Menopause and Memory

Coping with the menopauseFor eras women’s physical and mental suffering has been trivialized when it is associated with the condition of menopause.  But the reality of hot flashes, fatigue, sleep disturbance, moodiness, and discomfiting cerebral performance during menopause is virtually tangible.   Various traditional and alternative therapies are used to address these symptoms, from hormone replacement therapy at the allopathic end to black cohosh and essential fatty acids at the complementary end. The brain fog, on the other hand, has been viewed with less fervor until recently.

The Department of Neurology at the University of Rochester, In New York, reported that the memory problems described by women as menopause approaches are real (Weber, Mapstone, et al, 2012). Of course, this is nothing new to the millions of women who have had periods of forgetfulness or fogginess in their 40s and 50s.  Their experiences have been validated by a rigorous battery of cognitive tests administered by researchers at Rochester and the U. of Illinois at Chicago.  The goal of the study was to find a relationship between subjective reports of memory complaints and objective tests of cognitive function, described as the intellectual process by which a person perceives and comprehends ideas.   Included here are all aspects of thought, reason, and recollection.   Antipodal is the brain misstep that affects all ages and is characterized by confusion, decreased clarity of thought, and forgetfulness.  In some folks this can lead to minor depression on the one hand and delinquency on the other.  For as often as this happens to women all over the globe, it still is barely seen as a “real” condition.

The subjects who participated in the study completed a comprehensive neuropsychological battery of tests that measured attention, working memory, verbal memory and fluency, visual-spatial skills, and fine motor dexterity.  Self-report inventories of perceived memory symptoms were included.  The findings indicated a link between the subjective memory faults and actual memory deficits in some, but not all, realms.  Working memory and complex attention tasks were most affected.  Working memory is the ability to hold information in the mind long enough to perform a complex task regardless of interfering processes and distractions.  If this operation is hindered, the person is frustrated.  If this recurs, the presentation of depressive symptoms should not be a complete surprise.  The physical changes of menopause are identifiable, but the mental changes are not to be identified with the mental aberrations of dementia.  Menopausal women can rate their own memory skills; demented ones cannot.

Brain fog can be triggered by physical, psychological, biochemical and even spiritual factors.  Some of these are adrenal exhaustion, food and chemical reactions, stress, and nutritional deficiencies.  There are, however, age-related cognitive changes that, though of non-dementia origin, can interfere with a person’s daily functioning, which makes this a relevant clinical issue.  Overcoming this situation may be as simple as getting enough sleep, exercising, or eating the right foods.  Meditation and prayer have been used as first-line treatment in some venues.  While the complex relationship of mood, memory and hormones is not identical in every case, it is inferred that the amount of attention paid to a novel situation or perception influences the persistence of memory (Weber & Mapstone, 2009).  Overall, if a woman says she experiences disconcerting bouts of forgetfulness, she deserves confirmation that these cognitive signs are part of the array of menopause symptoms (Schaafsma, 2010).

There are factors in the aging process that interact with menopause itself, among them  homocysteine values, hypercholesterolemia, metabolic syndrome or type 2 diabetes, hypertension, and depression.   If drugs are used to address any of these concerns, and if a drug has anticholinergic properties, there likely will be cognitive impairment to some degree.  This compounds the matter, and may lead to improper diagnoses and unneeded treatment for a condition that does not really exist.  This class of drugs—the anticholinergics—is used to treat gastric disturbances, urinary problems, respiratory matters, and insomnia, among others disorders that may display themselves as menopause signs in the first place.

The use of hormones to improve mental function in menopause has been hit and miss.  Observational studies say one thing, while randomized clinical trials report something else.   In a Wake Forest University study it was concluded that using estrogen with progestin to mediate global cognitive function in women over age 65 was less effective than the placebo.  In fact, it increased cognitive decline (Rapp, 2003).  While no clinically relevant adverse effects were reported, the trial was stopped because of “certain increased health risks for women” (Ibid.).  Hedging its bets, another study, following a similar protocol, found a negative effect on verbal memory, but a “trend to” a positive impact on figural memory, with other domains unaffected by the combination of estrogen and progestin (Resnick, 2006).  For those who put all their eggs into one basket—the basket of allopathic medicine and Big Pharma—this is an eye-opener.

Walking down the primrose path, we stumble upon complementary medicine or functional medicine or integrative medicine, all of which are supported by evidence-based science, none of which is a sham.  Because it can’t be a money-maker for mega-corporations, since natural substances cannot be patented, complementary medicine raises a jaundiced eye.  And because your physician has little time to examine the research for himself, being directed by the verbal testimonies of the pharmaceutical representative, he knows little or nothing about the efficacy of alternative modalities.

It’s uncertain whether money, time, compassion, or philosophy drives the Euro-Asian medical community to study alternatives to allopathic treatment more earnestly than happens in the States.  Studies on ginkgo biloba that were performed in the last century in the UK have determined that this extract has profound impact on working memory and psychomotor performance at doses of 120 mg a day, with those between ages 50-59 reaping the most benefit (Rigney, 1999).  An earlier study, employing 600 mg of ginkgo extract, found significant improvement in memory one hour after administration (Subhan, 1984).  If there is concern that these studies are too old to carry any weight, work done in this century agrees (Scholey, 2002) (Kennedy, 2000) In order to “kick it up a notch,” scholars of neuroscience and cognition, also in the UK, decided to combine ginkgo with Panax ginseng—the adaptogen that purportedly increases the body’s resistance to stress, anxiety and fatigue—and to measure the combined efficacy on cognitive benefit in tests of serial arithmetic tasks with varying cognitive load and in tests of memory quality.  Two studies found this phytopharmaceutical blend to offer substantial cognitive profit (Wesnes, 2000) and (Scholey, 2002)

Why settle for cognitive improvement alone when the whole body can capitalize on a protocol?  Ever hear of phosphatidylcholine?  It’s the number one phospholipid from which you are made.  It’s a component of each of the trillions of cells that make you, you.  You’ve heard the expression, “When Mama’s happy, everybody’s happy?”  When the cells are healthy, everything is healthy.  That’s what phosphatidylcholine (PC) does:  it restores and elevates cellular function and stability.    And it enhances learning and memory, and improves cognitive disorders (Nagata, 2011) (Fioravanti, 2005)  As an unseen but additional benefit, PC is accompanied in its extraction by phosphatidylethanolamine, a phospholipid that helps to manufacture phosphatidylserine, an ingredient known to attenuate many neuronal effects of aging, and to restore normal memory on a variety of tasks (McDaniel, 2003)  It’s possible to lift that fog, after all.


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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.

Mood Boosts Elder Brain Power

pleased-manWhen you’re in a good mood, it’s almost amazing what you can accomplish. This has little to do with emotions and even less with temperament. The former are short-lived and specific, and may be turned on by a single stimulus. The latter are characteristics that are seemingly innate rather than learned. Moods may be disarrayed, as in depression and bipolar disorder, and are subjective, although they may be inferred by conduct or body language. Many things can trigger a bad mood, and what disturbs one person might be ridiculous to another. In some circles, bad mood is believed to originate when one’s ego becomes threatened by a situation, event or condition beyond his control. Foul moods can interfere with many of our individual enterprises and ventures, not the least of which are the mental acrobatics that have seen us through thick and thin from youth to the extremes of middle-age. With age there may come decline, physically, emotionally and mentally. But we may have more control over this than previously thought. Is it possible that we can improve physical health, which will improve mood, which will improve mental faculties?

We already know that diet and exercise can enrich physical well-being and probably extend life…and the quality of life as we live it. Newspapers, magazines, the internet, television programs, and even the beauty parlor help to deliver information about longevity and agelessness. With a little thought, it’s possible to separate the wheat of the message from the chaff. The time at which old age begins is subjective, and ranges from sixty-five to the mid seventies, depending on whom you ask. Most of us believe that old age is for other people. That attitude will bless you with almost-eternal youth.

A vagary of aging is the diminution of working memory and instant decisiveness. The invincibility of youth gives way to the deliberations of middle-age and eventually to the tentativeness of senior citizenship. The culmination of this time line puts us on the game board square labeled “moody” or “testy” or “cranky.”  Modern research tells us that good mood can counterbalance these vagaries, and that trivial gestures, like giving a person a small bag of candy, can help to improve performance on tests of decision making and working memory.

In an interesting work done at Decision Research, in Oregon, good mood in twenty-three seniors was engendered with a bag of candy and a Thank-you card as a reward for agreeing to take part in the study. An equal number of seniors received no reward, and were considered the control group. Both groups were assigned to individual computers. The candy group saw happy faces and smiling suns on their sky-blue backgrounds. The control group saw neutral round images with no facial features. In tests of speed and accuracy that entailed experiential, sequenced learning, the candy group made significantly better choices than the neutral group. An extension of this mode to real life is analogous to meeting a person for the first time, and having to decide if she or he is trustworthy. What the study suggests is that people in a good mood are able to make such a determination faster and more accurately.

Working memory is linked to learning outcomes, encompassing the recall of instructions and the ability to complete an activity based on them. It boils down to how much information you can hold onto at one time. This function is important to decision making. The seniors in the happy group fared better than the others (Carpenter, 2013). It can be such that those who are suddenly elated forget their aches and pains and their trials and tribulations, thus vouching for the promises of a good mood. If good mood improves memory, then being able to remember might just improve mood, particularly for those beleaguered with cognitive interruptions.

Lots of factors can throw the body out of balance, but if you are chemically balanced, your moods will also be. It has been established that positive feelings facilitate working memory and decision making. Nutrients can do the same, especially if they are proportioned to maintain stable blood sugar. Because some seniors are prone to the loss of gustatory sensation, eating may be a chore rather than a pleasure, in which case nutrient supply may be shallow. Supplementation with at least one nutrient–vitamin B6, for example—has been found to improve storage of information (Deijen, 1992).

When the elderly are able to cheer each other on, as in a community setting, they are more apt to comply with those dietary interventions aimed at physical and mental maintenance. That flavor enhancement induces appetite by overcoming perceptual losses has been demonstrated at home and institutional settings (Schiffman, 1993), and the inclusion of essential fatty acids, whether from foods or supplements, has been found to enhance cognitive function (Yehuda, 2012) and, thereby mood (Parker, 2006) (Stahl, 2008).

Keeping Grandpa or Grandma in a good mood is essential to family serenity. In a time when several generations might live together, this could be as simple as letting them control the remote. Trading Ed Sullivan reruns for peace of mind is probably worth it if Gramps can simultaneously offer a compelling review of last Sunday’s pot roast dinner.


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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.

Stress and Childhood Obesity

weigh-inBeing a kid doesn’t necessarily mean having a carefree life, yet that’s how most adults view childhood. Because kids don’t have jobs, bills to pay, and children to raise what could they possibly have to worry about? More than we realize. Even the very young among us have stressors, slight though they may be. Stress is a function of the demands we face and our ability to handle them. Often it comes from outside sources. You know—family, job, friends, school, and expectations. Sometimes stress comes from inside, related to what we think we should do compared to what we actually do, say or think.

Today, kids have to learn scores of times more information than their parents did at the same age. That we can blame on an electronic era. And they have to learn these things in the same allotted time. Preschoolers get stressed when their moms leave them at daycare. As they get older, kids are pressured by academics and social position. After all, they need to fit in. Their lives get so hectic they seldom have time for themselves, for creative play, or even for relaxation. They are overscheduled with activities that would tax even the adult mind. Disturbing images on TV, news of wars, terrorism and natural disasters, and concerns for personal and family safety add to the burden. Illness, death and divorce don’t help.

All stressors are not created equal, and all people do not respond to stress the same way. Children often learn to handle stress from their parents. Sometimes that’s good; sometimes not. The idea that, “If it doesn’t kill me, it’ll make me stronger,” doesn’t apply to youngsters who’ve not yet developed a coping mechanism. What does this have to do with obesity, a childhood plague that’s more than doubled in the last few decades?  Lots.

A person’s reaction to stress will likely invoke the fight-or-flight (-or freeze) response as the primary means of dealing with a novel situation perceived as threatening. Children who overreact to stress will manufacture more cortisol than the body can dump, and that’s where the problem begins—emotional eating (Michels, 2012). Cortisol is a steroid hormone made by the adrenal glands, released in response to stress. Its main job is to increase blood sugar to power the fight-flight machinery. Cortisol counteracts insulin and contributes to insulin resistance (Goran, 2010) by lowering glucose transport to the cell membrane. Small increases in cortisol can provide a quick burst of energy in an emergency. At the same time it can heighten memory, briefly but powerfully enhance immunity and lower sensitivity to pain. But the return to normal is needed lest the body idle at high rpm’s. With our high-stress culture that has become the norm…chronic stress. That eventually induces impairment of cognitive function, suppresses thyroid activity, throws blood sugar out of whack, menaces bone density, elevates blood pressure, and actually lowers immune responses. And it increases deposition of abdominal fat, setting the stage for metabolic syndrome, depressed affect (Endocrine Society, 2009) (Dockray, 2009) and cardiovascular entanglement, even at a young age.

Children’s biological response to stressors was examined recently by researchers from Penn State and Johns Hopkins Universities.  A group of pre-teens was assigned public speaking and mathematical tasks with little preparation time allowed for either. Cortisol content of their saliva was measured before and after. Following the assignment, the children were offered an array of snack foods regardless of their hunger status. The amount of calories they consumed varied, but those with the highest body mass indexes, who also had the highest cortisol levels, consumed more calories, even in the absence of hunger, than did those with lower cortisol levels. The outcome suggests that children with poor response to stress are at risk for becoming overweight or obese (Francis, 2013). Other factors that contribute to eating in the absence of hunger include poverty, living in a violent environment and food insecurity.

The determination of childhood obesity needs to be made on an individual basis, not from a chart developed by an insurance company that focuses on only one ethnicity or population. Anthropometric measurements and family history need to be included in an evaluation. Pathologies need to be ruled out, genetics must be considered, and psychosocial factors scrutinized. The comorbidities of obesity are varied and many, and their prophylaxis calls for early intervention, some of which transcends diet. Overweight children face the same health conditions as their parents, with hypertension, discordant lipid panels, abnormal glucose levels, and elevated inflammation markers among them. Lifestyle changes, where parents are the managers, may be all that is needed. This may include dietary interventions that eliminate simple carbohydrates, especially sugars and refined starches common to the foods kids like the most. These foods will spike insulin, which will spike cortisol, which will encourage eating, which will add pounds. Avoiding pharmaceutical anorectic agents is strongly encouraged.

Mental stress is associated with emotional eating, which typically ignores healthy dietary patterns (Michels, 2013). Cortisol levels peak in the morning, but can remain elevated in stressful surroundings. Admittedly, some of those surroundings are beyond a parent’s control, so coping mechanisms are helpful. Without being a helicopter parent, it’s possible to create a comfortable atmosphere for a child, even when he is away from you. Teaching coping skills by example starts early. Believe it or not, kids watch, listen and emulate. There are three-year-olds with vocabularies that would make you wince. If kids can learn to be tense and confrontational, they can also learn to relax and to take things in stride.

Limiting cortisol manufacture might be as easy as increasing magnesium in thediet. How?  Vegetables. Essential fatty acids, music therapy and phospholipids,and even vitamin C and tea have been shown to curtail cortisol release (Rains,2011) (Arent, 2010) (Peters, 2001).


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*These statements have not been evaluated by the FDA.
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Vitamin C and Mood

oj-drinking-womanFor a long time, emotions and logical thought have been portrayed as competing processes, with emotions depicted as obstacles to effective decision making. On the other hand, emotions and cognitions might work together to determine our behaviors. Whether or not one controls the other is still a question. If puppy dog eyes can influence a decision or alter a mood, well, “Aw, come on. Please?”  The rigidity of doctrine can be tempered by the plasticity of human thought and behavior, right? If so, a good mood can change outcomes, or at least change the behaviors that affect the outcomes.

Despite their best efforts, even positive people get in bad moods. It could be lack of sleep, or maybe being overworked or overwhelmed. Perhaps there is regret for having done something…or having done nothing. Emotional responses happen so quickly that it becomes a challenge to put a space between feeling and doing. Have you ever snapped at someone for no reason? Or fibbed and said you’re feeling great when you really felt like screaming? Maybe it’s time to figure out what’s standing between you and a smile, and to rewrite the story that precipitated the bad mood. The mood is yours. There’s no need to share it.

Nutritional deficiencies, mostly caused by poor diet, play a part in mood. Junk food equates to junk mood. Edible things devoid of nutritional value, washed down with sweetened, flavored and carbonated distilled water can make you feel depressed, irritable and sick. It’s little wonder that short tempers abound. Recent study has confirmed the importance of micronutrients to the expression of mood, and vitamin C is one of them. Hypovitaminosis is a term that describes vitamin deficiency, though most often associated with vitamin D. It happens when the system is unable to absorb the right amount of vitamins from food or supplements, and results in a number of medical conditions, like scurvy, beriberi, or pellagra, among others.

Vitamin C deficit is not very common in the general population, but does show up in cancer patients and in those with conditions that inhibit absorption. Age, poor diet, medications and obesity are contributing factors. The widowed elderly, for example, often do not eat properly because they don’t cook for themselves. Community settings can make a difference in their nutrient balance.

In acute care situations, as in a short-term hospital stay, hypovitaminosis is more common than one might think, and malnutrition of vitamin C (often accompanied by vitamin D) has been linked to mood disturbances and cognitive upset. In these cases, doses as little as 500 mg twice a day resolved issues with psychological distress and irascible mood (Wang, 2013). Because vitamin C is water-soluble, it needs to be replaced regularly. Most animals can make their own. Humans, apes and guinea pigs cannot. Without it, the body cannot make collagen or the neurotransmitter norepinephrine.

It’s not completely clear if hypovitaminosis C results from outright deficiency or from tissue redistribution as part of the acute-phase response. Investigations stand on both sides of the street (Evans-Olders, 2010). This response is an innate body defense during acute illness and involves the increased production of certain blood proteins, appropriately called acute phase proteins. Once activated, these substances cause the release of inflammatory molecules, the most well known being C-reactive protein (CRP), a marker unexpectedly related to mood disorders in the presence of even low-grade inflammation (DeBerardis, 2006) (Luukinen, 2010). Since CRP is also associated with increased risk of cardiovascular involvement, reducing it is a prudent objective on two fronts. Vitamin C was found to be as effective as statin drugs in lowering CRP levels by more than 25% in a study of individuals whose inflammatory markers put them at risk for a cardiac event (Block, 2009). In patients with active disease, such as cancer, intravenous vitamin C was found to have a salutary effect on CRP and pro-inflammatory cytokines (Mikirova, 2012).

Decrease in blood vitamin concentrations is common to the acute-phase response, but is more common because people fail to get the nutrition they need to maintain optimum health. A glass of orange juice just won’t cut it. Not only are mood and cognitive ability worthy of adequate nutrient intake, but also total physiological function. Supplements have been shown to improve mental processing and response to stress, to reduce fatigue, and even to attenuate psychological and physical damage from noise (Angrini, 2012), including high blood pressure (Fernandes, 2011). Vitamin C now has an identified mechanism of activity beyond that of anti-oxidant. It enhances mood.


Amr M, El-Mogy A, Shams T, Vieira K, Lakhan S
Efficacy of vitamin C as an adjunct to fluoxetine therapy in pediatric major depressive disorder: a randomized, double-blind, placebo-controlled pilot study.
Nutr J. 2013 Mar 9;12:31.

Angrini MA, Leslie JC.
Vitamin C attenuates the physiological and behavioural changes induced by long-term exposure to noise.
Behav Pharmacol. 2012 Apr;23(2):119-25.

Baumann H, Gauldie J.
The acute phase response.
Immunol Today. 1994 Feb;15(2):74-80.

Block G, Jensen CD, Dalvi TB, Norkus EP, Hudes M, Crawford PB, Holland N, Fung EB, Schumacher L, Harmatz P.
Vitamin C treatment reduces elevated C-reactive protein.
Free Radic Biol Med. 2009 Jan 1;46(1):70-7.

De Berardis D, Campanella D, Gambi F, La Rovere R, Carano A, Conti CM, Sivestrini C, Serroni N, Piersanti D, Di Giuseppe B, Moschetta FS, Cotellessa C, Fulcheri M, Salerno RM, Ferro FM.
The role of C-reactive protein in mood disorders.
Int J Immunopathol Pharmacol. 2006 Oct-Dec;19(4):721-5.

Evans-Olders R, Eintracht S, Hoffer LJ.
Metabolic origin of hypovitaminosis C in acutely hospitalized patients.
Nutrition. 2010 Nov-Dec;26(11-12):1070-4.

Fain O, Pariés J, Jacquart B, Le Moël G, Kettaneh A, Stirnemann J, Héron C, Sitbon M, Taleb C, Letellier E, Bétari B, Gattegno L, Thomas M.
Hypovitaminosis C in hospitalized patients.
Eur J Intern Med. 2003 Nov;14(7):419-425.

Fernandes PR, Lira FA, Borba VV, Costa MJ, Trombeta IC, Santos Mdo S, Santos Ada C.
Vitamin C restores blood pressure and vasodilator response during mental stress in obese children.
Arq Bras Cardiol. 2011 Jun;96(6):490-7.

Hamer M, Owen G, Kloek J.
The role of functional foods in the psychobiology of health and disease.
Nutr Res Rev. 2005 Jun;18(1):77-88.

David O. Kennedy, Rachel Veasey, Anthony Watson, Fiona Dodd, Emma Jones, Silvia Maggini,
Crystal F. Haskell
Effects of high-dose B vitamin complex with vitamin C and minerals on subjective mood and performance in healthy males
Psychopharmacology. July 2010, Volume 211, Issue 1, pp 55-68,

Lindblad M, Tveden-Nyborg P, Lykkesfeldt J.
Regulation of Vitamin C Homeostasis during Deficiency.
Nutrients. 2013 Jul 25;5(8):2860-79.

Louw JA, Werbeck A, Louw ME, Kotze TJ, Cooper R, Labadarios D.
Blood vitamin concentrations during the acute-phase response.
Crit Care Med. 1992 Jul;20(7):934-41.

Mikirova N, Casciari J, Rogers A, Taylor P.
Effect of high-dose intravenous vitamin C on inflammation in cancer patients.
J Transl Med. 2012 Sep 11;10:189.

William K. Summers, Roy L. Martin, Michael Cunningham, Velda L. DeBoynton, Gary M. Marsh
Complex Antioxidant Blend Improves Memory in Community-Dwelling Seniors
Journal of Alzheimer’s Disease. 2010; 19(2); 429-439

Luukinen H, Jokelainen J, Hedberg P.
The relationships between high-sensitivity C-reactive protein and incident depressed mood among older adults.
Scand J Clin Lab Invest. 2010 Apr;70(2):75-9.

Wang Y, Liu XJ, Robitaille L, Eintracht S, Macnamara E, Hoffer LJ.
Effects of vitamin C and vitamin D administration on mood and distress in acutely hospitalized patients.
Am J Clin Nutr. 2013 Jul 24.

Zhang M, Robitaille L, Eintracht S, Hoffer LJ.
Vitamin C provision improves mood in acutely hospitalized patients.
Nutrition. 2011 May;27(5):530-3.

*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,, 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 to get the American Academy of Family Physician’s take on memory. Here is the link:


  • 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]

    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.

    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.

    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.

    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).

    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.

    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).

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

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

    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.

    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.

    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.

    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]

    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]

    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.

    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.

    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.

    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.

    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.

    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.

    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.

    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.

    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.