Suffolk County Police have issued a Silver Alert on Feb. 26 for a missing Patchogue man with dementia.
William Stewart, 72, left his residence, located at 286 North Ocean Ave., on February 23 at approximately 7 p.m. and was seen getting into a taxi. He was reported missing on February 26.
Stewart is white, approximately 6 feet one inch tall and weighs 230 pounds. He has white hair and blue eyes.
Detectives are asking anyone with Stewart’s location to call the Fifth Squad at 631-854-8552 or 911.
Silver Alert is a program implemented in Suffolk County that allows local law enforcement to share information with media outlets about individuals with special needs who have been reported missing.
This rendered image of the brain via a technique called diffusion tractography reveals parts of the brain’s white matter in a compilation of WTC responders experiencing cognitive impairment (CT). These areas depicted by various colors illustrate where the brain is more vulnerable to neurodegenerative processes. The different colors represent differences in the heath of various parts of the brain including the limbic system. Credit: Chuan Huang
Stony Brook-led imaging study sheds light on PTSD-associated mental decline
A study that assessed the brains of 99 World Trade Center (WTC) responders by using diffusion tractography, a 3-D imaging technique, showed that WTC responders with cognitive impairment (CI), a possible sign of dementia, and post-traumatic stress disorder (PTSD), have a different presentation of the white matter in their brains compared to responders with CI without PTSD. Led by researchers at Stony Brook University affiliated with the Stony Brook WTC Health and Wellness Program, the study suggests a specific form of dementia could be affecting WTC responders who also have PTSD. The findings are published early online in the Journal of Alzheimer’s Disease.
According to the authors, this is the first study to examine white matter alterations using connectometry in a sample of WTC responders in mid-life (average age: 56) with and without concurrent PTSD. The goal of the study was to examine and elucidate the extent to which white matter tract integrity might be impaired in WTC responders with CI and/or PTSD. Previously, the researchers had identified changes in white matter diffusivity in small numbers of responder patients.
“Our findings are by no means conclusive in terms of defining CI or dementia in WTC responders, and if this study provides evidence of a new form of dementia emerging,” says Sean Clouston, PhD, lead author and Associate Professor in the Program in Public Health, and in the Department of Family, Population, and Preventive Medicine at Stony Brook University.
“Overall, the study supports the view that responders with CI have neurological changes consistent with neurodegenerative disease, but they are inconclusive as to the type of disease,” he adds. “Our findings do show that dementia due to PTSD is clearly different from non-PTSD dementia in this responder population.”
Subjects in the study were matched by age, gender, occupation, race and education. Cognitive status was determined by using the Montreal Cognitive Assessment, and PTSD status was determined by using the Diagnostics and Statistics Manual-IV. The researchers used diffusion tensor imaging via a mMR scanner, and they used connectometry to examine whole-brain tract level differences in white matter integrity as reflected by fractional anistrophy (FA) values.
In summary, the team found that FA was negatively correlated with CI and PTSD status in the fornix, cingulum, forceps minor of the corpus callosum, and the right uncinate fasciculus. Additionally, FA was negatively correlated with PTSD status, regardless of the CI status in the superior thalamic radiation and the cerebellum.
The authors conclude that the brain imaging results “suggest that WTC responders with early-onset CI may be experiencing an early neurodegenerative process characterized by decreased FA in white matter tracts.”
The technique and other findings
Clouston and colleagues used the imaging technique diffusion tractography to examine how healthy axons are in the brain’s white matter. The technique helped to determine that responders with CI had signatures in their white matter that did not match patterns seen in old-age Alzheimer’s disease and other related dementias.
By using the imaging technique, they also compared responders with PTSD and dementia to those with dementia but without PTSD. The imaging revealed a lot of similarities between the groups but also showed a remarkable difference in the white matter of those with PTSD and dementia – showing evidence of cerebellar atrophy, a finding that is inconsistent with other studies of dementia.
The research for the study was supported in part by the National Institutes of Health’s National Institute on Aging (grant # R01AG049953), and the Centers for Disease Control and Prevention (grant # U010H011314) and the National Institute for Occupational Safety and Health, NIOSH, (grant # 200-2011-39361).
The Alzheimer’s Foundation of America (AFA) has awarded the Long Island Museum a $6,000 grant to support the Museum’s “In the Moment” program, a free program designed to creatively engage those living with dementia-related illnesses and their care partners.
Created in 2011, this innovative program takes individuals living with dementia and their care partners on guided tours of the museum’s collection of art, historical objects, and seasonal exhibits. Additionally, the program offers hands-on art workshops which afford opportunities for creative expression, with all needed materials provided for free.
All programs are led by museum educators and designed to be cognitively stimulating. Programming is currently offered virtually through Zoom and as a hybrid, in-person/virtual option. Since its inception, the program served more than 3,200 individuals, according to the Museum.
“This AFA grant has allowed us to purchase a 75” Vibe Smartboard Pro to use as we return to in-person programming,” said Lisa Unander, Director of Education at the Long Island Museum. “We are building upon the lessons we learned through remote engagement and bringing the most successful aspects of these virtual programs to enhance our gallery sessions. Specifically, we have seen how powerful short video clips are as a way to engage and bring themes to life. With this grant, we won’t have to lose techniques we now heavily rely on, but instead will be able to incorporate these tools to create even more memorable multi-sensory moments together.
“Art can be a powerful tool to enhance quality of life for individuals living with a dementia-related illness and their caregivers. It stimulates the mind and creates opportunities for self-expression and socialization,” said Charles J. Fuschillo, Jr., AFA’s president and chief executive officer.“We are proud to support the Long Island Museum in delivering this impactful program to Long Islanders affected by Alzheimer’s disease and other dementias.”
From left, Robyn Nevin, Emily Mortimer and Bella Heathcote. Photo courtesy IFC Midnight
Reviewed by Jeffrey Sanzel
First-time director Natalie Erika James takes a new spin on the possessed residence genre with the atmospheric psychological horror film, Relic. James has co-written the heady screenplay with Christian White, and the result is ninety minutes of introspective dread that are grounded more in family than in fright. Relic had a buzzy debut at Sundance last year; it is equally arthouse and haunted house.
Three generations of women confront the dark but unexplained spirits possessing their family. When the elderly Edna (Robyn Nevin) disappears for three days and then suddenly reappears without explanation, daughter Kay (Emily Mortimer) and granddaughter Sam (Bella Heathcote) respond differently to the older woman’s erratic behavior.
The core of Relic is the portrait of a dysfunctional family staring down its matriarch’s slip into dementia. What is revealed is that years before, Edna’s grandfather suffered a fate similar to Edna’s.He died alone in a cabin on the property — the first structure put up on the land.(Kay has visions of both the old man and the cabin.) And while it no longer exists, pieces of it had been incorporated into the existing house, most notably the stained glass window now found in the front door.
It is as if the evil that destroyed the man followed it into the house, biding its time to possess its owner, in this case, Edna. But is it evil or illness? The answer is both.
While there are many traditional images, they feel fresh in James’s hands. In the opening moments, the house “breathes.” While an overflowing bathtub is a well-known trope, there is something about the water’s flow down the stairs that sets the tone for what will be the film’s creeping malevolence.
Initially, the house itself looks benign and suburban, if a bit cluttered. Yes, it is large and well-appointed, but this is not a caricature of the old dark house, and this is a very different kind of haunting. The black mold appears to be an insidious manifestation of the dementia, and it is consuming the family homestead.
At first, Edna seems to have a bruise on her chest. In actuality, the same mold is overrunning house and body. The possession is a slow poison that hovers around the edges before taking over; the metaphor is clear. Scattered around the house are Edna’s notes to herself — ranging from the simple “Flush” to the alarming “Don’t let it in.”
The layers and twists are neatly woven, alternating between the ever weakening bond between Edna and Kay and the malign forces that are present. The fact that they are joined makes the film unique as it is impossible to disconnect one from the other.The evil dwelling in the house is just as real as what has clearly been a disintegration of Edna’s mind.
This is a film that allows the narrative to slowly unravel. The scenes are short with staccato dialogue but the tempo remains at a slow burn for a majority of the time. It does not rely on gore or even visual scares.Instead, it allows us to peer into the shadows, unsure of what they — or we— are seeing.
It helps that all three actors — Mortimer, Nevin, and Heathcote — give understated and grounded performances. Nevin’s descent into confusion is marked by flashes of anger and disturbing behavior. There is a moment where she wanders away from the house and attempts to eat photographs before trying to bury the album itself. Wide-eyed, she looks at her daughter and cries, “Where is everyone?” It is a moment that is both horrifying and heart-breaking.
Mortimer’s struggle with ambivalence and obligation are palpable. Her love is mixed with resentment. She shows equal amounts of frustration and hurt in witnessing her mother’s desolation. Heathcote strikes the right balance in trying to be a loyal daughter and an attentive granddaughter. She also makes the climax (an extended sequence lost in the house’s impossible labyrinth) a showpiece in discovery. Both the spoken and unspoken pain and disappointment of this trio build the narrative.
Cinematographer Charlie Sarroff has effectively desaturated the color to the point of almost being absent. Robert Mackenzie’s eerie sound design — with ambient noise tamped down or oddly amplified — greatly enhances the off-kilter world. The distorted sounds of an empty washing machine and the gunshot bang of a bolt into a lock are jarring in just the right (wrong?) way.
For those looking for something different in the genre, Relic is an evasive but mysterious tale, cleverly flying in the face of traditional horror movie expectations. It masterfully blends many of the everyday fears for our loved ones with darker forces. Give it the time and it will stay with you long after its bizarre final moments.
Eat the colors of the rainbow to reduce the risk of dementia. Stock photo
Intensive lifestyle changes may grow protective telomeres
By David Dunaief, M.D.
Dr. David Dunaief
Dementia may be diagnosed when someone experiences loss of memory plus loss of another faculty, such as executive functioning (decision-making) or language abilities (speaking, writing or reading). The latter is known as aphasia. Alzheimer’s disease is responsible for approximately 60 to 80 percent of dementia cases (1).
Unfortunately, there are no definitive studies that show reversal or a cure for Alzheimer’s disease. This is why prevention is central to Alzheimer’s — and dementia in general.
In terms of dementia, there is good news and some disappointing news.
We will start with the good news. Though chronological age is a risk factor that cannot be changed, biological age may be adjustable. There are studies that suggest we may be able to prevent dementia through the use of both lifestyle modifications and medications.
Telomeres’ length and biological age
Biological age may be different from chronologic age, depending on a host of environmental factors that include diet, exercise and smoking. There are substances called telomeres that are found at the ends of our chromosomes. They provide stability to this genetic material. As our telomeres get shorter and shorter, our cellular aging and, ultimately, biological aging, increases.
In a preliminary case control study, dementia patients were shown to have significantly shorter telomere length than healthy patients (2). Interestingly, according to the authors, men have shorter telomere length and may be biologically older by four years than women of the same chronological age. The researchers caution that this is a preliminary finding and may not have clinical implications.
What I find most intriguing is that intensive lifestyle modifications increased telomere length in a small three-month study with patients who had low-risk prostate cancer (3). By adjusting their lifestyles, study participants were potentially able to decrease their biological ages.
Diet’s effect
Lifestyle modifications play a role in many chronic diseases and disorders. Dementia is no exception. In a prospective observational study, involving 3,790 participants, those who had the greatest compliance with a Mediterranean-type diet demonstrated a significant reduction in the risk of Alzheimer’s disease, compared to the least compliant (4). Participants were over the age of 65, demographics included substantial numbers of both black and white participants, and there was a mean follow-up of 7.6 years. Impressively, those who adhered more strictly to the diet performed cognitively as if they were three years younger, according to the authors.
Beta-carotene and vitamin C effect
In a small, preliminary case-control study (disease vs. healthy patients), higher blood levels of vitamin C and beta-carotene significantly reduced the risk of dementia, by 71 percent and 87 percent, respectively (5). The blood levels were dramatically different in those with the highest and lowest blood levels of vitamin C (74.4 vs. 28.9 µmol/L) and beta-carotene (0.8 vs. 0.2 µmol/L).
The reason for this effect may be that these nutrients help reduce oxidative stress and thus have neuroprotective effects, preventing the breakdown of neurons. This study was done in the elderly, average 78.9 years old, which is a plus, since as we age we’re more likely to be afflicted by dementia.
It is critically important to delineate the sources of vitamin C and beta-carotene in this study. These numbers came from food, not supplements. Why is this important? First, beta-carotene is part of a family of nutrients called carotenoids. There are at least 600 carotenoids in food, all of which may have benefits that are not achieved when taking beta-carotene supplements. Second, beta-carotene in supplement form may increase the risk of small-cell lung cancer in smokers (6).
Foods that contain beta-carotene include fruits and vegetables such as berries; green leafy vegetables; and orange, red or yellow vegetables like peppers, carrots and sweet potato. In my practice, I test for beta-carotene and vitamin C as a way to measure nutrient levels and track patients’ progress when they are eating a nutrient-dense diet. Interestingly, many patients achieve more than three times higher than the highest beta-carotene blood levels seen in this small study.
Impact of high blood pressure medications
For those patients who have high blood pressure, it is important to know that not all blood pressure medications are created equal. When comparing blood pressure medications in an observational study, two classes of these medications stood out. Angiotensin II receptor blockers (known as ARBs) and angiotensin-converting enzyme inhibitors (known as ACE inhibitors) reduce the risk of dementia by 53 and 24 percent, respectively, when used in combination with other blood pressure medications.
Interestingly, when ARBs were used alone, there was still a 47 percent reduction in risk; however, ACE inhibitors lost their prevention advantage. High blood pressure is a likely risk factor for dementia and can also be treated with lifestyle modifications (7). Otherwise, ARBs or ACE inhibitors may be the best choices for reducing dementia risk.
Ginkgo biloba disappoints
Ginkgo biloba, a common herbal supplement taken to help prevent dementia, may have no benefit. In the GuidAge study, ginkgo biloba was shown to be no more effective than placebo in preventing patients from progressing to Alzheimer’s disease (8). This randomized controlled trial was done in elderly patients over a five-year period with almost 3,000 participants. There was no difference seen between the treatment and placebo groups. This reinforces the results of an earlier study, Ginkgo Evaluation of Memory trial (9). Longer studies may be warranted. The authors stressed the importance of preventive measures with dementia.
You may be able to prevent dementia, whether through lifestyle modifications or, if medications are necessary, through medication selection.
Dr. Dunaief is a speaker, author and local lifestyle medicine physician focusing on the integration of medicine, nutrition, fitness and stress management. For further information, visit www.medicalcompassmd.com.
Every year, the country pauses on 9/11, remembering the victims of the terrorist attacks and reflecting on the safety and security of the country. At the same time, a Stony Brook University study continues not only to remember the first responders but also to understand the physical and mental consequences of the work police, firefighters and other first responders performed in the immediate aftermath of the attacks.
Benjamin Luft
Recently, Sean Clouston, an associate professor in the Department of Family, Population & Preventive Medicine at SBU Renaissance School of Medicine, and Ben Luft, the director of the SBU WTC Health and Wellness Program since 2003, published research in which they demonstrated a link between a protein commonly connected with Alzheimer’s disease to post-traumatic stress disorder, or PTSD, in first responders.
In a small preliminary study, the researchers found a difference in the level of the protein between first responders who are battling chronic PTSD and those who aren’t battling the condition. The Stony Brook scientists published their work in the journal Alzheimer’s & Dementia: Diagnosis, Assessment & Disease Monitoring.
The researchers cautioned that the presence of the markers doesn’t necessarily indicate anything about present or future changes in cognitive function.“We don’t know the specificity of the markers,” Luft explained in an email.
Amyloid is generally considered the earliest marker of Alzheimer’s disease, which includes cognitive decline. Some people, however, have significant amounts of amyloid and don’t develop problems with their thinking. Neurodegenerative diseases without amyloid rarely have severe symptoms, which don’t appear to worsen with time.
“This paper doesn’t look at cognitive symptoms,” Clouston said. “We do have papers looking at cognitive impairment and other memory-based differences. It wasn’t a part of this paper.”
The newest research is part of an ongoing program in which the university follows 11,000 responders who came to the World Trade Center. The study for this paper involved a smaller subset of this population. This type of research can and does have application to other studies of people who have traumatic experiences, the scientists suggest.
Most traumatic experiences are unique to each person, as people who suffer physical and emotional trauma in combat often confront the aftereffects of head injuries. Among the first responder population who survived the attacks on 9/11, most of them “faired pretty well physically,” Clouston said.
“We didn’t have a lot of head injuries. Understanding PTSD in this crowd is really useful for the literature as a whole because it allows us to focus on the long-term psychiatric fallout of an event without worrying about exposures that are different.”
The scientists had at least some idea of the timing and duration of exposures. This research suggests that it might be helpful to think about the kinds of problems that cognitive impairment can cause, which might involve managing other health-related problems.
Luft added that the population they are studying shows the benefit of immediate care. “One thing for sure is that the care of the first responders has to occur very quickly,” he said. “Now that we know the history, the greatest chance you have in mitigating the effect of this type of trauma is to deal with the problem from the get-go.”
Sean Clouston with his daughter Quinn at Benner’s Farm in Setaukt. with his daughter Quinn. Photo by Rachel Kidman
First responders have benefited from psychotherapy as well as from various pharmacological treatments. Luft suggested that they might even benefit from having therapists available in the field, where they can receive near instantaneous psychological support.
In addition to the psychological trauma, first responders have had physical effects from their work in the aftermath of the attacks, such as respiratory and gastrointestinal problems, as well as autoimmunity issues.
People have these problems because “of the pro-inflammatory effect of PTSD itself,” said Luft. The researchers believe trauma can affect the immune system and the brain.
According to Clouston, the next step with this work is to replicate it with a larger scale. The experiment was “fairly expensive and untried in this population and novel in general, so we started small,” he explained in an email. The scientists would like to “get a larger range of responders and to examine issues surrounding symptomatology and other possible explanations.”
Clouston has been at Stony Brook for six years. Prior to his arrival on Long Island, he worked on a collaborative project that was shared between University College London and the University of Victoria.
An expert in aging, he felt like his arrival came at just the right time for the WTC study, as many of the first responders were turning 50. After giving talks about the cognitive and physical effects of aging, he met Luft and the two decided to collaborate within six months of his arrival.
Clouston is focused on whether PTSD caused by the terrorist attacks themselves have caused early brain aging. A self-proclaimed genetics neophyte, he appreciates the opportunity to work with other researchers who have considerably more experience in searching for molecular signatures of trauma.
Clouston said his family has suffered through the trauma of cognitive decline during the aging process. His family’s struggles “definitely bring [the research] home,” reminding him of the “terror that many family members feel when they start noticing problems in their siblings, parents, spouses, etc.”
As for his work on the recent study, he said he is excited about the next steps. “Little is known about the subtypes of amyloid,” he suggested and there’s a “lot more to explore about the role [of this specific type] in the population. I do think it could be really informative about the types of symptoms.”
Making Memories with Music, a special program for people with dementia and their care partners, returns to the Cinema Arts Centre, 423 Park Ave., Huntington on Aug. 27 at 11 a.m. Facilitated by Marcy Rhodes, the morning will feature a performance by The Jazz Loft Trio — Tom Manuel on cornet and vocals, Steve Salerno on guitar and Keenan Zach on double bass. Admission is $5 per person. Popcorn and beverages will be served. Registration is required by calling 631-423-7610, ext. 0.
Temple Isaiah, 1404 Stony Brook Road, Stony Brook will host an event titled How Sweet It Is!, a perfect activity for those with memory impairment and their caretakers, on Sunday, Aug. 19 from 2 to 4 p.m. Participants will relive favorite memories of the 1950s with a sing-along, souvenir photos, soda fountain and snacks. Free and open to all. For more information or to RSVP, email Iris at [email protected] or call Penny at 631-751-8518.
In Europe, lipoic acid is classified as a drug, unlike in the United States, where it is a supplement.
Lipoic acid may have a significant effect on multiple chronic diseases
By David Dunaief, M.D.
Lipoic acid, also known as alpha lipoic acid and thioctic acid, is a noteworthy supplement. I am not a big believer in lots of supplements for several reasons: Diet contributes thousands more nutrients that work symbiotically; in the United States, supplements are not regulated by the FDA, thus there is no official oversight; and research tends to be scant and not well-controlled.
Dr. David Dunaief
So why would I write about lipoic acid? It is a supplement that has scientific data available from randomized controlled trials, which are the gold standard of studies. In Europe, lipoic acid is classified as a drug, unlike the United States, where it is a supplement (1).
Lipoic acid is an antioxidant, helping to prevent free radical damage to cells and tissues, but also is a chelating agent, potentially removing heavy metals from the body. Lipoic acid is involved in generating energy for cells; it is an important cofactor for the mitochondria, the cell’s powerhouse. It may also boost glutathione production, a powerful antioxidant in the liver (1). We produce small amounts of lipoic acid in our bodies naturally. Lipoic acid may be important in chronic diseases, including Alzheimer’s, multiple sclerosis and diabetic peripheral neuropathy. Let’s look at the evidence.
Diabetic peripheral neuropathy
Diabetic peripheral neuropathy, or diabetic neuropathy, involves oxidative stress and occurs in up to half the population with diabetes. One in five patients, when diagnosed, will already have peripheral neuropathy. The most common type is distal symmetric polyneuropathy — damage to nerves on both sides of the body in similar locations. It causes burning pain, numbness, weakness and pins and needles in the extremities (2).
The best studies with lipoic acid focus on peripheral neuropathy with diabetes. In a double-blinded, randomized controlled trial (SYDNEY I), results showed that the total treatment score had improved significantly more for those receiving 600 mg lipoic acid by intravenous therapy compared to the placebo group (3). Also, individual symptoms of numbness, burning pain and prickling significantly improved in the group treated with lipoic acid compared to placebo.
The study involved 120 diabetes patients with stage 2 neuropathy. Its weakness was its duration; it was a very short trial, about three weeks. The author concluded that this therapy would be a good adjunct for those suffering diabetic neuropathy.
In a follow-up to this study (SYDNEY II), the design and the results were the same (4). In other words, in a second double-blinded, placebo-controlled trial, the lipoic acid treatment group showed significantly better results than the placebo group. There were 180 patients with a similarly short duration of five weeks.
Why include this study? There were several important differences. One was that lipoic acid was given in oral supplements, rather than intravenously. Thus, this is a more practical approach. Another difference is that there were three doses tested for lipoic acid: 600, 1,200 and 1,800 mg. Interestingly, all of them had similar efficacy. However, the higher doses had more side effects of nausea, vomiting and vertigo, again without increased effectiveness. This suggests that an oral dose of 600 mg lipoic acid may help treat diabetic peripheral neuropathy.
Dementia and Alzheimer’s
In a recent randomized, placebo-controlled trial involving Alzheimer’s patients, results were significantly better for lipoic acid (600-mg oral dose) in combination with fish oil, compared to fish oil alone or to placebo (5). The amount of fish oil used was 3 grams daily containing 675 mg docosahexaenoic acid and 975 mg eicosapentaenoic acid of the triglyceride formulation.
The duration of this pilot study was 12 months with 39 patients, and the primary end point was a change in an oxidative stress biomarker, which did not show statistical significance. However, and very importantly, the secondary end point was significant: slowing the progression of cognitive and functional decline with the combination of fish oil and lipoic acid. Minimental status and instrumental activities of daily living declined less in the combination treatment group. This was encouraging, although we need larger trials.
However, another study showed 900 mg lipoic acid in combination with 800 IU daily of vitamin E (alpha tocopherol strain) and 500 mg vitamin C actually mildly reduced an oxidative stress biomarker but had a negative impact on Alzheimer’s disease by increasing cognitive decline on a minimental status exam (6). What we don’t know is whether the combination of supplements in this study produced the disappointing effects or if an individual supplement was the cause. It is unclear since the supplements were tested in combination. The study duration was 16 weeks and involved 78 moderate to severe Alzheimer’s patients.
Multiple sclerosis
In a study involving rats, giving them high doses of lipoic acid resulted in slowing of the progression of multiple sclerosis-type disease (7). The mechanism by which this may have occurred involved blocking the number of inflammatory white blood cells allowed to enter the cerebrospinal fluid in the brain and spinal cord by reducing the enzymatic activity of factors such as matrix metalloproteinases.
I know this sounds confusing, but the important point is that this may relate to a human trial with 30 patients that showed reduction in the enzyme MMP (8). Thus, it could potentially slow the progression of multiple sclerosis. This is purely connecting the dots. We need a large-scale trial that looks at clinical outcomes of progression in MS, not just enzyme levels. The oral dose used in this study was 1,200 to 2,400 mg lipoic acid per day.
Interestingly, the 1,200-mg dose used in the human trial was comparable to the high dose that showed slowed progression in the rat study (9). This only whets the appetite and suggests potential. So, we have lots of data. What do we know? In diabetic neuropathy, 600 mg oral lipoic acid may be beneficial. However, in Alzheimer’s the jury is still out, although 600 mg lipoic acid in combination with fish oil has potential to slow the cognitive decline in Alzheimer’s disease. It also may have a role in multiple sclerosis with an oral dose of 1,200 mg, though this is early data.
Always discuss the options with your physician before taking a supplement; in the wrong combinations and doses, supplements potentially may be harmful. The good news is that it has a relatively clean safety profile. If you do take lipoic acid, know that food interferes with its absorption, so it should be taken on an empty stomach (1).
Dr. Dunaief is a speaker, author and local lifestyle medicine physician focusing on the integration of medicine, nutrition, fitness and stress management. For further information, visit www.medicalcompassmd.com or consult your personal physician.
Dementia symptoms include impairments in thinking, communicating, and memory. Stock photo
By David Dunaief, M.D.
When you hear the word dementia, what is your reaction? Is it fear, anxiety or an association with a family member or friend? The majority of dementia is Alzheimer’s, which comprises about 60 to 80 percent of dementia incidence (1). There is also vascular dementia and Parkinson’s-induced dementia, as well as others. Then there are precursors to dementia, such as mild cognitive impairment, that have a high risk of leading to this disorder.
Dr. David Dunaief
Encouraging data
There is good news! A recent study, the Health and Retirement Study (HRS), a prospective (forward-looking) observational study, suggested that dementia incidence has declined (2). This was a big surprise, since predictions were for significant growth. Dementia declined by 24 percent from 2000 to 2012. There were over 10,000 participants 65 years old and older at both the 2000 and 2012 comparison surveys. There was also a decrease in mild cognitive impairment that was statistically significant. However, the reason for the decline is not clear. The researchers can only point to more education as the predominant factor. They surmise that more treatment and prevention of risk factors for cardiovascular disease may have played a role.
So how is dementia defined?
According to the American Psychiatric Association’s DSM-5 (“Diagnostic and Statistical Manual of Mental Disorders,” Fifth Edition), dementia is a decline in cognition involving one or more cognitive domains. In addition to memory, these domains can include learning, executive function, language, social cognition, perceptual-motor and complex attention (3).
What can be done to further reduce dementia’s prevalence?
Knowing some of the factors that may increase and decrease dementia risk is a good start. Those that raise the risk of dementia include higher blood pressure (hypertension), higher heart rate, depression, calcium supplements in stroke patients and prostate cancer treatment with androgen deprivation therapy (ADT).
What abates risk?
This includes lifestyle modifications with diet and exercise. A diet shown to be effective in prevention and treatment of dementia is referred to as the MIND (Mediterranean–DASH intervention for neurodegenerative delay) diet, which is a combination of the Mediterranean-type and Dietary Approaches to Stop Hypertension (DASH) diets. Surprisingly, there is also a cocktail of supplements that may have beneficial effects.
How does medication to treat dementia, specifically Alzheimer’s, fit into this paradigm?
It is not that I was ignoring this issue. Our present medications are not effective enough to slow the disease progression by clinically significant outcomes. But what about the medications in the pipeline? The two hottest areas are focusing on tau tangles and amyloid plaques. Recently, drugs targeting tau tangles from TauRx Therapeutics and amyloid plaques from Eli Lilly failed to achieve their primary clinical end points during trials. There may be hope for these different classes of drugs, but don’t hold your breath. The plaques and tangles may be signs of Alzheimer’s dementia rather than causes. Several experts in the field are not surprised by the results.
Let’s look at the evidence.
The quandary that is blood pressure
If ever you needed a reason to control high blood pressure, the fact that it may contribute to dementia should be a motivator. In the recent Framingham Heart Study, Offspring Cohort, a prospective observational study, results showed that high blood pressure in midlife — looking specifically at systolic (top number) blood pressure (SBP) — increased the risk for dementia by 70 percent (4). Even worse, those who were controlled with blood pressure medications in midlife also had significant risk for dementia.
There were 1,440 patients involved in the study over a 16-year period with an examination every four years. Then, those patients who were free of dementia were examined for another eight years. Results showed a 107-patient incidence of dementia, of which half were on blood pressure medications. And when there was a rapid drop in SBP from midlife to late in life, there was a 62 percent increased risk, to boot. Thus, the moral of the story is that lifestyle changes to either prevent high blood pressure or to get off medications may be the most appropriate route to reducing this risk factor.
Prostate cancer inflates dementia risk
Actually, the title above does not do justice to prostate cancer. It is not the prostate cancer, but the treatment for prostate cancer, androgen deprivation therapy (ADT), that may increase the risk of dementia by greater than twofold (5). Treatment duration played a role: those who had a year or more of ADT were at higher risk. ADT suppresses production of the male hormones testosterone and dihydrotestosterone. The study involved over 9,000 men with a 3.4-year mean duration; however, it was a retrospective (backward-looking) analysis and requires a more rigorous prospective study design to confirm the results. Thus, though the results are only suggestive, they are intriguing.
Calcium supplements — not so good
In terms of dementia, the Prospective Population Study of Women and H70 Birth Cohort trial has shown that calcium supplements, especially when given to patients who have a history of stroke, increase the risk of dementia by greater than sixfold (6). Those who had white matter lesions in the brain also had an increased risk. The population involved 700 elderly women, with 98 given calcium supplements. How do we reduce this risk? Easy: Don’t give calcium supplements to those who have had a stroke. This brings more controversy to taking calcium supplements, especially for women. You are better off getting calcium from foods, especially plant-based foods.
The MIND diet to the rescue
In a recent study, results showed that the MIND diet reduced the risk of Alzheimer’s dementia by 53 percent in those who were adherent. It also showed a greater than one-third reduction in dementia risk in those who only partially followed the diet (7). There were over 900 participants between the ages of 58 and 98 in the study, which had a 4.5-year duration. When we talk about lifestyle modifications, the problem is that sometimes patients find diets too difficult to follow. The MIND diet was ranked one of the easiest to follow. It involves a very modest amount of predominantly plant-based foods, such as two servings of vegetables daily — one green leafy. If that is not enough, the MIND diet has shown the ability to slow the progression of cognitive decline in those individuals who do not have full-blown dementia (8).
Supplement cocktail
To whet your appetite, a recent study involving transgenic growth hormone mice (which have accelerated aging and demonstrate cognitive decline) showed a cocktail of supplements helped decrease the risk of brain deterioration and function usually seen with aging and in severe Alzheimer’s dementia (9). The cocktail contained vitamins, minerals and nutraceuticals, such as bioflavonoids, garlic, cod liver oil, beta carotene, green tea extract and flax seed. Each compound by itself is not considered to be significant, but taken together they seem to have beneficial effects for dementia prevention in mice.
The reasons for dementia may involve mitochondrial dysfunction, oxidative stress and inflammation that are potentially being modified by these supplements. Hopefully, there will be more to come on this subject. It comes down to the fact that lifestyle modifications, whether in terms of reducing risk or slowing the progression of the disease, trump current medications and those furthest along in the drug pipeline. There may also be a role for a supplement cocktail, though it’s too early to tell. The MIND diet has shown some impressive results that suggest powerful effects.
Dr. Dunaief is a speaker, author and local lifestyle medicine physician focusing on the integration of medicine, nutrition, fitness and stress management. For further information, visit www.medicalcompassmd.com or consult your personal physician.
