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Friday, December 19, 2014

Medications To Avoid If You Have bvFTD Or Other Dementias

It has been almost 3 months since I have written anything. In September I was having many difficult days, and attributed them to allergies and antihistamines. Here in Northwest Ohio we had a cold snap before Thanksgiving accompanied by a few inches of snow. That put an abrupt end to the hayfever season. Now that the weather has turned colder my allergy symptoms have all but disappeared, and I have not been regularly taking any antihistamines. I am also feeling much better.

Surprisingly my recovery was not as rapid as I would have predicted. It has taken a couple months. Once in a while I still have a really bad day where I lock myself away in a dark room and read, but they are becoming less frequent. I am still having great difficulty getting things done, and going out. Christmas shopping has become an almost insurmountable task. Almost! I will manage. Online shopping helps, but seems like too much of a compromise. I need to get out there in the world and do some shopping.
Simple, but SO difficult at the time!

As an example of one of those "bad days", I was putting new tires on a bicycle for Cindy. She had found it at a garage sale. I have changed bicycle tires countless times, but this time I was totally incapable of figuring out how to re-assemble the chain and derailleur. I was SO frustrated. I took a break, and looked up a picture of it on the internet. I finally got it, and it was so simple. bvFTD can strike at the oddest of times.

Back to antihistamines. I have been having some trouble sleeping through the night for a very long time. I tend to wake up after sleeping a few hours, watch TV for a couple hours, and then go back to bed. I very rarely sleep through the entire night.

I saw an advertisement on TV for a sleep aid. I checked up on it, and found that its only ingredient was Benadryl - an antihistamine! Well, since I have been having so much difficulty with antihistamines anyway, I figured I would try some as a sleep aid. bvFTD can really assist in making smart decisions like this. I took a couple tablets before I went to bed, matching the dose in the sleep aid, and slept the whole night through for the first time in months. That was nice.

But, over the following couple of days I was confused, and was right back having what I have come to refer to as a "bad day". Fortunately the bad affects didn't last long. Though I appreciated the good nights sleep overall it wasn't worth it.

This led me to do a little research on just which medications are NOT RECOMMENDED for people with bvFTD and related dementias. The list is surprisingly long, and includes some very commonly prescribed medications. I am going to skip the technical studies for a change, and just include some of the recommendations gleaned from several websites dedicated to dementia. The bulk of this information came from the Alzheimer’s Association, and the University Of Southern California.

Following is the list, some alternatives, and other interesting and related information. Interesting to note that antihistamines figure prominently on this list. As always, remember: Every case of bvFTD is different. Everything here is for informational purposes only. See the medical disclaimer through the link located to the right of this page.

Anticholinergic medications

Anticholinergics decrease acetylcholine activity to balance out the production of dopamine and acetylcholine. They are used to treat incontinence, depression and sleep disorders. Medications with strong anticholinergic effects, such as antihistamines that cause drowsiness, are well known for causing acute cognitive impairment in individuals with dementia and may cause confusion and hallucinations. Furthermore, with the cholinergic deficit in some forms of dementia, they could potentiate this deficit and antagonize any cholinesterase inhibiting medications. Adverse effects may include blurred vision, dry mouth and urinary retention. Single or combination gastrointestinal/urinary antispasmodics products should be avoided.

Several factors that may influence whether a patient develop cognitive impairment when exposed to
anticholinergic drugs:

    the number of AC drugs and the doses of the drugs used,
    baseline cognitive function (determines susceptibility) and
    the patient's response to medications (sensitivity and metabolic processing as determined by their liver and kidney function status).

Carefully evaluate the risk/benefit for these medications and consider alternatives. For example with incontinence, consider the following:

    Functional vs urge incontinence
    Scheduled toileting
    Check post void residuals (especially in males as these medications can cause retention)
    Reducing dose of cholinergic medication

If used, carefully evaluate effectiveness of medication and consider discontinuing if there is no improvement in six weeks.

    Belladonna alkaloids
    Benzotropine mesylate (Cogentin®)
    Dicyclomine (Bentyl®)
    Flavoxate (Urispas®)
    Hyosyamine (Levsinex®)
    Oxybutynin (Ditropan®)
    Tolterodine (Detrol®)
    Trihexyphenidyl HCL (Artane®)


Antihistamines block the action of histamine, a substance in the body that causes allergic symptoms.

    Azatadine (Optimine®)
    Brompheniramine (Dimetane®)
    Carbinoxamine, Chlorpheniramine (Chlor-Trimeton®)
    Clemastine (Tavist®)
    Cyproheptadine (Periactin®)
    Dexchlorpheniramine (Polaramine®)
    Diphenhydramine (Benadryl® or Sominex®)
    Hydroxyzine (Atarax®)
    Phenindamine (Nolahist®)
    Promethazine (Phenergan®)
    Tripolidine (Actifed/Myidyl®)

Physicians also recommend that individuals with dementia avoid over-the-counter sleep remedies. The active ingredient in many of these preparations is diphenhydramine (Benadryl®), an antihistamine that tends to make people feel drowsy. Diphenhydramine further suppresses the activity of one of the main brain cell messenger chemicals whose activity is reduced by Alzheimer’s disease.

Examples of over-the-counter sleep aids containing diphenhydramine that should be avoided include:

    Compoz®, Nytol®, Sominex®  and Unisom® diphenhydramine (Benadryl!!! ed.) is also an ingredient in many “nighttime” or “PM” versions of popular pain relievers and cold and sinus remedies 


Barbiturates cause relaxation and sleepiness. Excessive and prolonged dosages of barbiturate drugs, such as phenobarbital, may produce memory loss, irritability, changes in alertness and decreased interpersonal functioning. Barbiturates may also cause an acute, life-threatening overdose syndrome.

    Phenobarbital (Luminal® Sodium)


In general, benzodiazepines are frequently associated with increasing confusion, falls and memory impairment in elderly patients. In people with FTD, benzodiazepines have been associated with an increase in behavioral problems and impair both memory and psychomotor skills. Repeated use of large doses or, in some cases, daily use of therapeutic doses of benzodiazepines is associated with amnesia, hostility, irritability and vivid or disturbing dreams, as well as tolerance and physical dependence. Use can result in reduced inhibition and impaired judgment. Benzodiazepines have also been associated with anticholingeric-like effects, such as urinary retention and dry mouth. Anxiolytics recognized as benzodiazepines should be avoided.

Carefully evaluate alternatives for these medications, and if they cannot be avoided, consider using them for only a short time. When used for anxiety, consider nonpharmacological supportive strategies. If co-existing with depression, consider use of paroxitene (Paxil®), citalopram (Celexa®) or buspirone (Buspar®). When used for sleep:

    Consider good sleep hygiene
    Encourage adequate physical activity during the day
    Try melatonin
    Try trazodone (Desyrel®)


    Short-acting benzodiazepines: triazolam (Halcion®) and Midazolam (Versed®)
    Intermediate-acting benzodiazepines: lorzepam (Ativan®), temazepam (Restoril®), alprazolam (Xanax®), oxazepam (Serax®), estazolam (ProSom®)
    Longer-acting benzodiazepines: diazepam (Valium®), chlordiazepoxide (librium®), clorazepate (Tranxene®), halazepam (Paxipam®), prazepam (Centrax®), quazepam (Doral®) and clonazepam (Klonopin®), flurazepam (Dalmane®)

CNS stimulants

Increased sensitivity to medications affecting the CNS can produce impaired memory and delayed psychomotor performance.

    Amitriptyline (Limbitrol® or Limbitrol® DS): Amitriptyline is used to treat symptoms of depression
    Fluoxetine (Prozac®, Prozac® Weekly, Sarafem®, Symbyax®): Fluoxetine (Prozac) is used to treat depression, obsessive-compulsive disorder, some eating disorders and panic attacks. Fluoxetine (Sarafem) is used to relieve the symptoms of premenstrual dysphoric disorder, including mood swings, irritability, bloating and breast tenderness.

Muscle relaxants

Muscle relaxants may be used to treat spasticity or muscle spasms associated with spinal cord injuries, stroke, multiple sclerosis, cerebral palsy or other conditions. Several of them can cause severe liver damage.

    Carisoprodol (Soma®)
    Chlorzoxazone (Parafon Forte®)
    Cyclobenzaprine (Flexeril®)
    Dantrolene Oral (Dantrium®)
    Metaxalone (Skelaxin®)
    Methocarbamol (Robaxin®)
    Orphenadrine (Norflex®)
    Baclofen (Lioresal®)

Tricyclic antidepressants

Some of these medications have anticholinergic properties which may worsen cognition in patients with mild memory problems and antagonize the effects of cholinesterase inhibitors. Carefully evaluate alternatives for these medications. Desipramine (Norpramin® or Pertofrane®) has the least anticholinergic side effects of any of the tricyclics.

When used for neuropathic pain, patients over the age of 65 may do better on gabapentin (Neurontin®) due to a lower risk of side effects. When used for sleep, please consider possible use of trazodone (Desyrel®) due to lower risk for anticholinergic side effects. When used for depression, consider using an alternative antidepressant class.

    Amitriptyline (Elavil®)
    Clomipramine (Anafranil®)
    Desipramine (Norpramin® or Pertofrane®)
    Doxepin (Sinequan®)
    Imipramine (Tofranil®)
    Protriptyline (Vivactil®)
    Trimipramine (Surmontil®)

There are no medications available to cure or delay the progression of FTD, but there are a number of medications available for symptomatic relief. Medical management includes treatment of concomitant medical conditions including infections, parkinsonian symptoms, seizures, pain and improving nutritional status. It is imperative to review all medications that the patient is taking. This includes prescription drugs, non-prescription drugs, social drugs (caffeine, nicotine, alcohol) and/or alternative products (e.g., herbals, vitamin or minerals). A number of medications can exacerbate behaviors or cognitive problems (e.g., stimulants, depressants, some anti-epileptic medications), so any unnecessary drug should be discontinued. All medications the patient is taking should be fully reassessed for optimal response at the dose prescribed and the patient should only be on necessary medication that are effective in treating underlying conditions.

Early interventions

Nonpharmacological forms of therapy should be initiated first for the management of inappropriate or aggressive behavior. This includes discussing tolerance for disruptive but non-dangerous behavior, a medical alert bracelet for the patient and a note or card to be given to strangers explaining the patient has a disease (click here to download cards that can be printed), providing distraction so that patient diverts attention or alters behavior, and mild forms of bribery with favorite snacks. The family and caregivers should be referred to support groups and local chapters that in addition to providing information and advice, organize respite care. Depression in caregivers is common and leads patients to earlier nursing home placement (Litvan et al, 2001). The need for a power of attorney cannot be overemphasized as the patients quickly, if not at the time of diagnosis, are no longer able to make medical and financial decisions. The behavioral symptoms are often the cause for the institutionalization of patients and so need to be addressed and adequately treated.
Pharmacological review

There are no medications available to cure or delay the progression of FTD, but there are a number of medications available for symptomatic relief. Medical management includes treatment of concomitant medical conditions including infections, parkinsonian symptoms, seizures, pain and improving nutritional status. It is imperative to review all medications that the patient is taking. This includes prescription drugs, non-prescription drugs, social drugs (caffeine, nicotine, alcohol) and/or alternative products (e.g., herbals, vitamin or minerals). A number of medications can exacerbate behaviors or cognitive problems (e.g., stimulants, depressants, some anti-epileptic medications), so any unnecessary drug should be discontinued. All medications the patient is taking should be fully reassessed for optimal response at the dose prescribed and the patient should only be on necessary medication that are effective in treating underlying conditions.
Selective serotonin reuptake inhibitors (SSRIs)

While there is no known treatment that can delay progression, environmental and pharmacological interventions can help with the behavioral management. Certain behaviors, especially aggression and extreme disruptiveness, as well as delusions require medication. Patients with FTD show serotoninergic deficits which appears largely related to postsynaptic defects although presynaptic deficits have been reported (Huey et al, 2006). Selective serotonin reuptake inhibitors (SSRIs) have been used with some success (Huey et al, 2007; Lebert et al, 2004; Swartz et al, 1997). SSRIs have been used to treat compulsions, ritualistic behaviors, carbohydrate cravings, anxiety and behavioral symptoms in patients with FTD (Swartz et al, 1997). Another study reported that paroxetine decreased or eradicated repetitive, ritualistic behavioral in a large proportion of patients (Chow & Mendez, 2002). The side effects were tolerable for most patients. Paroxetine compared to piracetam improved behavioral symptoms (Moretti et al, 2003). However, there is one study, albeit using paroxetine at a higher dose (40mg) that showed no improvement in behavioral symptoms and some learning difficulties in the paroxetine group (Deakin et al, 2004). Trazodone, was shown to be effective compared with placebo in controlling behavior in patients with FTD (Lebert et al, 2004).

Patients with SD share many similarities with FTD and so SSRIs can be tried for the compulsive behaviors. SSRIs can be warranted in PNFA because patients with this condition are often very aware of their deficits, so depression and social withdrawal are common. There are, however, no reported studies of antidepressant efficacy in this group.
Atypical antipsychotics

Low doses of atypical antipsychotics such as quetiapine, olanzepine or risperidone can be used for agitation, aggression or psychotic behavior. The potential benefit of all antipsychotics must be weighed against the potential risks such as cerebrovascular adverse events and even mortality. Typical antipsychotics are associated with extrapyramidal side effects and usually should be avoided, since patients with FTD are likely to show parkinsonism. Medications for behavioral symptoms should be initiated at a low starting dose and then subsequently titrated slowly based on the patient’s response and the presence of adverse effects.
Acetylcholinesterase inhibitors (AChEIs)

Acetylcholinesterase inhibitors, although helpful in AD, do not seem to be effective in managing symptoms of FTD and have been reported to cause agitation in patients with FTD. (Perry & Miller, 2001). They can be dangerous in patients with FTD-MND as they cause increased oral secretions. The most probable explanation for their lack of effectiveness in FTD is that the cholinergic system, in particular the cholinergic neurons in the nucleus basalis of Meynert, are relatively spared in FTD.
NMDA-receptor antagonist

Memantine, an NMDA-receptor antagonist, is approved for the treatment of Alzheimer's disease (AD). Preliminary evidence suggested transient, modest benefit on neuropsychiatric symptoms in FTD, but a prospective trial at UCSF showed no benefit for patients.
Valproic acid

Valproic acid and derivatives (divalproex sodium) have been reported as useful for aggressive behavior and for impulse control, primarily in individuals diagnosed with Alzheimer's disease. In placebo-controlled studies valproic acid displayed little or no benefit. Valproic acid and related drugs may cause liver damage and require blood tests to periodically check liver function. Many practitioners also order blood levels, which adds to the cost of drug therapy.

Gabapentin has also been reported to be helpful in managing behavioral problems in a few case reports.
Non-pharmacological therapies

Individualized exercise programs can have a positive impact on functional performance in persons with mild to moderate dementia and can be helpful for patients with FTD (and their caregivers). Adequate sleep may reduce behavioral problems. Recognizing and treating concomitant illnesses or infections can also improve dispositions.
Complementary and alternative medicine

Many individuals also use non-prescription and herbal/alternative remedies for symptoms. However, at this time there is no evidence for any herbal/alternative remedies. Gingko biloba (GB) has been widely used in Asian and European medicine, and recent animal studies support a GB antioxidant effect but, to date, there is no evidence of a beneficial effect on cognition or behavior. Vitamin E was reported to be an antioxidant possibly beneficial in Alzheimer's disease (AD), but recent evidence suggests otherwise. There is no evidence to support its use in FTD (Sano et al, 1997, Peterson 2005).
Future treatments

The lack of randomized, placebo-controlled data on most symptomatic treatments for FTD greatly hinders our ability to determine optimal therapies at this time. The development of mouse models of FTD as well as a greater understanding of the pathophysiology offers hope for the development of future therapies. (Lee and Trojanowski 2001)
Language impairment

While there aren't useful medications to help with language impairment. PNFA, but also early SD and bvFTD, warrants a speech pathology assessment and intervention. Maintaining adequate communication can decrease frustration, a common problem in FTD. Refer your patient to our practical tips section for different communication strategies.

(More. . . this didn't copy well, and the table from the article was indecipherable. I am too lazy to fix it, so I deleted the table, but left the rest. If you are interested in the entire piece it is online as a PDF file. Just Google it. I am sure you can figure it out if I did.)

Copyright © 2008 by Therapeutic Research Center
Pharmacist’s Letter / Prescriber’s Letter
~ P.O. Box 8190, Stockton, CA 95208 ~ Phone: 209-472-2240 ~ Fax: 209-472-2249
pharmacistsletter.com ~
Detail-Document #240510
-This Detail-Document accompanies the related article published in-
May 2008 ~ Volume 24 ~ Number 240510
Drugs To Avoid in Patients with Dementia
Elderly people with dementia often tolerate drugs
less favorably than healthy older adults. Reasons
include increased sensitivity to certain side effects,
difficulty with adhering to drug regimens, and
decreased ability to recognize and report adverse events
. Elderly adults with dementia are also more
prone than healthy older persons to develop drug-induced cognitive impairment.
Medications with strong anticholiner
gic (AC) side effects, such as
sedating antihistamines, are well-
known for causing acute cognitive impairment in people with dementia.
Anticholinergic-like effects,
such as urinary retention and dry mouth, have also b
een identified in drugs not typically associated with
major AC side effects (e.g., narcotics, benzodiazepines).
These drugs are also important causes of acute
confusional states. Factors that may determine
whether a patient will develop cognitive impairment
when exposed to ACs include: 1)
total AC load (determined by number of AC drugs and dose of agents
utilized), 2) baseline cognitive function, and 3) individual patient pharmacodynamic and pharmacokinetic
features (e.g., renal/hepatic function).
Evidence suggests that impairment of cholinergic tr
ansmission plays a key role in the development of
Alzheimer’s dementia. Thus, the development of th
e cholinesterase inhibitors (CIs). When used
appropriately, the CIs (donepezil [
], rivastigmine [
], and galantamine [
Razadyne, Reminyl
in Canada]) may slow the decline of cognitive and f
unctional impairment in people with dementia. In
order to achieve maximum therapeutic effect, they id
eally should not be used in combination with ACs,
agents known to have an opposing mechanism of action.
Roe et al studied
AC use in 836 elderly
Use of ACs was found to be greater in patie
nts with probable dementia than healthy older
adults (33% vs. 23%, p = 0.001). Patients with dementia may be more apt to take ACs because of
increased prevalence of urinary incontinence (comm
only treated with ACs), us
e of AC antipsychotic
agents for behavioral and psychotic sympto
ms, and side effects caused by CIs.
When selecting drug therapy fo
r patients with dementia, the use of AC medications should be
avoided, or at least limited to medications within a
therapeutic class that have the least AC adverse

Friday, October 3, 2014

eExtremely Low Doses Of THC Reduce The Production Of Amyloid Beta

Alright! This looks like the best evidence yet that marijuana may have some beneficial properties for dementias.

Marijuana compound may offer treatment for Alzheimer's disease, study suggests
Date: August 27, 2014
Source: University of South Florida (USF Health)
Summary: Extremely low levels of the compound in marijuana known as delta-9-tetrahydrocannabinol, or THC, may slow or halt the progression of Alzheimer's disease, a recent study from neuroscientists suggests.

A new study tested the effects of the marijuana compound THC on an Alzheimer’s disease cell model.
Credit: © Uros Poteko / Fotolia

Extremely low levels of the compound in marijuana known as delta-9-tetrahydrocannabinol, or THC, may slow or halt the progression of Alzheimer's disease, a recent study from neuroscientists at the University of South Florida shows.

Findings from the experiments, using a cellular model of Alzheimer's disease, were reported online in the Journal of Alzheimer's Disease.

Researchers from the USF Health Byrd Alzheimer's Institute showed that extremely low doses of THC reduce the production of amyloid beta, found in a soluble form in most aging brains, and prevent abnormal accumulation of this protein -- a process considered one of the pathological hallmarks evident early in the memory-robbing disease. These low concentrations of THC also selectively enhanced mitochondrial function, which is needed to help supply energy, transmit signals, and maintain a healthy brain.

"THC is known to be a potent antioxidant with neuroprotective properties, but this is the first report that the compound directly affects Alzheimer's pathology by decreasing amyloid beta levels, inhibiting its aggregation, and enhancing mitochondrial function," said study lead author Chuanhai Cao, PhD and a neuroscientist at the Byrd Alzheimer's Institute and the USF College of Pharmacy.

"Decreased levels of amyloid beta means less aggregation, which may protect against the progression of Alzheimer's disease. Since THC is a natural and relatively safe amyloid inhibitor, THC or its analogs may help us develop an effective treatment in the future."

The researchers point out that at the low doses studied, the therapeutic benefits of THC appear to prevail over the associated risks of THC toxicity and memory impairment.

Neel Nabar, a study co-author and MD/PhD candidate, recognized the rapidly changing political climate surrounding the debate over medical marijuana.

"While we are still far from a consensus, this study indicates that THC and THC-related compounds may be of therapeutic value in Alzheimer's disease," Nabar said. "Are we advocating that people use illicit drugs to prevent the disease? No. It's important to keep in mind that just because a drug may be effective doesn't mean it can be safely used by anyone. However, these findings may lead to the development of related compounds that are safe, legal, and useful in the treatment of Alzheimer's disease."

The body's own system of cannabinoid receptors interacts with naturally-occurring cannabinoid molecules, and these molecules function similarly to the THC isolated from the cannabis (marijuana) plant.

Dr. Cao's laboratory at the Byrd Alzheimer's Institute is currently investigating the effects of a drug cocktail that includes THC, caffeine as well as other natural compounds in a cellular model of Alzheimer's disease, and will advance to a genetically-engineered mouse model of Alzheimer's shortly.

"The dose and target population are critically important for any drug, so careful monitoring and control of drug levels in the blood and system are very important for therapeutic use, especially for a compound such as THC," Dr. Cao said.

Tuesday, September 23, 2014

Bad Days With bvFTD. Lost Another Month. What Happened?

Gracie dressed up for a Party last Fall.

"The only thing I'm allergic to is criticism."
-David Lee Roth

This is a rather long post, but hopefully I can help gain some insight into dealing with bvFTD by rambling on a bit, and exploring some interesting symptoms. I have had a challenging time since my last post. I had stopped taking all of my medications for 14 days to detoxify my system, and get a sense of how I was functioning without medication. As I wrote previously, that went well after the first few days. As planned, I started taking my medications again. I did not have any difficulties with side effects when I started taking the pills again except for some gastric disturbance probably due to the Metformin/Glyburide mix (generic Glucovance) to control my blood sugar. I was feeling pretty good, and most of my days were good days. I was fat, dumb, and happy!

Then all of a sudden with no warning I had a really bad day. I was a little confused, and had a lot of difficulty thinking of words and names. Over the next few days I could feel my anxiety growing and strangling me like a vine. I felt my stress growing. Instead of getting better, each day seemed a little worse than the day before.

To reduce my stress level I limited my contacts with outside people. Just having to "act normal" in a social situation, even with friends, added too much more stress and anxiety. I did not want to see anyone. I did not want to talk to anyone on the telephone. I did not even want to read emails or texts. Saying "I did not want..." is not a very accurate description. More accurately, I was incapable of seeing anyone, talking with anyone, or even texting. It just kept getting worse every day. It was getting scary. I spent many days in a darkened room reading. I don't remember how many, but it was too many.

Just when I was starting to feel a little more normal, I had a friend who should have known better drop by unannounced. Most folks know that I do better if they call first to make sure a visit is welcome. I never did well with drop-ins, and now they are intolerable. Anyway, I visited with him for a couple of hours, but when he finally left I had to lock the doors after him. I did not want even a remote chance of any more unexpected company. I went upstairs and closed myself into a locked darkened bedroom. Gracie was "on guard" snoring loudly right outside the bedroom door to make doubly sure I was not disturbed. I read for a while, and fell asleep. I felt better after a short nap. Well now, the nap isn't all that unusual since my medications can make me sleepy sometimes, but this felt different. I was stressed to the breaking point, and just being a hermit for a while was the only way I knew of to cope.

I should clarify that I do not have anything going on in my life that is any more or less stressful than usual. The every day dealings with Frontotemporal Degeneration, bvFTD in my case, is a constant stress I have been managing over the past few years (more like 4 years, 7 months and 10 days ...but who counts?) since my first diagnosis. Some days are better than others, and I have come to accept that most of the time. I am still not making quite enough money, and still having all of the other daily little problems like always. There were a couple incidents which added more stress than I could handle, but I dealt with them the best I could. I removed the stress.

First, I was buying a television from someone who was moving. Payment was to be made when they actually moved, and needed the money most which was a few months away. Unfortunately, every time I saw them I was asked for early payment, or reminded about the TV until it got to the point where every time I looked at it there was a conflict. I looked at that TV a LOT! It became an unbearable burden. I managed the stress it was causing by removing it. I gave the television back, and cancelled the deal. As soon as it was gone I felt as if a huge weight had lifted. Even I hadn't realized how much stress it had been causing. Of course Cindy thought I was totally crazy, and I am sure she made some excuse about it just being a symptom of my disease, and rightly so.

Then there were the books. Someone brought me a case of 20 books to try to sell, and split the profit. I stupidly agreed because I have FTD and I sometimes I make stupid decisions. After fretting about it for several weeks, I finally had a day where I was feeling better, and I contacted a friend who frequently bought such items. It is so difficult for me to do stuff like that. It sometimes takes me days to work up to actually doing something instead of thinking about doing it. This took me weeks!

I was really looking for some assistance since I was in no condition to be negotiating prices for collectible books with strangers when I was incapable of even talking to a friend on the phone. I still couldn't do it. When I was asked to come up with a price for the books I fretted for several days before finally just saying I wanted them to make me an offer. I was totally incapable of making any kind of decision about a price after it had taken me weeks just to finally make the contact. I really needed help. Though the books are selling online from other dealers for $75-80 each, I would have taken a buck each just to remove the stress. Any extra money is helpful. Money is so tight that even $20 would make a noticeable difference. The person I contacted wouldn't even bother to make me an offer. Their answer, and I quote, was "Shit happens!" Well, I should have known better than to ask anyone for help. I managed the stress. I put the box of books out for the trash on Monday morning. Once again I felt like a huge weight was lifted as soon as they were gone.

What I am babbling about here are a couple examples to point out that neither the books nor the TV is enough to cause any insurmountable stress under normal circumstances. In the past I would have cussed out the tv-person for being such a dick, and set a price so high the shit-happens-bastard would have cried when he paid, or I would have found another buyer. However, at the time, for me, added to the way I was feeling, it was entirely too much. Besides, I am way nicer than I used to be ...mostly.  Well, maybe they were each having a worse day that I was at the time. Both are wonderful friends. See how complicated bvFTD can be?

Each incident caused me to pull back further and further away from the world. All I wanted was to be a hermit, and be left alone. I knew instinctively that is what I needed. Poor Cindy! I don't think anyone can totally understand, but she helped me the best she could. Now and then I received a reassuring or encouraging text from a friend which though I couldn't answer, I read and appreciated. Gracie was always there too, checking to make sure I was OK (Gracie is an Akita, and very protective), so even though I limited my contact with the outside world to manage the stress I was never really alone.

On a side note: I did learn that Cindy is extremely protective of me. She is like a momma bear when her cub is threatened. When I was feeling really bad, and needed a lot of lone-time and personal space she protected me from the outside world. She gave me the space I needed, and made damn sure others did also. Though I do not think I need protecting all that much because after all, with FTD I can still go from zero to rage in 0.24 seconds anytime and anywhere, she did good. Maybe she was actually protecting the other poor fools from me instead. I was a bear cub on the edge!

This had been going on for over 4 weeks!

This is still going on, but getting better. I am switching tenses all over the place as I write this because some of what happened is from weeks ago, and some is current. In my mind time is compressed, so then is the same as now. It feels like everything is yesterday. My past and present tenses have mingled and reflect my state of mind. I think I will not correct them with an edit as it shows how my mind is working, or not working. I am not so much confused, but time is all mashed together.

The whole point of writing this is because I realized something had drastically changed. Cindy realized something had drastically changed. I really don't think it is just the natural progression of my disease because it happened so quickly. The pattern of my bvFTD has been a slow and steady march rather than periods of rapid decline. What I was dealing with was a very rapid decline in my ability to function. I couldn't do anything. I was confused. I had very little memory of what happened yesterday, or the past week, or weeks. If I really thought about it I could remember, but it was as if the time was missing or compressed. Sometimes I could barely talk because I couldn't think of the words. All I wanted to do was lock the doors, and be a hermit.

Together Cindy and I tried to think of anything environmental that may have changed. It only made sense that if it was not directly related to the progression of my disease there must be some other cause. We eliminated just plain stress because that hadn't changed any. I had taken a different dose of Aricept for a week because I used up an old sample pack of 23mg pills before getting a refill of my usual quick-acting 10mg pills. Nothing changed when I switched back, so we decided that probably wasn't it. I had recently refilled most of my prescriptions, and I thought that maybe one or more of the generic substitutions was not what it was supposed to be. This seemed most likely until I got another bunch of refills, and still nothing changed. What could it be? Fumes from the new insulation? We were wracking our brains trying to figure it out.

One night I was sitting on the couch about 3 AM. I had been asleep, and gotten up. I rarely sleep all night anymore. Thinking about what was going on, I wondered if it had happened to me before. Duh! All of a sudden I remembered. April 2012! My missing month. II just re-read my post from back then, and it is exactly the same now as it was then. In April of 2012 I had forted-up and become a hermit, and barely remembered any of it afterwards. Back then I was living alone, so almost nobody noticed. Could something so devastating really be so simple?

It had been a warm spring back in 2012, and my allergies were much worse than usual. I was taking antihistamines. I have not been bothered much by allergies in fall for many years. This year has been different. It has been an unusually cold summer here in Ohio following a harsh winter. For some reason the allergy season started weeks earlier than usual, and pollen counts have been through the roof. Couple that with very little rain, and I guess conditions are perfect. I have all of the symptoms of classic hayfever: Itchy eyes and throat, sneezing, runny nose, sinus congestion, and even a little asthma thrown in now and then just to make it interesting. I have lived with allergies all of my life, so though they hadn't bothered me much in the fall lately it was nothing out of the ordinary. I did what I have always done - took some antihistamines, and went on with what I had to do without giving it a second thought.

Well. Things have changed since I was younger and dealing with allergy season. I now have bvFTD, and take some very robust medications. Even small changes have big impacts. When talking about this with my neurologist back in 2012, we came to the conclusion that the additional stress of allergies coupled with the action of the antihistamines on my already challenged brain chemistry was causing my difficulties. It was just a theory back then, but it made sense. There is convincing evidence that the histamine pathway is intermingled with both cognition and memory.

It is just a theory now, but it still makes sense. We finally got a few days of rain, and pollen counts are more normal. I changed antihistamines, too. Same generic Zyrtec, but from a different manufacturer. I am starting to feel better. Well enough to sit down and write something. I was unable to do that for weeks. Maybe it is just coincidence, but then again, maybe not.

I am looking forward to the first frost!

Some days are better than others, and lately most days have been very difficult. Better times are coming!

Comments and questions are always welcome.

Friday, August 29, 2014

Cold Turkey - Withdrawal Symptoms - Ritalin, Namenda, and Aricept

This "high" is when snorted, overused, and abused, but look at the temporal lobes all alight.
I stopped taking my medications for a period of 14 days. It was my intention to cleanse myself of all of my medications for two reasons. First was too avoid addiction and long term side effects. Though it probably wont help it makes me feel better about taking such powerful and addictive medications. The other reason 
was that I periodically check and see how my progression is coming along, and it seemed like time to do it again. I have been doing this kind of self-evaluation roughly once a year since my diagnosis with FTD. If you haven’t already, please read the medical disclaimer.
I am currently taking Ritalin, 20 milligrams a day, donazapel 20 milligrams a day, namenda 20 milligrams a day, and losartan 5 milligrams a day. Though it is recommended that these doses be split up morning and evening I have always taken the full dose of all of them in the morning ...or mid-day when I forget or sleep late. I also started taking a glyburide/metformin combination (generic for Glucovance) again, and have increased the dose of that to 2000 milligrams a day. That one I do take twice daily, and it still has some side effects.

 In addition to the prescription medications, I also occasionally take some supplements. I am not taking as many supplements as previously because I cannot afford them. I have been fairly consistent taking a Ginko Biloba extract, but other than a very occasional vitamin D3 or Niacin not much else. I have not taken the Lions Mane Mushroom Extract all summer, but it is time to reorder. I have been taking that one consistently 3-4 months on, and 3-4 months off. It is very expensive, so I give it some time to work between courses of treatment. When it is on sale I also still drink pomegranate juice. Other than a generally healthy diet that avoids most processed foods and additives that is about all I am currently doing.

I stopped taking my pills on Sunday, and that included supplements too. The first 3 days were easy, but it is not recommended that anyone stop taking any medication cold turkey without consulting a physician. This can lead to both physical and psychological withdrawal symptoms, side effects, or worse. Of course I did indeed have some withdrawal symptoms and side effects. After all, nothing is really easy with frontotemporal degeneration and I am taking some pretty serious medications here.

Probably the worst of the medication I am taking that is known for having withdrawal symptoms is the Ritalin. The higher doses (up to 60 mg/day or greater) are reportedly far worse than the 20 milligrams I am taking for having withdrawal from addiction. Even at only 20 milligrams after the first few days I started to feel very tired during the day. I had some bouts of nausea, and couldn't sleep hardly at all at night. When I did manage to sleep I had some very vivid dreams. Not bad, just more realistic and detailed than normal, or I remembered them better. Poor Cindy might say I was irritable, but she is a very kind and loving person. I was irascible, and very short tempered. Sometimes I could barely stand to be in the same room with myself. It was in the middle of the night. though, that things were the most difficult. I found myself tossing and turning, unable to lie still, and a couple times I even had the shakes!

After a week I did not notice any more side effects or withdrawal symptoms. They just dwindled and finally went away. That does not mean that I was feeling all fine and dandy. After the withdrawal symptoms were gone I was able to get an idea of what I would like be like without any medication. It was not good. 

The places where I noticed the biggest degradation or progression was with motivation, and my ability to think of words. I did not accomplish much of anything during the time I was not taking my medications except lay around on the couch and watch TV. I couldn't get myself to do anything but think of all the things I wanted to do. I did not want to see or talk to anyone either. My short-term and working memory went out the window. I had to make notes or I would not remember much of what happened over that 2 week period.

When I spoke, I had to pause every few sentences to think of a word. I am talking about a long pause that completely stops conversation, and frequently I never did think of the word I was looking for and got very frustrated because I forgot what I was going to say. I could not remember names of places or actors, movies, or TV shows. Communication was very difficult. I had a very halting speech pattern. This is a huge change because when I am taking my medications I speak well even when I don't talk very good.

There are a few other areas where I noted some changes. The other night when I tried to think of a simple math problem, I was trying to figure out how old I was back in 2010, instead of a mental math problem I got a mental image like I was looking up an empty metal spiral staircase. That was kind of weird! Apparently that is all that's left in that part of my brain that used to be able to do mental arithmetic. The metal staircase looked rusty, like my brain. I could still  subtract backwards from the current year, but I was totally blank when I tried to figure my age forward from my date of birth. My ability to do mental arithmetic is steadily degrading, but advanced statistics, and percentages are still easy for me.
So that is what I was doing the last couple of weeks, as for the rest of the Summer...
 It has been about 4 months since the last time I wrote anything to post here. There is nothing more wrong than usual. I am doing as well as can be expected. Cindy and Gracie have been keeping me busy, but that is for another post.

As always - comments are welcome. I know it is a nuisance to have to register to leave a comment or question, but I was being deluged with spam comments. Maybe I will try opening it up again soon.

Please take a few seconds to click on an ad link before you leave. Every penny helps!

Some days are better than others, but I am still doing percentages as needed!!!!!!

Monday, April 28, 2014

Marijuana cannabinoids slow brain degradation and aging, reverse dementia: here's how

My personal take on this is - the jury is still out. Yeah! It is always a nice "high", but as for any real beneficial effects ...I don't think I have seen any on the few occasions I have experimented. I have never been what could be considered a "user" because I did not like thew effect it had on my brain. My brain was always my strongest asset, so why would I ever want to put it at a disadvantage. Now that my brain is slowly turning to Lime Jell-o ...it just doesn't matter so much. Anyways - here is some information on some recent research on this subject. I really cannot endorse it, but it seems to be a current trend.

Amy Corderoy
Health Editor, Sydney Morning Herald
Yeah! That's me! In Michigan medical marihuana is legal. Not yet in Ohio.

It makes most people a little foggy-headed, but scientists are investigating whether an active ingredient in cannabis could actually stave off dementia.

A team from Neuroscience Research Australia is in the early stages of research examining if one of the main active ingredients in cannabis, called cannabidiol, could reverse some of the symptoms of memory loss in animals.

Tim Karl, a senior research fellow with the group, said cannabidiol does not have the same psychoactive effects as the main component of marijuana, THC, but it has been found to have anti-inflammatory, antioxidant and other effects that could be beneficial for the brain.

“Back in the day cannabis was used for medical purposes, I'm talking 200 years, 100 years back, then at some point people discovered it had other effects and, as quite often happens in our society, people decided it was a bad drug,” he said.

“But it's not one compound, it is a mixture of 60 different compounds, and you just have to look at those different compounds because some of them might be good for you.”

His study involved injecting cannabidiol into mice that had been bred to have similar symptoms as those seen in Alzheimer's, as well as examining what would happen to brain cells treated with the drug.

Dr Karl found that when the mice were given the cannabidiol they showed drastic improvement on parts of the tests that were related to recognising and remembering objects and other mice.

“It basically brings the performance of the animals back to the level of healthy animals,” he said. “You could say it cured them, but we will have to go back and look at their brains to be sure.”

The study was done as part of the PhD of student David Cheng, who has also collected the brains of the mice and intends to examine them to see if they showed physical improvements.

As part of the research, which is being presented at the Australian Neuroscience Society annual meeting in Melbourne this week, the team also treated animal brain cells that produced a protein linked to the development of plaques in the brain in humans with Alzheimer's disease, amyloid precursor protein.

The cell research, done at the University of Wollongong, found treating the cells with cannabidiol also reduced the amount of the harmful protein that they produced.

Dr Karl said there had been case reports in medical literature of marijuana smokers who had developed Alzheimer's disease, only to find their smoking seemed to relieve some of their symptoms.

“Most of the components [of marijuana] are detrimental, they worsen your cognitive performance and have psychoactive effects… cannabidiol seems to not have any of these negative effects,” he said.

Marijuana cannabinoids slow brain degradation and aging, reverse dementia: here's how
Thursday, May 23, 2013 by: Ethan A. Huff, staff writer

(NaturalNews) The human brain contains an extensive network of special receptor sites that modulate nervous system function only when activated by the appropriate cannabinoid compounds, many of which are found in abundance in the marijuana plant. And emerging research continues to uncover the unique role these cannabinoids play in protecting brain function, which in turn helps deter the aging process and even reverse the damaging effects of Alzheimer's disease and other forms of dementia and cognitive abnormality.

One of the latest discoveries concerning cannabinoids involves their ability to act as antioxidants in the brain. Researchers from Germany found that the brain's cannabinoid system is fully capable of not only cleansing damaged brain cells from the brain, but also triggering the production of new brain cells within the brain, a concept that contradicts years of conventional thinking about how the brain works. Cannabinoids also supercharge mitochondria in the brain, which are the powerhouses of energy that maintain proper cell function.

Published in the journal Philosophical Transactions of the Royal Society B, these discoveries shed new insight on how natural marijuana cannabinoids hold the capacity to literally quell the brain inflammation responsible for causing cognitive decline, neural failure, and brain degeneration. By supplying these receptor sites with cannabinoids, patients may be able to overcome brain conditions like Alzheimer's disease, Parkinson's disease, Huntington's disease, and many other conditions, not to mention premature brain aging, all conditions for which modern science has failed to find real solutions.

"I've been trying to find a drug that will reduce brain inflammation and restore cognitive function in rats for over 25 years; cannabinoids are the first and only class of drugs that have ever been effective," said Gary Wenk, a professor of neuroscience, immunology and medical genetics at Ohio State University (OSU) who helped with the research. "I think that the perception about this drug is changing and in the future people will be less fearful," he added, referencing the fact that marijuana is still viewed mostly negatively by many people.

Marijuana cannabinoids help restore the body's own natural cellular abilities
Ever since researchers first discovered the existence of cannabinoid receptor systems in rat brains back in 1988, independent scientists largely unconcerned with the stigma of marijuana have been gradually forming a piecemeal understanding of how the system works, and how cannabinoids can help prevent and reverse all sorts of chronic conditions that result from a lack of these important compounds. Today, marijuana research is moving forward more strongly than ever, and this taboo plant is finally receiving proper recognition as the medical "superfood" that it truly is.

"Cannabis actually goes upstream, it provides feedback from the postsynaptic nerve to the presynaptic nerve, which is unheard of in neural chemistry," explains Dr. William Courtney, founder of the Cannabis International Foundation (CIF), which is actively working to consolidate all available and relevant science on marijuana's medical uses for the purpose of promoting a reformation in health maintenance, restoration, and wellness around the world.

"The phytocannabinoids from this plant augment the body's attempt to restore an increased function to a normal level. So [marijuana cannabinoids] mimic the regulatory system of cellular physiology."

Cannabis use and cognitive decline in persons under 65 years of age

AMERICAN JOURNAL OF EPIDEMIOLOGY, Vol. 149, No.9 pages 794-800, 1999
Constantine G. Lyketsos, Elizabeth Garrett, Kung-Yee Liang, and James C. Anthony


The purpose of this study was to investigate possible adverse effects of cannabis use on cognitive decline after 12 years in persons under age 65 years. This was a follow-up study of a probability sample of the adult household residents of East Baltimore. The analyses included 1,318 participants in the Baltimore, Maryland, portion of the Epidemiologic Catchment Area study who completed the Mini-Mental State Examination (MMSE) during three study waves in 1981, 1982, and 1993-1996. Individual MMSE score differences between waves 2 and 3 were calculated for each study participant. After 12 years, study participants' scores declined a mean of 1.20 points on the MMSE (standard deviation 1.90), with 66% having scores that declined by at least one point.

Significant numbers of scores declined by three points or more (15% of participants in the 18--29 age group).

There were no significant differences in cognitive decline between heavy users, light users, and nonusers of cannabis.

There were also no male-female differences in cognitive decline in relation to cannabis use. The authors conclude that over long time periods, in persons under age 65 years, cognitive decline occurs in all age groups. This decline is closely associated with aging and educational level but does not appear to be associated with cannabis use.

Cognitive capacity has multiple determinants, including genetic makeup, nutritional status, health status, formal education, and age-related developmental processes. This capacity generally reaches its peak in early adulthood and then declines later in life (1). Cognitive decline is a significant public health problem, given its association with impaired functioning and increased mortality (1) and its close link to dementia (2-4). Dementia is defined as the occurrence of measurable, global cognitive decline sufficient to impair functioning (5). The prevalence and incidence of dementia, now one of the most common and serious diseases of the elderly, is rapidly increasing as the world population ages (6, 7).

Epidemiologic studies of dementia and of cognitive decline have typically investigated individuals over the age of 60 years. The expected prevalence of dementia in these age groups is 2 percent or higher (6, 7), and prevalence might be as high as 48 percent in those over age 85 (6, 7). In late life, dementing processes hamper the study of cognitive decline as a phenomenon distinct from dementia. Additionally, recent research suggests (8) and scientific consensus concurs (9) that dementia is best understood as the result of cumulative effects on the brain from diseases (e.g.. Alzheimer's disease or cerebrovascular disease) and other exposures (e.g. alcohol or tobacco use), all occurring against background, possibly lifelong, declines in cognition associated with aging itself. However, epidemiologic knowledge regarding cognitive decline in persons younger than age 65 is very limited. Indeed, we could find only one published epidemiologic study of cognitive decline in younger persons: the Seattle Longitudinal Study (10).

The Seattle Longitudinal Study followed a series of community-based cohorts of individuals enrolled in a health maintenance organization. Sample sizes for individual cohorts were between 500 and 997. Participants were assessed according to a large number tests of intelligence and cognitive capacity. The main findings were that individual cognitive abilities did not change much before age 60, with the exception of verbal fluency. Because of attrition, the Seattle Longitudinal Study did not have sufficient sample sizes to detect small cognitive declines in younger age groups. Furthermore, very few individual participants were followed for spans of more than 5 years.

The major correlate of cognitive decline is increasing age (10-14). Higher educational level (14) and higher functioning (13) are associated with less cognitive decline. Being female or encountering stressful life events is not associated with cognitive decline (II,13). Risk factors for dementia include age, prior cognitive impairment, stroke, high blood pressure, heart disease, diabetes mellitus, alcohol consumption, and depression (15-28). The use of nicotine via smoking has also been associated with a lower risk for dementia, although this finding is controversial (29). Being female has not been associated with the incidence of dementia (15, 17). Two recent studies (30, 31) have reported that lesser educational attainment is a risk factor for dementia. However, this finding has not been supported universally (17, 32, 33).

The relation between cognitive functioning or cognitive decline and use of cannabis (marijuana) has received limited attention in epidemiologic studies. Two cognitive effects of cannabis must be distinguished: acute effects, those associated with intoxication, and residual effects, which persist after the drug has left the central nervous system (34). The latter effects might be short term or long term. Cross-sectional studies, either experimentally administering cannabis or comparing users with nonusers, support the existence of short term residual effects of cannabis use on attention, ability to perform psychomotor tasks, and short term memory (34, 35). These effects are more severe in women (36) and in heavy users of cannabis as compared with light users (37).

To our knowledge, no study with published results has investigated the long term effects of cannabis use on cognition in an epidemiologic sample. According to Pope et al. (34), study designs best suited to addressing this issue are naturalistic comparisons, in large epidemiologic samples, of heavy users, light users, and nonusers of cannabis. These studies must also account for the concurrent use of alcohol and other drugs, both illicit and legal (e.g., nicotine). In Addition such studies must adjust for other factors known to influence cognition over time, such as age and education, and must investigate possible interactions between the cognitive effects of cannabis use and gender (being female).

We recently reported findings from a 13-year follow-up of 1,488 persons of all ages who had participated in the Baltimore, Maryland, portion of the Epidemiologic Catchment Area study (38). The Mini-Mental State Examination (MMSE) (39), a widely used quantitative measure of cognition, was administered to participants during wave 1 (1981) and during two follow-up waves in 1982 and 1993-1996. The design of the study allowed us to examine cognitive decline between waves 2 and 3 in a large epidemiologic sample. We found that cognitive decline occurred in all age groups. Age, education, and minority status were all significantly associated with greater cognitive decline.

In this follow-up paper, we focus our investigation on persons under age 65 years. To our knowledge, this is the first population study that has investigated cognitive decline in this age group, in which the prevalence of dementia is very low. This permits better study of cognitive decline as a phenomenon distinct from dementia, as well as its associated risk factors. We had two goals: 1) to further delineate the epidemiology of age-specific cognitive decline in persons under 65 and 2) to investigate any long term association between cognitive decline and use of cannabis using a design similar to the one proposed by Pope et al. (34).


Baltimore Epidemiologic Catchment Area follow-up

The Epidemiologic Catchment Area program has been described in detail elsewhere (40, 41). The Baltimore arm of this five-site study first entered the field in 1981, when the first wave of in-person assessments was completed. A second wave of assessment (including wave 2 administration of the MMSE) was conducted 1 year later, in 1982. The Baltimore Epidemiologic Catchment Area target population consisted of the adult household residents of eastern Baltimore City, an area with 175,211 inhabitants. During wave 1, 4,238 individuals were designated for interview by probability sampling methods, and 3,481 (82 percent) completed interviews. Of these persons, 2,695 completed interviews during wave 2.

In 1993, all 3,481 initial participants were targeted for tracing and interviewing. A total of 848 participants were found to have died; the remaining 2,633 were presumed to be alive, but 415 of them could not be successfully traced. Of the 2,218 persons located, 298 refused to participate, and 1,92O completed interviews. Of these, 1,488 had completed the MMSE during all three waves, approximately 11.5 years after wave 2. All study participants signed informed consent statements approved by the Institutional Review Board of the Johns Hopkins University School of Hygiene and Public Health.


In these analyses, we included only those participants who were under age 65 at wave 1 and who completed the MMSE during all three study waves (n = 1,318).

Measurement of cognitive decline.

For each participant, an MMSE score difference was calculated by subtracting the wave 3 (1993-1996) MMSE score from the wave 2 (1982) MMSE score, The mean time interval between the points at which these MMSEs were administered was 11.6 years (standard error 0.01 years). The median interval was 11.5 years, the 25th percentile was 11.3 years, and the 75th percentile was 11.9 years. Change in MMSE score between waves 2 and 3 Has the primary dependent variable in the analyses.

Classification of participants according to use of cannabis. Participants were separated into five groups based on their self-reported drug use during all three waves of the study. Group 1 ( nonusers) were those who reported in all three waves that they had never used cannabis in any form (n = 806 (61 percent)). Group 2 (light users) were participants who had used cannabis but had never used it daily or more often for over 2 weeks (n = 235 (18 percent)). Group 3 were light users who reported use of any other illicit substance in any study wave (n = 131 (10 percent)). Group 4 (heavy-users) reported during at least one study wave that they had used cannabis daily or more often for over 2 weeks (n = 137 (10 percent)). Group 5 were heavy users of cannabis who reported use of other illicit drugs as well (n = 8 (1 percent)). Information on cannabis use was missing for one participant.

Classification of participants according to use of alcohol or tobacco.

On the basis of the highest alcohol intake reported for the past month during any of the three study waves, participants were placed into three groups: never drinkers (n = 67 (5 percent), light-to- moderate drinkers (n = 778 (59 percent)), and heavy drinkers, defined as those who had had more than four drinks on any one day during the past month (n = 473 (36 percent)). With respect to smoking, three groups were defined on the basis of self-report during any of the three waves: never smokers (n = 347 (26 percent)): occasional smokers (n = 573 (44 percent)); heavy smokers, defined as those who smoked 20-39 cigarettes per day (or the equivalent in cigars or pipefuls of tobacco (n = 310 (24 percent)) and very heavy smokers, those who smoked two or more packs of cigarettes per day (or the equivalent (n = 85 (6 percent)). Information on smoking was missing for three participants.

Other variables associated with cognitive decline used as covariates.

Information on other variables associated with cognitive decline was recorded at wave 1. Gender was indicated as male or female. Age was grouped as follows: 18-30, 31-40, 41-50, 51-60, and 61-64 years. Minority status was indicated as African-American or Hispanic versus other ethnicity (non-Hispanic white). Five educational subgroups were developed: 0-8 years, 9-11 years, 12 years or General Equivalency Diploma, 13-15 years, and 16 or more years, in conformance with common educational landmarks (grade school, some high school, completed high school or the equivalent, some college, and completed college). It is possible that some study participants, especially those in younger age groups at wave 1, completed their education after wave 1 and were thus misclassified.


Mean MMSE score changes between waves 2 and 3 (with 95 percent confidence intervals) are reported in the tables for the entire cohort and for subgroups by age. The proportions of individuals who evidenced any increase, no change, a one-point decline, a two-point decline, a three-point decline, or a four-point or greater decline are also reported by age group. Mean change in MMSE score (with its 95 percent confidence interval) by level of cannabis use was estimated for men and women separately. The relation between level of cannabis use and MMSE score change between waves 2 and 3 was examined in a series of linear regression models with MMSE score change as the dependent variable and cannabis use as the independent variable, with or without inclusion of the other covariates. For both univariate and multiple regression models, the association of cannabis use with change in MMSE score is reported in the form of regression coefficients (with 95 percent confidence intervals). Subgroups were entered into regression models individually as "dummy" variables to allow direct comparisons of remission coefficients using one of the subgroups as the reference category.

To validate the findings from the linear regression models, we also constructed a series of proportional odds logit models (42) relating diseases or substance use to MMSE score change. These were bivariate or multivariate “analogs” to the linear models. The dependent variable was “change in MMSE score,” grouped as follows: any increase, no change, a one-point decline, a two-point decline, a three-point decline, or a four-point or greater decline. Findings from these models were similar to those obtained from the linear models. For simplicity, we report only findings from the linear models.


Table 1 provides a description of the study cohort at wave 1 with regard to sociodemographic variables. It also shows mean MMSE scores at each study wave.

TABLE 1. Sociodemographic characteristics at the Baltimore Epidemiologic Catchment Area study cohort at wave 1 (n = 1,318) and mean MMSE scores at waves 1-3
Variable    Number    %
Age (years)        
18-30    545    41
31-40    319    24
41-50    179    14
51-60    185    14
61-64    90    7
Male    488    37
Female    830    63
Minority (African-American or Hispanic)    490    37
Nonminority (other)    828    63
Education (years)        
0-8    161    12
9-11    280    21
12/GED    541    41
13-15    211    16
16 or more    125    10
Mean MMSE score        
Wave 1(1981)    28.65 (1.9 standard deviation)   
Wave 2 (1982)    28.65 (1.81 standard deviation)   
Wave 3(1993-1996)    27.46 (2.23 standard deviation)   

Cognitive decline between waves 2 and 3

Table 2 shows the mean change in MMSE score between waves 2 and 3 for every age group. It also shows the proportions of participants in each age group with specific changes in MMSE score, as described above. Persons in all age groups had mean declines greater than zero, with two thirds declining in score by at least one point. The mean decline and the proportion of persons with declining scores increased steadily with age, as expected. It is noteworthy that in every age group there was a notable proportion of participants whose score declined three points or more-- a change of a magnitude that merits clinical attention (43, 44). These estimated declines must be considered in the context of MMSE measurement error, the MMSE ceiling effect, and normal variation in MMSE scores over time (see Discussion).

TABLE 2. Mean change in Mini-Mental State Examination (MMSE) score from wave 2 (1982) to wave 3 (1993-1996) and proportions of participants evidencing specific MMSE score changes, by age group, Baltimore Epidemiologic Catchment Aiea study follow-up
Age group (years)   
Change in MMSE score
     Mean change    95% confidence interval
18-30 (n=545)    -0.98    -0.83 to -1.13
31-40 (n=319)    -1.08    -0.89 to -1.27
41-50 (n=179)    -1.25    -0.92 to -1.58
51-60 (n=185)    -1.52    -1.20 to -1.84
61-64 (n=90)    -2.12    -1.52 to -2.72
All ages (n=1318)    -1.20    -1.10 to -1.30

(EDITORIAL NOTE: Only the first part of TABLE 2 is included to save space.)

Association between cannabis use and score decline

Table 3 displays estimated mean changes in MMSE score according to level of cannabis use for men and women separately. Women who were nonusers of cannabis had scores that declined more than those of men who were nonusers. However, within male-female groups, there were no evident differences in score decline by cannabis use for either men or women.

TABLE 3. Mean change in Mini-Mental State Examination (MMSE) score between wave 2 (1982) end wave 3 (1993-1996) in men and women, by level of cannabis use, Baltimore Epidemiologic Catchment Area study follow-up
Gender and level of cannabis use    Number    Mean score change in MMSE    95% confidence interval
Nonusers    251    -1.00    -0.73 to -1.27
Light users    104    -1.03    -0.67 to -1.39
Light users & use of drugs    47    -1.06    -0.57 to -1.55
Heavy users    82    -0.84    -0.46 to -1.22
Heavy users & use of drugs    3    -0.33    +5.93 to -6.59
Nonusers    555    -1.46    -1.29 to -1.63
Light users    131    -1.04    -0.71 to -1.37
Light users & use of drugs    83    -1.07    -0.77 to -1.37
Heavy users    55    -1.15    -0.47 to -1.83
Heavy users & use of drugs    8    -0.60    +3.09 to -4.29

Table 4 displays results from the linear regression models with MMSE change between waves 2 and 3 used as the dependent variable. The numbers shown in the table are regression coefficients estimating the relative change in MMSE score for a given group of cannabis users relative to nonusers. Model 1 included only cannabis use as the covariate. Model 2 included cannabis use and use of alcohol and tobacco. Model 3 included cannabis use plus age, gender, education, minority status, alcohol use, and tobacco use. Model 4 included cannabis use plus all of the variables from models 2 and 3. Both light and heavy users of cannabis evidenced less cognitive decline than nonusers, although this finding was not statistically significant at the conventional level of p < 0.05 (model 1). After adjustment for the other variables in models 2-4, there was no association between cannabis use and cognitive decline.

TABLE 4. Regression coefficients indicating relative differences in Mini-Mental State Examination (MMSE) score change between wave 2 (1982) and wave 3 (1993-1996), by level of cannabis use, in four regression models, Baltimore Epidemiologic Catchment Area study follow-up
Level of cannabis use   
Model 1 (cannabis use)
     Regression coefficient    Standard error
Light users    0.28*    0.15
Light users & use of drugs    0.25    0.19
Heavy users    0.35*    0.18
Heavy users & use of drugs    0.81    0.71

* p < 0.10

(EDITORIAL NOTE: Models 2, 3 and 4 were not included in this table, see note at end of this article)


Cognitive decline is an age-related phenomenon that affects persons of all ages, including those under age 30 years. It becomes more pronounced with increasing age and is most evident in persons over age 59. A significant proportion (>15 percent) of persons in all population age groups evidence declines that approach clinical significance. We offer two interpretations of this finding. One is that cognitive decline might be an inevitable phenomenon of aging, perhaps modified by genetic makeup, education, nutrition, disease, and environmental exposure. Another is that the declines are the result of slowly progressive neurodegenerative diseases (such as Alzheimer's disease) which might be lifelong in evolution but do not lead to clinical symptoms until much later in life (8). While these two lines of reasoning are not mutually exclusive, the relation between age and cognitive decline across all age groups reported here lends greater support to the former.

To our knowledge, this was the first long term prospective study in the United States that had a community sample large enough to investigate the relationship between cannabis use and cognitive decline in persons under age 65 years. Other studies have found short term residual effects of cannabis use on memory and cognition (34, 35) that are more severe among women (36) and heavy users (37). However, our data suggest that over the long term cannabis use is not associated with greater declines in cognition among men, women, or heavy users. The study design we used included several of the features proposed by Pope et al. (34) as critical to addressing the long term effects of cannabis on cognition: naturalistic follow-up, a large sample size, a population basis, comparison of light cannabis use with heavy use, and the construction of models accounting for the effects of gender and use of illicit drugs, alcohol, and tobacco. Therefore, these results would seem to provide strong evidence of the absence of a long term residual effect of cannabis use on cognition.

Notable limitations of this study include loss to follow-up and mortality. Cognitive functioning at base-line was a predictor of both mortality and loss to follow-up in the Epidemiologic Catchment Area study (40). Additionally, it is possible that some cannabis users in the study may have used cannabis on the day the MMSE was administered. Given the acute effects on cannabis on cognition (34), this would have tended to reduce their MMSE score on that day. This may have adversely affected accurate measurement of MMSE score changes over time.

Given that a lower level of cognitive functioning was associated with greater cognitive decline, these estimates of decline may be underestimates. The assessment of cannabis use was based on self-reports and was not confirmed with biologic measures or controlled in an experimental setting. This may have led to underestimation of cannabis use in persons with poor memory.

Another important limitation of the study is that the MMSE is not a very sensitive measure of cognitive decline, even though it specifically tests memory and attention. Thus, small or subtle effects of cannabis use on cognition or psychomotor speed may have been missed. The MMSE is not intended for the purpose for which it was used in this study, and it contains some items that assess neurologic function as well as cognition. Additionally, MMSE item analysis was not performed in this study. Given the MMSE's ease of use and widespread application, it was the most practical instrument available for brief assessment of cognitive functioning at the time the multisite Epidemiologic Catchment Area study was planned in the late 1970s. Also, given its limited sensitivity, declines noted on the MMSE are probably under estimates of true declines.

Other limitations of the MMSE include the fact that small errors. such as forgetting the present day's date, may be due to measurement error and not to true decline. Measurement error on the MMSE might be caused by a variety of factors, including the ambient environment in which the test is taken, the respondent’s mood or emotional state, the respondent’s adequacy of sleep the night before, the time of day at which the test is given, and other factors. However, such errors ought to be random and not systematic (equally distributed between study waves), so the effect on mean estimates should "average out across the population and across waves of assessment.

MMSE scores in this study exhibited a ceiling effect, given that most participants scored in the 27-30 range during wave 1. However, the ceiling effect was limited to a minority of participants, those who scored 30 points at baseline, since most declines were small.

Finally, the small but tangible beneficial "practice effect" of repeated testing on MMSE score would tend to lead to higher, not lower, MMSE scores at follow-up.

We conclude that cognitive decline occurs across all age groups. with a significant proportion of persons of all ages showing declines near clinically significant levels after 12 years. Such decline is not associated with cannabis use in either men or women. A better understanding of predictors of cognitive decline in persons under age 65 years might lead to interventions designed to slow or arrest such decline. This in turn might reduce the incidence of dementia at older ages.


This study was supported by grant 1R01-MH47447 from the National Institute of Mental Health for Baltimore Epidemiologic Catchment Area study follow-up.


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Copyright: 1999 Johns Hopkins University School of Hygiene and Public Health

EDITORIAL NOTE: Models 2, 3 and 4 were not included in Table 4, partly because there is no specific discussion of how these models were mathematically created. They begin to compensate for other variables, however, it is not fair to lower the existing differences between cannabis users and nonusers - by compensating for alcohol and tobacco use. Since these variables accelerate cognitive decline, particularly alcohol according to this article and many other sources, one questions whether they should be used to diminish this important finding of lower cognitive decline among marijuana smokers as compared to nonusers. Many people would argue that the use of cannabis helps cut down on the use of these two legal drugs, and this is part of its beneficial effect - rather than something that must be subtracted away from it.

Also, the p < 0.10 probability for “Light users” and “Heavy users” means that there is a greater than a ten to one chance that this observed difference is real or an actual difference. This is less than the p < 0.05 probability often used in research, which is greater than a twenty to one chance that this observed difference actually reflects a similar real difference in the population and thus, is “statistically significant”.

Since this is the first major study to be published in this area of marijuana research, more studies are needed to see if this observed trend of lowered cognitive decline continues in marijuana smoking populations in the future. At least the authors report that there is absolutely no evidence that marijuana causes a long-term decline in mental functioning - as the false assertions that marijuana did indeed cause brain damage were popular in legislative circles in the 1980’s and were used to increase marijuana penalties

Wednesday, April 23, 2014

Allergies, Antihistamines, bvFTD ...and a kitchen project.

Here it is nearly the end of April, and I have not posted anything since February. Here is a link to my February update. There are a few good reasons, or maybe a few good excuses for not posting anything. I have been a little busy, and I have not had anything to say. I have had some good days, and some bad days as usual. I had a string of bad days all in a row which was (...)(I wrote something here which disappeared when I tried to put in a picture. Gotta love Blogger! I have no idea what I wrote, but those days were totally lost to me. Pretty sucky!)

April seems to be a difficult month for me. I have suspected that my allergies play a large part in the impact of my symptoms on everyday living, and this year just adds more support to my theory. There is plenty of research available regarding the histamine pathway, allergies, allergy medications, and memory. There isn't anything directly looking at bvFTD or other forms of dementia and antihistamines. I should probably say bvFTD (Behavioral Frontotemporal Dementia, and Frontotemporal Degeneration) just so Google knows I am still here!).

My anecdotal account is that the allergy symptoms themselves make my symptoms worse. It happens every year when the tree pollen levels climb in the Spring. I notice my short-term and working memory take an especially hard hit when my allergies are bad. I also notice a huge lack of energy and motivation when I take antihistamines. I currently take a generic for Zyrtec. My former neurologist thought that my allergies acted as a general stressor making my symptoms worse. The Zyrtec is probably interacting with my other medications, but I am not planning to t4est it by discontinuing my other meds while I take the Zyrtec. I will just get through the allergy season as best I can.

The end result is that I have a few more bad days than usual, and sometimes when I take the antihistamines I just want to stay in bed or lay around watching TV all day. I would prefer to be outside enjoying the Spring weather, but somehow on those days it is way too much of a struggle to make it out the door. Then the next day everything is fine again. It is very inconsistent. The symptoms seem to mirror depression, but I am not in the least bit depressed. I can see why doctors often misdiagnose bvFTD as depression.

Well, I have not just been sitting around on my butt this whole time watching TV. I have had a couple projects. Together, Cindy and I redecorated the kitchen. It took a couple weeks working mostly on the weekends. All we really did was paint, and move some furnishings and knick-knacks, but I am still very proud of the accomplishment. I was able to stick to it, and complete a fairly large project.

The only real time when I noticed my bvFTD was when I was doing some electrical wiring. I added a receptacle to the back kitchen, and a light over the sink. That is huge! This house is 115 years old, and it has never had a light over the kitchen sink, or any receptacles in the kitchen except a couple on the counter. Having a plug in the back kitchen is really nice.

So, I turned off the breaker that controlled the circuit I wanted to add the light to. I drilled, and ran the wires, and put up the light without any unexpected difficulty. Then it was time to add the receptacle. I cut the hole in the wall, and wired in the box. I decided to add it to an existing circuit in the basement which was conveniently located, and did not have much load on it. I turned off the breaker, and proceeded to cut the wire.

That is when things got interesting. I shot sparks halfway across the basement. OOPS! Wrong breaker! It was labelled incorrectly in the breaker-box. I quickly tested, and found the correct breaker, and turned it off. No real problem. I completed the wiring.

I turned on the juice, and the receptacle was not working. I changed the light I was using to test it. Nothing. I pulled the box out, and changed it for another. Still nothing! I figured there must be a break in the wire, so I totally re-did everything. Still nothing. I re-wired the box where I was tying into the existing circuit 4 times. Still nothing! I was really frustrated.

Then I noticed something. My bvFTD had struck again. Remember I had flipped the incorrect breaker at first because it was mis-labeled? Well - every time I tested my new addition I turned that same damn breaker back on. Never once did I remember that I was now working on the breaker right next to it. Yup! I did everything right the first time. I just turned on the wrong switch so of course it didn't work. That is how sneaky this disease is. I can still wire a building, but I can't remember 10 seconds ago exactly which breaker I switched off.

Yeah. I know it was no big deal, but it was frustrating, and a very good example of how bvFTD enters into everyday projects. Oh! There were lots of little things doing the painting and decorating. I sometimes didn't do things in the correct sequence, but nothing major. Painting is a pretty forgiving project.

I must give credit to Cindy. She painted the downstairs bathroom all by herself, and did a great job. It used to be a warm off-white, and now it is light green. As long as it is not blue I like it just fine. Of course my bvFTD intruded by making it nearly impossible for me to help choose a color scheme. I just couldn't decide on anything, so I finally just told her to do whatever she wanted - and I tell you that was scary! It worked out well.

I finally got the results of my EEG. Some overall changes noted by a diminished amplitude. There was too much noise activity from my medications to tell much of anything else. I find it refreshing to see that an EEG shown that the medications I am taking have my brain working overtime. It needs it!

In order to get the results of my EEG I saw my General Practitioner. My Neurologist, or more accurately "my former neurologist" never returned my calls. I am moving on. He didn't listen anyway, and seemed pretty clueless about bvFTD. I have a good recommendation for another neurology specialist, but I am in no hurry to go unless something changes.

Actually I saw my regular doctor as part of an annual physical,  and asked about my EEG while I was there. Except for my triglycerides being elevated (as usual), and having bvFTD, I am fairly healthy.

Somewhere during the past couple months we managed to host a Murder Mystery Party - OK - actually Cindy did all of the work, but I was there - and in spite of bvFTD I think I did as well as anyone else. Everyone, including me, had a great evening.  Also mixed in there were some visits with friends, and a Birthday celebration. Easter was a nice family dinner at Cindy's brother's house. I managed to make it through the day, but was ready to leave when it was time to go. The Saturday before Easter was what I would consider a rough day. Mostly I napped. I don't remember if I did anything else. That is indicative of the way things have been this Spring.

I am still taking Aricept, Namenda, and Ritalin. When I do not take them even for a couple days I notice a huge worsening of my symptoms. Everyone else notices it also, so at least for now I am going to continue taking them. in spite of the occasional side-effects. Right now due to tight finances I am not taking any additional supplements except occasionally some pomegranate juice.

Cindy, Gracie, and I are doing well. Of course I have days when everything is a challenge, but between Cindy and Gracie my rough days are not as difficult as they used to be. Well - at least for me!

Some days are better than others, but most days are good.unpleasant, but I managed to get through it.

 Following are a few pictures. I tried to put them into the post, but this blogger program is totally screwing up the placement, moving everything around, and randomly deleting text where I put a picture - and then it still moves it to the beginning or the end. As a former programmer all I can say is ...OK - I won't say that!. ...so- I am just gonna stick them here at the end and let you sort them out.


Front kitchen before

Back kitchen after.

For the first time in 115 years this room has a light and plug

Gracie likes Spring!

Crocuses mean allergy season has arrived