We all forget things once in a while. How many times, for example, have you struggled to come up with the name of a recent acquaintance or forgotten where you put your car keys? These memory hiccups are common and merely constitute a by-product of your brain’s continuous striving to sort, file, and prioritize the incessant barrage of information it receives.
We used to think that such 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.
In the past, scientists and clinicians believed that these innocent memory lapses were associated with normal wear and tear on your brain and that normal aging is associated with loss of brain cells (neurons). Results of more recent research, however, strongly suggest that there may be very little nerve cell loss with normal aging. Moreover, early memory loss IS associated with loss of brain cells.
Our brain cells normally diminish by half percent a year as we get older, and with cognitive impairment and Alzheimer’s disease, the rate of atrophy speeds up. But the good news is cognitive impairment and Alzheimer’s disease is not a normal part of aging as opposed to what most people believe. Although the incidence of Alzheimer’s disease has increased in the recent years, the majority of elderly aged 65 years and above still have good mental health. The implication of this is that we can do something to prevent many forms of cognitive impairment.
For this reason, it is more important than ever to identify and aggressively address signs and symptoms of early memory loss. Furthermore, in addition to screening for early memory loss, we must proactively promote the health of nerve cells and optimize neurotransmitter and hormonal balance before
you begin to experience memory and other cognitive decline.
Moreover, 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.
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:
- Medications. Single or multiple medications, particularly in older adults, can mimic symptoms of dementia. Even some herbal remedies and topical analgesics for arthritis can cause memory lapses when the liver fails to eliminate the chemicals quickly enough.
- Chronic use of alcohol and drugs causes a deficiency of vitamin B1, which results in memory lapses.
- Environmental toxins such as lead, mercury, carbon monoxide, and chemicals in hobby items and pesticides can lead to confusion and a reduced ability to concentrate.
- Hormone changes during menopause/perimenopause can cause temporary disconnects in the ability to recall information.
- Stress, depression and anxiety may actually lead to loss of neurons in the parts of the brain that are affected, leading to an inability to focus, and memory loss.
- Head injuries such as concussion can cause a temporary lapse of memory.
- Infections, particularly those which affect the lining of the brain, can lead to memory loss.
- Impaired thyroid function leads to hormonal imbalances which can affect memory.
- Sleep deprivation from any cause can affect proper memory function.
- Nutritional deficiencies such as lack of vitamins B1 and B12 can also have an effect on memory.
- Natural aging, after all, does cause some brain function to slow down. This slowing of cognitive ability is sometimes misinterpreted as memory loss.
- Stroke, or “vascular accident,” is a significant cause of memory loss.
- Mild Cognitive Impairment, or MCI for short. When memory loss moves beyond a few lapses into something more significant, like forgetting a weekly social event or blanking out on where you were going when you left the house, MCI may be the culprit. While frightening, and often seen as a precursor to dementia or Alzheimer’s, many patients with MCI never progress to those later stages. While MCI can disrupt some day-to-day functions, many of those with mild cognitive impairment manage to live independently.
- Alzheimer’s Disease, AD, is the most common type of senile dementia. It is progressive and degenerative, caused by protein deposits in the brain known as amyloid plaques and tangled nerve fibers. AD has a genetic component, and it may also be linked to a history of severe concussion. It slowly destroys a person’s ability to communicate, make judgments, and engage in social activities. AD may cause significant changes in personality, and eventually loss of speech, incapacitation, and death.
- Other types of dementia – there are a number of other types of dementia, with varying causes but similar results. In most cases, the patient’s ability to function deteriorates, leading to inappropriate social behavior, loss of independence, emotional disturbance, loss of language skills, and eventually, incapacitation and death. These forms of dementia include vascular dementia (caused by blockages in the arteries), Parkinson’s disease, and Huntington’s disease.
- Fortunately, many types of memory loss can be prevented or reversed. With an eye to your long-term health and quality of life, there are several preemptive steps you can take to improve and enhance your memory.
PROTECT YOUR BRAIN NOW
Here at Integrative Psychiatry, we are, after all brain doctors. Our focus on the brain is easy to understand. Your brain is not only your life’s master of ceremonies coordinating all of the intricate physical, emotional, cognitive, social, and interpersonal functions necessary to survive and thrive. It is indeed also the enduring repository of your memories and experiences, hopes and aspirations. Simply put, your brain is the cradle of your identity and the seat of your soul. Take good care of it.
The following recommendations are derived from the most recently published peer-reviewed scientific research. They are appropriate no matter what your overarching goals are:
- Relief of symptoms (mood, memory, sleep, energy)
- Prevention of disease
- Promotion of health
In the most general terms, we try to accomplish these goals as follows:
- “Seal and heal” your likely leaky gut
- “Right-size” inflammation
- Balance neurotransmitters, hormones (thyroid, vitamin D, insulin, and reproductive)
- Replenish adrenal stores
- Reduce oxidative stress
- Eliminate environmental, interpersonal, dietary, and metabolic toxins
Because no prescription medications have ever been shown to protect the brain, prevent memory loss and cognitive decline, or modify the disease course of Alzheimer’s and other neuro-degenerative disorders, the cornerstones of our Therapeutic Brain System to accomplish these vital goals are lifestyle and nutraceuticals.
- Optimize your diet. Try to stick to a low-glycemic, anti-inflammatory, hormonally correct diet (for example a Mediterranean-esque diet) that limits refined carbohydrates, simply sugars, gluten, and red meat.
- Regulate your sleep. Aim for ~8 hours per night. Fall asleep faster; stay asleep longer (i.e. increase sleep efficiency).
- Reduce stress. Interpersonal strife and hectic pace of living are two of the most potent contemporary contributors to brain inflammation.
- Move. Regular exercise and non-exercise activity, along with proper diet and adequate sleep, are the best ways to enhance cognition (and mood it turns out) and prevent brain rot.
- Engage. Maintaining social interactions is an important part of maintaining a healthy mind. While loneliness has been shown to be a factor in Alzheimer’s disease, keeping healthy social interactions can reduce stress levels and promote cognition and memory.
DIETARY SUPPLEMENTS AND NUTRACEUTICALS
Think of supplements and nutraceuticals not as alternatives to medications but rather complements to diet and lifestyle. Those we emphasize based on rationale and data include the following:
- Methyl folate
- Methyl cobalamine
- N-acetyl-cysteine (NAC)
- Vitamin D3
- Alpha lipoic acid
- Gingko biloba
- Omega-3 fatty acids (found in fish oils)
- Huperzine A (Chinese club moss)
- Acetyl-L-carnitine (an amino acid)
- Vinpocetine, an alkaloid extract of the periwinkle plant which acts like dopamine
This list of potentially beneficial nutraceutical ingredients boggles the mind. To simplify things and prevent “pill fatigue,” we have formulated and incorporated products that combine as many of these key ingredients as possible.
Please click on the following link to learn more about our Core Cognitive Cocktail.
If I could only choose one of the nutraceuticals that make up our Core Cognitive Cocktail it would have to be our best-selling FolaNAC.
I will elaborate in the next few sections.
MORE RECENT VIEWS OF EARLY MEMORY LOSS
I mentioned previously that 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:
- It is more important than ever to identify and aggressively address signs and symptoms of early memory loss, and
- In addition to screening for early memory loss, we must proactively promote the health of nerve cells and optimize neurotransmitter and hormonal balance before you begin to experience memory and other cognitive decline.
THE LINK BETWEEN DEMENTIA AND HOMOCYSTEINE
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. This condition is called hyperhomocysteinemia (HHcy) and is a common condition with estimates of prevalence ranging from 5% to 29% in individuals over 65. Accumulating data demonstrates a relationship between elevated homocysteine and neurodegenerative diseases including cognitive disorders and dementia, conditions associated with chronic inflammation and oxidative stress. Past research has found that with an elevated homocysteine level, you’re twice as likely to become demented, twice as likely to have a heart attack, twice as likely to have a stroke, and ten times more likely to experience brain atrophy.
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.
THE FOLATE CONNECTION
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:
- High total folate intake is associated with reduced risk of AD (Corrada M, Kawas C. et al. Reduced Risk of Alzheimer’s Disease with High Folate Intake: The Baltimore Longitudinal Study of Aging. Alzheimer’s & Dementia. 2005 July;1(1):11-18.
- High total folate intake may protect against AD (Luchsinger JA, Tang MX, Miller J, Green R, Mayeux R. Relation of higher folate intake to lower risk of Alzheimer disease in the elderly. Arch Neurol. 2007 Jan.;64(1):86-92.
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.
WHAT ABOUT THE OTHER B VITAMINS?
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.
SLOWING BRAIN DEGENERATION
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:
- Homocysteine activates a specific brain receptor – NMDA – that has been implicated in many different brain disorders including depression, dementia, Parkinson’s, migraines, epilepsy, and Lou Gehrig’s disease. Some believe that homocysteine is at least as neurotoxic as excess glutamate.
- Activation of the NMDA receptor ultimately leads to nerve cell death.
- Homocysteine causes oxidative stress that accelerates the rate at which you burn through your acetycholine.
- Homocysteine, at the same time, slows down the rate at which you make acetylcholine.
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.
ONE LAST POINT
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.
A new study published in the Journal of Alzheimer’s Disease
evaluated the effect of a medical food, Cerefolin/CerefolinNAC (CFLN), in patients with HHcy and Alzheimer’s disease or cognitive impairment due to cerebrovascular disease. An earlier study by the same group of researchers demonstrated significantly slower cognitive decline in patients with Alzheimer’s disease and related disorders (ADRD) who were treated for HHcy with CFLN compared to those without HHcy who did not receive CFLN. In that study, slower cognitive decline was observed in learning and memory, constructional praxis, and visual-spatial executive function, and was more significant in patients with milder baseline severity and who were treated with CFLN for at least a year.
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 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.