system.  There has been considerable support over the past decade for the role of vitamin D in brain development and function.  It was noted by Kesby and colleagues at Australia’s Queensland Brain Institute that, “…this vitamin is actually a neuroactive steroid that acts on brain development, leading to alterations in brain neurochemistry and adult brain function.”  (Kesby. 2011)  Deficiencies have been related to depression, as well as to Parkinson’s disease and cognitive decline.

Of particular interest to American researchers at the U. of South Carolina is the relationship of vitamin D deficit to postpartum depression as one of the several mood disorders studied in 2010.  Using a moderate sample size at the outset, scientists found that low levels of vitamin D are associated with increased postpartum depression, as measured by evaluation on the Edinburgh Postpartum Depression Scale. (Murphy. 2010)  Even though larger studies are encouraged, the outcomes are likely to be the similar.

When the immune system abandons its competence because of nutritional deficit, inflammation ensues, often with a mighty wrath.  Such is the case with deficit of vitamin D in various maladies that include diabetes and multiple sclerosis, as well as depression.  Depression is a family affair characterized by feelings of hopelessness, despair, anxiety, irritability and restlessness.  Depression understandably accompanies degenerative disease, in part by the hopelessness is may engender.  If vitamin D is able to address depression, might it also be able to help get a handle on these conditions?   Whatever the cause of vitamin D deficiency, levels lower than 30 nanograms per milliliter have been associated with heart disease, type 2 diabetes, infectious diseases, autoimmune disorders, and neurological conditions. (Nimitphong. 2011)


Dr. Blaylock
Up Vitamin D3 for Your Brain
Thursday, June 23, 2011 10:11 AM

Mol Cell Endocrinol. 2011 Jun 1. [Epub ahead of print]
The effects of vitamin D on brain development and adult brain function.
Kesby JP, Eyles DW, Burne TH, McGrath JJ.

Source Queensland Brain Institute, University of Queensland, St. Lucia, Qld 4076, Australia.

J Am Psychiatr Nurses Assoc. 2010 May;16(3):170-7.
An exploratory study of postpartum depression and vitamin d.
Murphy PK, Mueller M, Hulsey TC, Ebeling MD, Wagner CL.

SourceMedical University of South Carolina, Charleston, SC, USA, [email protected]

Curr Opin Clin Nutr Metab Care. 2011 Jan;14(1):7-14.
Vitamin D, neurocognitive functioning and immunocompetence.
Nimitphong H, Holick MF.

SourceSection of Endocrinology, Diabetes, Nutrition, Department of Medicine, Boston University Medical Center, Boston, Massachusetts, USA.

Acta Psychiatr Scand. 2011 Apr 12. doi: 10.1111/j.1600-0447.2011.01705.x. [Epub ahead of print]
D’ for depression: any role for vitamin D?: ‘Food for Thought’ II.
Parker G, Brotchie H.

SourceSchool of Psychiatry, University of New South Wales, and Black Dog Institute, Randwick, Sydney, NSW, Australia.

Psychopharmacology (Berl). 2011 Jun;215(4):733-7. Epub 2011 Jan 29.
Exploring the relationship between vitamin D and basic personality traits.
Ubbenhorst A, Striebich S, Lang F, Lang UE.

SourceDepartment of Physiology, University of Tuebingen, Gmelinstr. 5, 72076, Tuebingen, Germany.

FASEB J. 2008 Apr;22(4):982-1001. Epub 2007 Dec 4.
Is there convincing biological or behavioral evidence linking vitamin D deficiency to brain dysfunction?
McCann JC, Ames BN.

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

Sleep and Kids

boy-watching-tv-with-remoteIt would be too easy if we put our kids to bed and they fell asleep in the average nine minutes it takes for an adult to drop into the arms of Morpheus. If your child struggles to fall asleep, know that this is not likely to resolve merely by moving from crib to bed. As he ages, there will fewer cries and screams, and more pleas and refusals. Could there be a reason behind this? Maybe television? Video games?

Each child is unique and has his own distinct needs for sleep.  Generally, a preschooler needs 10 to 12 hours a night, maybe with a nap during the day.  The surprise is that the school-age and preteen group benefit from the same, except for the nap.  But, “media use has been shown to negatively affect a child’s sleep,” according to researchers at Seattle’s Children’s Research Institute.  In their randomized controlled study of preschoolers, they found that the children had more than 70 minutes of screen time a day, with a fifth of that after 7 PM.  Almost 20% of the parents interviewed indicated at least one sleep problem with their preschooler.  Daytime TV showing violent behavior exacerbated problems.  (Garrison. 2011)  In a similar study a decade earlier, investigators at Brown University discovered that the sleep domains most affected by television were “bedtime resistance, sleep onset delay, and anxiety around sleep, followed by shortened sleep duration.”  (Owens. 1999)  In both studies—and in several between— it is agreed that a TV in the child’s bedroom compounds the matter and translates into less-than-stellar academic performance.

Recent assaults on Sponge Bob and his kin have raised the hackles of the entertainment industry.  But theirs is not righteous indignation, and transcends the humor of a “Who?  Me?” response.  It has been suspected for decades that the electronic babysitter would require a payback.  If a person believes that life is a series of trade-offs, here’s one of them, usually showing up during the school years, unknowingly invited earlier.

Children who watch fast-paced programs—even for as little as nine minutes — perform poorly in executive function tasks, those that control and regulate other behaviors and abilities, and are necessary for goal-directed activities.  These might include knowing when to start and stop behaviors and when to change them if the situation calls for it.  It also includes being able to plan ahead, to pay attention, and to fine tune memory and motor skills.  Although they are not easy to assess, their absence is noticeable.  (Lillard. 2011)  Teachers have lamented since the 1970’s that too many children start school with five-minute attention spans.

The U.S. is not the only nation facing this problem.  German researchers realized that 25% of their children do not get the ten hours of sleep they need.  They advise that parents and care givers limit TV time in order to prevent the negative consequences of sleep deprivation.  (Heins. 2007)  The Japanese learned that not only TV, but also after-school activities that last past 8 PM can interfere with sleep / wake patterns.  (Oka. 2008)

Other electronic entertainment, not only TV, plays a role in cerebral interference.  Electronics may induce the fight-or-flight state, increase blood pressure and pulse, and disrupt overall brain performance.  The unnatural brightness of the screen can interfere with production of melatonin, the signaling molecule that tells you to fall asleep.  Fast-moving and quick-changing scenes can interrupt the wiring of a young brain, possibly leading to bad dreams and restlessness.  Electromagnetic radiation is a by-product of anything electronic, affecting children more than adults, considering that their brain tissue is more conductive, radio frequency penetration is greater relative to head size, and children will have a longer lifetime exposure than adults.  (Kheifets. 2005)

Problems begin to manifest by age seven, the time when academic load may become a family affair.  When and if you help your child with his homework, you’re sure to notice what all this is about.  A two-hour delay between electronic stimulation and bedtime is not a bad idea.   Prior to that, naturally-paced shows, or even those seemingly in slow motion (Mr. Rogers), can offset, or even prevent, the surreal experiences that occur later. (Christakis. 2011)


Garrison MM, Liekweg K, Christakis DA.
Media use and child sleep: the impact of content, timing, and environment.
Pediatrics. 2011 Jul;128(1):29-35.

Owens J, Maxim R, McGuinn M, Nobile C, Msall M, Alario A.
Television-viewing habits and sleep disturbance in school children.
Pediatrics. 1999 Sep;104(3):e27.

Angeline S. Lillard, PhD,  Jennifer Peterson, BA
The Immediate Impact of Different Types of Television on Young Children’s Executive Function
Pediatrics. Published online September 12, 2011   (doi: 10.1542/peds.2010-1919)

Heins E, Seitz C, Schüz J, Toschke AM, Harth K, Letzel S, Böhler E.
Bedtime, television and computer habits of primary school children in Germany. [Article in German]
Gesundheitswesen. 2007 Mar;69(3):151-7.

Oka Y, Suzuki S, Inoue Y.
Bedtime activities, sleep environment, and sleep/wake patterns of Japanese elementary school children.
Behav Sleep Med. 2008;6(4):220-33.

Leeka Kheifets, PhD, Michael Repacholi, PhD, Rick Saunders, PhD, Emilie van Deventer, PhD
The Sensitivity of Children to Electromagnetic Fields
Pediatrics Vol. 116 No. 2 August 1, 2005 pp. e303 -e313

Dimitri A. Christakis
The effects of Fast-Paced cartoons
Pediatrics. 2011; peds. 2011-2071;  Published Online, 12 Sept., 2011

Gröer M, Howell M.
Autonomic and cardiovascular responses of preschool children to television programs.
J Child Adolesc Psychiatr Ment Health Nurs. 1990 Oct-Dec;3(4):134-8.

Christakis DA, Zimmerman FJ, DiGiuseppe DL, McCarty CA.
Early television exposure and subsequent attentional problems in children.
Pediatrics. 2004 Apr;113(4):708-13.

Al-Khlaiwi T, Meo SA.
Association of mobile phone radiation with fatigue, headache, dizziness, tension and sleep disturbance in Saudi population.
Saudi Med J. 2004 Jun;25(6):732-6.

Owens J, Maxim R, McGuinn M, Nobile C, Msall M, Alario A.
Television-viewing habits and sleep disturbance in school children.
Pediatrics. 1999 Sep;104(3):e27.

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

Anxious About Anxiety?

mid-adult-male-portraitYou’re not anxious about going on vacation or performing a pleasant task. You’re enthusiastic (but not enthused). You could be anxious about going to the dentist or to defend your last income tax return. Here, you’re entertaining a feeling of dread or apprehension, probably lacking clear justification.  Anxiety results from a subjective way of looking at a situation in the absence of a clear and actual danger. Of course, the sweating, increased pulse, and tension coupled with self-doubt about being able to handle the matter tell a different story. Sometimes respirations increase, the mouth gets dry and the intestines gurgle. All this is part of a defense mechanism. Anxiety can be particular, such as a panic attack in a crowd of people, in which case the stimulus can be identified. Or it may be generalized, being a long-term experience with no explanation of its cause. Obsessive-compulsory disorder (OCD) is an anxious state characterized by quandaries of uncertainty and compulsions to act. If the act is frustrated, the uncertainty remains and anxiety is intensified. Anxiety is considered a normal, but transient, response to stress, encouraging a person to take action in order to deal with what is perceived to be a difficult situation.

What’s The Risk?

Women are twice as likely as men to become anxious, mostly because of hormones and the archaic expectations that women are supposed to take care of everybody else before themselves. Age plays a minor role, in that OCD, separation anxiety and social phobias that include panic disorder show up in childhood and the teenage years. Early identification and treatment can forestall later problems. Certain environmental factors, such as poverty, separation from family, overly strict parents, family conflicts, anxious family members and lack of support can induce anxiety disorders. That anxiety runs in families is accepted, but it’s not known if the onset is genetic or learned, or both.

Physiologically, anxiety may be prompted by faulty brain chemistry, where an imbalance of serotonin, for instance, may result in irregular moods and emotions. There may be a structural fault, too.  The amygdala is the part of the brain in charge of processing emotional reactions and memory consolidation, including the recollection of fear.  If it’s overactive, this structure will heighten the fear response and increase anxiety in social situations.   Non-structural physical concerns, such as health problems, can cause anxiety.  Diabetes, alcoholism, heart disease, odd sensations that have no apparent cause, and thyroid disease are a few.

How Do I Handle Anxiety?

Besides the traditional psychotherapy practices and anti-anxiety medications, there are a few things you can do to take charge. First, you need to know that withdrawal from a psychoactive drug can cause anxiety. So, weaning from benzodiazepines causes the thing for which you took the drug in the first place. But beta-blockers, typically used for blood pressure control, have no such effect. They’re used off label to control rapid heartbeat, nervousness, trembling voice and shaky hands that accompany anxiety attacks. Alcohol withdrawal causes anxiety in many people.

Alternative approaches to anxiety treatment include things you can do and things you can swallow. Some modalities that require active participation include music therapy, art therapy, aromatherapy and meditation. With these you have to turn the music on, wield a paintbrush, light a candle, or think about pleasant things. But many people are unwilling or unable to be so engaged because of time constraints, family and job obligations, or simple faineance. Deglutition is the answer.

Options to psychological interventions for anxiety were sought in order to overcome limitations on time and resources. Because of adverse side-effects, alternatives to anxiolytic drugs also were explored. There is a shrub from the South Pacific islands that’s been used for centuries to calm the nerves, Piper methysticum, commonly known as kava kava. In a meta-analysis performed by the Cochrane Database at England’s Exeter University, researchers found that anxious subjects who took kava extract as a sole constituent in their treatment experienced a substantial reduction in symptoms compared to those taking a placebo (Pittler, 2000, 2003). One of the differences between a natural substance and a synthetic one is the time it takes to demonstrate effectiveness.  With a natural substance—in this example, herbal—you get the active ingredient and all the supportive components of the plant. Many enjoy an unexplainable synergy.  With a synthetic one—a drug—you get an isolated chemical that is not toned down by collaborative elements. Although earlier study found kava to be effective at taming anxious moments, it took eight weeks for kava’s superiority to placebo to be displayed (Volz, 1997).

Benzodiazepines are the drugs commonly used to treat anxiety. Their side effects, besides excessive drowsiness and decreased alertness, include paradoxical consequences, such as aggression, impulsivity, and irritability. Cognitive impairment and tolerance can result, as well. Tapering off these medications requires deliberation and a watchful eye. Using kava kava during such an ordeal, patients who were weaned from the drugs while being introduced to the herbal showed good tolerance and improved symptoms over a period of two weeks in a five-week trial in Germany (Malsch, 2001).

Generalized anxiety disorder has responded well to another folk remedy, passion flower. In a study comprising three dozen individuals, half received passion flower plus placebo and half received a benzodiazepine plus placebo in a one-month trial. The outcome showed both the herb and the drug to be effective in controlling anxiety symptoms. The drug, with rapid onset of action, impaired job performance (Akhondzadeh, 2001). The herb did not. Pharmacologically, extracts of the upper parts of the passion flower plant are most dynamic (Dhawan, 2001).

If you’ve taken fish oil for heart and brain health, that’s good. It’s been discovered that low levels of omega-3 fatty acids play a significant role in a number of mental irregularities (Buydens-Branchley, 2008) and that mood disorders respond especially well to omega-3 supplementation, with EPA getting better press than its companion, DHA (Ross, 2007). With a ratio of 3 to I, EPA to DHA, a fish oil product called Kirunal appears more than adequate to satisfy the mono- or adjunctive therapy approach in treating mood anomalies. For decades it’s been given that omega-3 fats are effective in the treatment of major depressive disorders, so it is reasonable to submit that they be likewise in anxiety disorders (Ross, 2009). If the presence of a substance yields a specific result, then the absence of that substance should yield the opposite. A deficit of n-3 fats has been identified in the red cell membranes of anxious persons (Greena, 2006), specifically those with social anxieties. Overall, it’s been proposed that human foods be supplemented with omega-3 fats as a strategy to improve behaviors and cognitive functions (Vinot, 2011). This makes one wonder if the education community needs to sit up and take notice. If that’s an inflammatory statement, n-3 supplementation can ameliorate that while reducing self-induced anxiety (Kiecolt-Glaser, 2011).

A relative newcomer on the anti-anxiety supplement stage is curcumin, the active ingredient of the turmeric spice common to Southern Asian and Middle Eastern cuisine.  Known predominantly as an anti-inflammatory agent, curcumin was found to have antidepressant like activity similar to tricyclic antidepressants, such as fluoxetine and imipramine (Sanmukhani, 2011). Because it is a natural substance, doses of curcumin used in an Indian trial were extraordinarily high, at 100 mg per kilogram of body weight, which equates to about 6,800 mg (6.8 grams) for a 150-pound person. Lesser dosages, from 10 to 80 mg/kg, demonstrated a positive effect on serotonin and dopamine activity, acting similarly to commonly prescribed drugs (Kulkami, 2008).

If you maintain a healthy diet, making sure to get the full array of macro and micro minerals, especially magnesium and zinc, as well as sufficient B vitamins, focusing on B 12, you’ll be able to avoid at least one cause of anxiety. Cutting back on alcohol and caffeine, and getting ample sleep are others. A caveat: before embarking on a supplement regimen to address anxiety, check with a healthcare professional to look for interactions with medicines and foods.


Andreatini R, Sartori VA, Seabra ML, Leite JR.
Effect of valepotriates (valerian extract) in generalized anxiety disorder: a randomized placebo-controlled pilot study.
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Akhondzadeh S, Naghavi HR, Vazirian M, Shayeganpour A, Rashidi H, Khani M.
Passionflower in the treatment of generalized anxiety: a pilot double-blind randomized controlled trial with oxazepam.
J Clin Pharm Ther. 2001 Oct;26(5):363-7.

Buydens-Branchey L, Branchey M.
n-3 polyunsaturated fatty acids decrease anxiety feelings in a population of substance abusers.
J Clin Psychopharmacol. 2006 Dec;26(6):661-5.

Buydens-Branchey L, Branchey M, Hibbeln JR.
Associations between increases in plasma n-3 polyunsaturated fatty acids following supplementation and decreases in anger and anxiety in substance abusers.
Prog Neuropsychopharmacol Biol Psychiatry. 2008 Feb 15;32(2):568-75. Epub 2007 Nov 1.

Dhawan K, Kumar S, Sharma A.
Anti-anxiety studies on extracts of Passiflora incarnata Linneaus.
J Ethnopharmacol. 2001 Dec;78(2-3):165-70.

Dhawan K, Kumar S, Sharma A.
Anxiolytic activity of aerial and underground parts of Passiflora incarnata.
Fitoterapia. 2001 Dec;72(8):922-6.

Ernst E.
The risk-benefit profile of commonly used herbal therapies: Ginkgo, St. John’s Wort, Ginseng, Echinacea, Saw Palmetto, and Kava.
Ann Intern Med. 2002 Jan 1;136(1):42-53.

Ernst E.
Herbal remedies for anxiety – a systematic review of controlled clinical trials.
Phytomedicine. 2006 Feb;13(3):205-8. Epub 2005 Aug 15.

G. Fontani, F. Corradeschi, A. Felici, F. Alfatti, S. Migliorini, L. Lodi
Cognitive and physiological effects of Omega-3 polyunsaturated fatty acid supplementation in healthy subjects
European Journal of Clinical Investigation. Vol 35, Iss 11, pages 691–699, Nov 2005

Pnina Greena, Haggai Hermeshb, Assaf Monselisec, Sofi Marom, Gadi Presburger, Abraham Weizman
Red cell membrane omega-3 fatty acids are decreased in nondepressed patients with social anxiety disorder
European Neuropsychopharmacology. Feb 2006; 16(2): 107-113

Harauma A, Moriguchi T.
Dietary n-3 fatty acid deficiency in mice enhances anxiety induced by chronic mild stress.
Lipids. 2011 May;46(5):409-16. Epub 2011 Feb 7.

Jadoon A, Chiu CC, McDermott L, Cunningham P, Frangou S, Chang CJ, Sun IW, Liu SI, Lu ML, Su KP, Huang SY, Stewart R.
Associations of polyunsaturated fatty acids with residual depression or anxiety in older people with major depression.
J Affect Disord. 2012 Feb;136(3):918-25. Epub 2011 Nov 21.

Kiecolt-Glaser JK, Belury MA, Andridge R, Malarkey WB, Glaser R.
Omega-3 supplementation lowers inflammation and anxiety in medical students: a randomized controlled trial.
Brain Behav Immun. 2011 Nov;25(8):1725-34. Epub 2011 Jul 19.

Kinrys G, Coleman E, Rothstein E
Natural remedies for anxiety disorders: potential use and clinical applications.
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Kulkarni SK, Bhutani MK, Bishnoi M.
Antidepressant activity of curcumin: involvement of serotonin and dopamine system.
Psychopharmacology (Berl). 2008 Dec;201(3):435-42. Epub 2008 Sep 3.

Lakhan SE, Vieira KF.
Nutritional and herbal supplements for anxiety and anxiety-related disorders: systematic review.
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Malsch U, Kieser M.
Efficacy of kava-kava in the treatment of non-psychotic anxiety, following pretreatment with benzodiazepines.
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McBride S, Graydon J, Sidani S, Hall L.
The therapeutic use of music for dyspnea and anxiety in patients with COPD who live at home.
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Pittler MH, Ernst E.
Efficacy of kava extract for treating anxiety: systematic review and meta-analysis.
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Pittler MH, Ernst E.
Kava extract for treating anxiety.
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Ross BM, Seguin J, Sieswerda LE.
Omega-3 fatty acids as treatments for mental illness: which disorder and which fatty acid?
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Brian M. Ross
Omega-3 polyunsaturated fatty acids and anxiety disorders
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Saeed SA, Bloch RM, Antonacci DJ.
Herbal and dietary supplements for treatment of anxiety disorders.
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Sanmukhani J, Anovadiya A, Tripathi CB.
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Song C, Li X, Leonard BE, Horrobin DF
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Vinot N, Jouin M, Lhomme-Duchadeuil A, Guesnet P, Alessandri JM, Aujard F, Pifferi F.
Omega-3 fatty acids from fish oil lower anxiety, improve cognitive functions and reduce spontaneous locomotor activity in a non-human primate.
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Volz HP, Kieser M.
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tYehuda S, Rabinovitz S, Mostofsky DI.
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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.

Feeling Anxious? Maybe Not

anxious-womanGood for you. You’re going to Disney World. But don’t say you’re anxious about it. It’s okay to be anxious about going to the dentist. It’s understandable that you’d be anxious about your debut at an IRS audit. Unless you‘re terrified by the characters, you’re eager, not anxious, about visiting Walt’s place. To be anxious is to be afraid, apprehensive, uneasy, or distressed, but not enthusiastic. Anxiety is a disorder with more than one characterization. It can display as panic disorder, obsessive-compulsive disorder, post-traumatic-stress disorder, social anxiety, and a few others, including various phobias. It’s even possible to be anxious about being anxious, to the point that the subsequent distress precludes a normal life.

A common emotion, anxiety is felt by most humans once in a while. Taking a test, facing a novel problem at the office, or making a difficult decision is enough to get you anxious. Being lost in a strange town makes you feel like a rat in a laboratory maze. These little upsets are supposed to go away. If they cause a lingering burn, it’s time to talk about it. Frustration with a task can cause anxiety, and anxiety about doing it in the first place can cause frustration, which then perpetuates the cycle. Replacing uncomfortable cognitions with calming thoughts—something you can learn to do yourself—is one path to serenity.  The Roman Emperor Marcus Aurelius wrote about dealing with frustration and anxiety two thousand years ago. So, this isn’t a new challenge. However, what is new is the discovery that the ninety percent of the cells that compose the body have the potential to respond to anxiety. These would be the intestinal bacteria that have the uncanny ability to communicate with the brain, a conclusion attributed to evolution but more than likely decided at the ontogeny. That a bidirectional communication system between the gut and the cerebrum exists has been established, and that it influences brain development and behavior through complex signaling mechanisms is amply defined (Diaz-Heijtz, 2011) (Collins, 2012) (Chen, 2013).

The connection between gut and brain is controlled by the vagus nerve, which is the longest cranial nerve, passing through the neck and thorax into the abdomen, where it directs motor and secretory impulses of the viscera—your innards. Stimulation of this nerve can instigate activity in a body process known as the HPA axis (Hosoi, 2000) (O’Keane, 2005), the hypothalamic-pituitary-adrenal axis, the control center for most of the body’s hormones, one of which is the steroid hormone cortisol. Cortisol is used as a biomarker for psychological stress (Djuric, 2008).  In response to physical or mental stress, the hypothalamus produces corticotropin-releasing factor, which binds to specific receptors in the pituitary gland, where adrenocorticotropic hormone (ACTH) is made. ACTH then moves to the adrenals to direct the secretion of cortisol. The idea behind cortisol is to break down body tissue to be used as energy. When rampant, it breaks down lean tissue to liberate amino acids that can be used to raise blood sugar. In adipose tissue, cortisol breaks fats into fatty acids and glycerol, which also elevate blood sugar.

To calm this activity in a kind of physiological riot control, the body enlists the major inhibitory neurotransmitter, called gamma-aminobutyric acid—GABA—to slow down the firing of nerve cells in the brain. Emily Dean, M.D., a psychiatrist practicing in Massachusetts, likens GABA to a glass of wine in front of a fire, to restful sleep, or to tranquility and yoga ( Paints a nice picture, eh? Negative alterations in GABA receptor expression are implicated in the development of anxiety and depression, which are comorbid with functional bowel disorders.

It’s been hypothesized that probiotics are able to make compounds that enhance the brain-gut link by acting as delivery vehicles for neuroactive substances, with each neurochemical being related to a specific strain of intestinal flora (Lyte, 2011). The strain Lactobacillus rhamnosus is known to modulate the immune system by manipulating tumor necrosis factor alpha (TNFa) and Interleukin 8 (Ma, 2004), two cytokine signaling molecules related to immunity and inflammation. In mouse studies performed in Ireland a couple years back, those animals preloaded with L. rhamnosus were spared a frantic response to physiological insult and stress, contrasted to their cage mates denied the probiotic, whose cortisol levels were extreme (Bravo, 2011). As expected, mice whose vagus nerves were severed had no similar neurochemical and behavioral effects, indicating the vagus nerve as the major thoroughfare between gut bacteria and the brain (Ibid). Even in the absence of insult, mice treated with lactobacillus presented with higher levels of anxiety-reducing receptors, the observation of which could not be made until their sacrifice. A lactobacillus, then, reduces stress-induced levels of corticosterone (the rodent equivalent of cortisol) by normalizing the HPA axis (Gareau, 2007).

The HPA axis helps to regulate physiological processes that include temperature, digestion, immunity, mood, sexuality and energy usage, besides controlling your response to stress, trauma and injury. If, as believed, the hypothalamus is involved with fibromyalgia and the adrenals with chronic fatigue syndrome, the use of a probiotic to tend to the HPA axis should ameliorate these assaults. If GABA plays a major role in the HPA stress response (Herman, 2004) (Cullinan, 2008), and if GABA production is enhanced by lactic acid bacteria (Dhakal, 2012), then a five-dollar treatment for anxiety is at hand.  Not only L. rhamnosus, but also L. brevis (Li, 2010), L. reuteri (Ma, 2004), and strains of Bifidobacteria (Barrett, 2012) work to produce GABA. This should settle once and for all that not all bacteria are bad.


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Bercik P, Park AJ, Sinclair D, Khoshdel A, Lu J, Huang X, Deng Y, Blennerhassett PA, et al
The anxiolytic effect of Bifidobacterium longum NCC3001 involves vagal pathways for gut-brain communication.
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Bravo JA, Forsythe P, Chew MV, Escaravage E, Savignac HM, Dinan TG, Bienenstock J, Cryan JF.
Ingestion of Lactobacillus strain regulates emotional behavior and central GABA receptor expression in a mouse via the vagus nerve.
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Xiao Chen, Roshan D’Souza, Seong-Tshool Hong
The role of gut microbiota in the gut-brain axis: current challenges and perspectives
Protein & Cell. June 2013, Volume 4, Issue 6, pp 403-414

Collins SM, Surette M, Bercik P.
The interplay between the intestinal microbiota and the brain.
Nat Rev Microbiol. 2012 Nov;10(11):735-42.

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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 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.

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These statements have not been evaluated by the FDA.
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