Everyone forgets things once in a while. How many times have you forgotten the name of a recent acquaintance, or put your car keys in a place where you were sure you would remember them, then forgotten where you set them down? These slight lapses in memory are common and are simply part of the brain's continuous striving to sort, file, and prioritize the constant bombardment of information it receives.
Forgetfulness is a normal part of the aging process, and in general it is nothing to worry about. You may joke about having a "senior moment" every now and then, and it may take a bit longer to remember what you were looking for in the other room or the name of your neighbor's grandson.
However, when memory lapses begin to interfere with daily life, there is greater cause for concern. Unlike minor lapses in memory, forgetting things like the name of a lifelong friend or close relative, repeating the same question during the same conversation, or getting lost and confused in a familiar place can be a red flag signaling something more serious.
For many people, the realization that they are beginning to suffer from memory loss conjures up the unwelcome and ominous thought of impending Alzheimer's disease. The good news is that many cases of memory loss are not due to Alzheimer's disease, and not all age-related memory loss becomes as severe as senile dementia.
Often, what appears to be significant loss of memory is actually treatable, even reversible, and brain cell growth and learning can take place at any age. Believe it or not, maintaining healthy brain function into the later years is in large part under your own control.
Remembering is not one unique cognitive process, and memory is not confined to one certain area of the brain. For this reason, there are any number of causes of memory loss, and there are many ways to prevent, reverse, and compensate for poor recall ability.
First, though, we should look at the way the brain forms and retrieves memories. There are three unique stages to forming, storing and retrieving memories:
Acquisition is the process of taking in new information along the nerve pathways of the brain and the neurons. During this stage, only the information you intentionally focus on takes up residence in your brain.
Consolidation is the process of encoding new information your brain has received and storing it in long-term memory.
Retrieval consists of recalling information along the same nerve pathways that were used to store it. The more often you use a memory, the easier it is to retrieve, provided the associated neurons remain healthy.
With the understanding that different nerve pathways and different locations of the brain are involved with the processing and storage of memory, it stands to reason that there are many different factors which can precipitate memory loss. The following list describes some of the many issues which are causes of memory loss:
Now, for the more serious age-related memory loss causes:
Some effective memory supplements include:
Physical exercise improves blood flow to the brain and may reduce the risk of memory loss. It also reduces stress and enhances the body's own abilities to regenerate itself.
Early memory loss is associated with loss of brain cells (neurons). At some point this loss crosses over from everyday annoying forgetfulness to clinically significant symptoms. In the past, scientists and we clinicians believed, in contrast, that normal aging is associated with similar loss of neurons, just at a slower rate. Results of more recent research, however, strongly suggest that there may be very little nerve cell loss with normal aging.
Think about the far reaching ramifications of this new data. Two in particular stand out:
To this end, we have been developing better ways of assessing your risk for the most aggressive form of memory loss: Alzheimer’s disease (AD). One of the best predictors of your future risk for this dreaded form of dementia is whether or not you have elevated levels of homocysteine in your blood.
For example, the Framingham Study, one of the most well-known and informative studies on the prevalence of diseases (epidemiology), demonstrated that plasma homocysteine level is a strong predictor of future Alzheimer’s disease. In fact, for every 5 units increase in homocysteine, the risk of AD was increased by 40%. Moreover, plasma homocysteine concentrations > 14 μmol/L nearly doubled the risk of AD.
Their finding led investigators in this study to conclude that plasma homocysteine (Hcy) is a strong, independent risk factor for the development of dementia in general, or specifically, AD. Not only that, in persons who already have Alzheimer’s, increased Hcy levels in the brain may accelerate the progression of the disease.
Another set of studies has found that these elevations of homocysteine are associated with low levels of folate in the central nervous system. As such, early intervention with a certain type of folate supplementation will help prevent the age-related increase in homocysteine.
One quick cautionary note. You may be fortunate enough to have a savvy primary care clinician who is familiar with this data. He or she may even have been proactive enough to measure folate levels in your blood. If so, and your level came back normal, be aware that brain levels of folate do not correlate to serum folate levels. In fact, a study by Serot, et al, found that people with AD often have normal serum folate levels despite very low CNS (central nervous system) folate levels. So, if your homocysteine levels are high, even if your serum folate levels are normal, you still need treatment with folate supplementation.
In addition, several other studies linking low folate levels to high homocysteine levels concluded the following:
Yet another study found that folate supplementation for 3 years significantly improved 5 domains of cognitive function (memory, sensorimotor speed, information processing, complex speed, global cognitive function – some to the level of performance of an individual 7 years younger) that tend to decline with age.
Good question. It turns out that elevated plasma homocysteine is also an important bio-marker for low vitamin B12 levels. The story on B12 is particularly interesting. For example, studies have shown that there is a direct relationship between serum B12 and serum folate such that optimum levels of both vitamins are necessary to protect you from cognitive decline. More specifically, low B12 and normal or even high folate levels do not protect against memory loss. Hence, the need to ensure normal B12 levels when supplementing with folate. It is for this reason that in our best-selling memory supplement – FolaNAC – we have combined both of these crucial vitamins.
It has historically been believed that vitamin B12 had to be given via shots. The more recent data, however, is very reassuring: oral cobalamin is as effective and possibly superior to parenteral (IV or IM) therapy.
The net effect of this dynamic duo is to ensure that you are able to continue to make that neurotransmitter most closely aligned with memory and cognition: acetylcholine.
As you might suspect, in the earliest stages of memory loss, you have an imbalance in your acetylcholine activity that results in increased need for new synthesis of this all-important brain chemical. New acetylcholine is formed through a series of chemical reactions first initiated by L-methyfolate (the type of folate that your brain can utilize) along with methyl-B12 and, in the process, reduces your elevated homocysteine levels.
A logical question arises: how exactly does elevated homocysteine cause memory loss and brain deterioration? The answer to this question is obviously complex but several possible mechanisms have been identified:
Because of the havoc elevated homocysteine levels can wreak, in addition to combining L-methylfolate and B12, we have added a powerful anti-oxidant and NMDA receptor stabilizer, namely, n-acetyl-cysteine (NAC), to FolaNAC. NAC is one of the most widely studied and used supplements in the field of integrative psychiatry because of its potential effectiveness and its proven safety and tolerability.
In addition to its potent antioxidant properties, NAC lowers homocysteine and prevents nerve cell death.
Not all folate is created equal. There is a good chance, particularly if you already have early memory loss (or depression for that matter), that the dietary folate you get from green leafy vegetables (you have to eat them first) and the synthetic folic acid that pollutes your multi-vitamin or your B complex, cannot get from your gut/blood past your blood-brain-barrier and into your brain. If it can’t, it won’t reduce your brain homocysteine levels and won’t protect you from cognitive decline.
It is imperative that you take folate in the L-methylfolate form that readily crosses from your systemic circulation into your brain.
I find it ironic how powerfully the organ cartels – heart, lung, endo, kidney, etc. – preach the good word on end-organ protection. For my money, however, the most precious organ (ok second most precious among men) is the brain. Protect it at all cost. For when it is gone, you and I are gone. So, you guessed it: I take my FolaNAC...Every Day.
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