Conventional medicine is still taking baby steps when it comes to preventing or treating Alzheimer’s – or even slowing its progression. Even though there are proven benefits of natural products such as mixed forms of vitamin E, conventional medicine seems to insist the only valid treatment will come in the form of a chemical produced in a lab by a pharmaceutical company.
And of course, one that is patented, so no one else can make it (or grow it).
This isn’t to say they might be able to find one. Meanwhile, conventional medicine has ignored proven natural treatments for Alzheimer’s disease.
This doesn’t mean that we will give up. Surely U.S. medical doctors care about their patients and as the valid research becomes more evident, they are bound to someday embrace the effectiveness of natural medicines such as huperzine A.
But this isn’t the only potential natural strategy to slow the progression of Alzheimer’s for those who have been struck with this condition. And even the most basic of nature’s resources has been shown to beat one of the most popular pharmaceutical Alzheimer’s treatment: memantine.
This expensive pharmaceutical is branded as Mimetix by Abbott, Ebixa and Abixa by Lundbeck aand Namenda by Forest Pharmaceuticals. It is prescribed for existing Alzheimer’s patients – with mild to moderate forms of the condition. It is also often prescribed for some other forms of dementia.
Memantine is a acetylcholinesterase inhibitor and a dopaminergic receptor agonist – it binds with this receptor. It is also non-competitive antagonist with the binding of 5HT receptors and acetycholine receptors.
Okay, I’m not expecting you to understand all that. What is important is that this chemical has complex responses within the body – it is a complex pharmaceutical that significantly affects the nervous system. And while it has shown some benefit in some situations, it also comes with various adverse effects, including anxiety, headaches, insomnia, dizziness, drowsiness, vomiting and even hallucinations.
Yes, that was hallucinations. And insomnia and anxiety. In a drug that is supposed to help with dementia.
Consider the contrast between this drug and vitamin E – notably one form of vitamin E, alpha-tocopherol. This is a nutrient that is prevalent in a number of natural foods. These include some of the highest levels in sunflower seeds, almonds, beets, pumpkin, peanuts, peppers, avocado and many other foods. It has no known adverse effects – only positive side effects.
Could such a basic, simple vitamin beat out the billion-dollar pharmaceutical, memantine?
First of all, this is research published in the most respected U.S. medical journal – the Journal of the American Medical Association – JAMA. The research was conducted by a large team of researchers – at 14 Veteren’s Administration research centers in Minneapolis, New York, Madison, Albuquerque, Cleveland, Washington, DC, Philadelphia, Miami, Baltimore, Charleston, Ann Arbor, Boston, Seattle, Iowa City, and elsewhere. Researchers from medical schools of the University of Maryland, the University of Washington, the University of Iowa, the University of South Carolina and Yale University’s School of Public Health were involved in the research.
The research was randomized, double-blinded and placebo-controlled. It began in 2007 and concluded in 2012, and was published in 2014.
The research involved 613 patients with mild to moderate Alzheimer’s disease. They were veterans treated at the 14 VA centers mentioned above.
The patients were divided into four groups: 152 patients were given 2000 IU per day of alpha tocopherol; 155 were prescribed 20 milligrams per day of memantine; 154 patients were given both of these together, and 152 were given a placebo. This placebo group provided the control group with which to compare the treatments of the other three groups.
The results of the study was measured by the Alzheimer’s Disease Cooperative Study/Activities of Daily Living (ADCS-ADL) Inventory test. The ADCS-ADL Inventory test has a range of scores, from 0 to 78 – with 78 being the highest and best score. This bases its measure on functioning levels of dementia – the ability to function on a day-to-day basis.
The researchers also otherwise measured the patients’ cognition, nervous and mood-related symptoms, their ability to function and the levels of caregivers they required during the five –year period. One of the more prominent alternative tests they used was the MMSE test – the widely used mini–mental state examination – along with the Alzheimer Disease Assessment Scale–Cognitive Subscale (ADAS-cog).
After an average of nearly two-and-a-half years of treatment, a total of 561 patients completed the study with appropriate analytical results. (Some died during the study and some had to drop out for different reasons). Completed were 140 vitamin E patients, 142 memantine-treated patients, 139 who took both and 140 who were treated with a placebo.
To summarize, the research found that the vitamin E-treated group had Alzheimer’s progression that were from between nearly 1 point up to 5.4 points lower than the placebo group declines. The average difference in reduced scores was 3.15 points. This means that the vitamin E group’s decline in functioning – their Alzheimer’s condition worsened less than the placebo group’s decline by 3.15 points.
This difference was significant. The difference was calculated to be equivalent to a delay of nearly 20% of Alzheimer’s disease progression. This was also converted to be about six months of reduced progression over the total four year trial period.
The researchers also found that the vitamin E-alone group scored better for caregiver time – meaning the vitamin E group required significantly less caregiver time than the other groups.
These positive effects of the vitamin E occurred throughout the group, but better among those with more advanced stages of the condition.
Meanwhile, the memantine treatment group also slowed their Alzheimer’s disease progression. However, the difference between the placebo group and the memantine treatment group’s Alzheimer’s progression was a meager 1.98 points – which the researchers qualified was too low to be considered a significant difference:
“There were no significant differences in the groups receiving memantine alone or memantine plus alpha tocopherol.”
This means that not only was the memantine not effective for delaying the progression of Alzheimer’s, but when the Vitamin E – which was effective – was mixed with memantine – the significant positive effect of Vitamin E was lost:
“When compared with placebo, the alpha tocopherol alone group showed significant benefit, but paradoxically, the combination of alpha tocopherol and memantine had less effect than either alpha tocopherol alone or memantine alone. Although it is possible that memantine could have interfered with the effectiveness of alpha tocopherol, it is difficult to postulate a plausible mechanism. To our knowledge, no studies have examined whether memantine interferes with alpha tocopherol’s antioxidant effects.”
In contrast, the researchers were clear that Vitamin E had a clear positive effect:
“These findings suggest benefit of alpha tocopherol in mild to moderate Alzheimer’s disease by slowing functional decline and decreasing caregiver burden.”
Many of the patients who were tested were older. So there were deaths during the trial period. When it comes to mortality, the Vitamin E group suffered significantly fewer deaths during the study. This of course contradicts the study showing greater mortality among Vitamin E takers.
Statistically, the Vitamin E group had a nominal death rate of 7.3% – over 25% lower than the death rate of 9.4% among the placebo group. And the memantine group had a whopping 11.3% mortality rate during the trial – over 50 percent higher than the Vitamin E group.
In addition, adverse effects were significantly greater in the memantine group. The memantine suffered 31 adverse events among 23 patients, while the combination groups suffered 44 events among 31 patients. The placebo group had 13 events among 11 patients.
Wow, you say – why didn’t we know this before?
Yes, we do find a previous study that proves Vitamin E’s effectiveness in reducing Alzheimer’s disease progression. But this is in a study from nearly two decades ago. That illustrates how little focus conventional medicine has been putting on testing natural solutions. Meanwhile dozens of studies have been done on potential pharmaceutical solutions that have little or no effect.
This doesn’t mean that this previous research on Vitamin E and Alzheimer’s isn’t valid. In 1997, researchers from the Columbia University’s College of Physicians and Surgeons studied 341 moderately severe Alzheimer’s patients for two years. In this study, the Mini-Mental State Examination was used to test the patients. The group that was treated with alpha-tocopherol had significantly less progression of Alzheimer’s compared to the placebo group – by a score of 670 to 440 days.
To be fair, in this study, the pharmaceutical drug Selegiline was tested as well. And it did result in a slower progression similar to that of the Vitamin E group. However, further study on Selegiline has proven it to not be such a hot Alzheimer’s drug. After a large 2003 Cochrane Database review from Oxford University medical researchers concluded:
“Despite its initial promise, ie the potential neuroprotective properties, and its role in the treatment of Parkinson’s disease sufferers, selegiline for Alzheimer’s disease has proved disappointing. Although there is no evidence of a significant adverse event profile, there is also no evidence of a clinically meaningful benefit for Alzheimer’s disease sufferers. This is true irrespective of the outcome measure evaluated, ie cognition, emotional state, activities of daily living, and global assessment, whether in the short, or longer term (up to 69 weeks), where this has been assessed. There would seem to be no justification, therefore, to use it in the treatment of people with Alzheimer’s disease, nor for any further studies of its efficacy in Alzheimer’s disease.”
Yet we do not find this sort of disappointment among the Vitamin E research and among other studies of natural remedies for slowing the progression of Alzheimer’s disease.
As we’ve discussed elsewhere, synthetic vitamin E doesn’t work as well as nature’s versions.
It must be understood that the alpha-tocopherol version of vitamin E is only one dimension of this critical brain vitamin. Nature provides eight different molecules categorized as vitamin E. Four are tocopherols – alpha-tocopherol, beta-tocopherol, gamma-tocopherol, and delta-tocopherol. Of these, alpha-tocopherol is the more prevalent within the body – easily stored and used.
But there are also four important tocotrienol forms of vitamin E – alpha-tocotrienol, beta-tocotrienol, gamma-tocotrienol, and delta-tocotrienol.
Research from Sweden’s Karolinska Institute has shown that Alzheimer’s disease and cognition decline is linked to not to just tocopherol levels – but also to tocotrienols.
The researchers studied 81 Alzheimer’s patients, 86 patients with mild cognitive impairment and 86 matched volunteers who where cognitively healthy.
The researchers found that plasma levels of both tocotrienols and tocopherols corresponded with levels of cognitive decline: Those with Alzheimer’s disease had the lowest levels of both.
Furthermore, MRI scans were compared with blood levels of gamma-tocotrienols and alpha-tocotrienols – along with gamma-tocopherols. The researchers found that lower levels of these different forms of Vitamin E were associated with greater levels of cognitive decline.
Another study from the Karolinska Institute and Stockholm University followed 140 advanced-age people without cognitive issues at the beginning of eight years. They measured their blood-levels of vitamin E together with the advancement of cognitive decline.
They tested for all eight vitamin E molecules as mentioned above.
The researchers found that over the eight-year period, cognitive decline was less among those who had higher blood levels of gamma-tocopherol and beta-tocotrienol. Those with higher levels of total tocotrienols also had significantly less cognitive decline.
In their conclusion they summarized their findings:
“Elevated levels of tocopherol and tocotrienol forms are associated with reduced risk of cognitive impairment in older adults.”
Multiple studies have also found that tocotrinols are significantly beneficial to cardiovascular health.
A mix of different forms of Vitamin E can be found with a diverse diet containing whole grain foods, whole rice, coconut and palm foods. This combination will provide both tocotrienols and tocopherols.
Dysken MW, Sano M, Asthana S, Vertrees JE, Pallaki M, Llorente M, Love S, Schellenberg GD, McCarten JR, Malphurs J, Prieto S, Chen P, Loreck DJ, Trapp G, Bakshi RS, Mintzer JE, Heidebrink JL, Vidal-Cardona A, Arroyo LM, Cruz AR, Zachariah S, Kowall NW, Chopra MP, Craft S, Thielke S, Turvey CL, Woodman C, Monnell KA, Gordon K, Tomaska J, Segal Y, Peduzzi PN, Guarino PD. Effect of vitamin E and memantine on Alzheimer disease: the TEAM-AD VA cooperative randomized trial. JAMA. 2014 Jan 1;311(1):33-44. doi: 10.1001/jama.2013.282834.
Sano M, Ernesto C, Thomas RG, Klauber MR, Schafer K, Grundman M, Woodbury P, Growdon J, Cotman CW, Pfeiffer E, Schneider LS, Thal LJ. A controlled trial of selegiline, alpha-tocopherol, or both as treatment for Alzheimer’s disease. The Alzheimer’s Disease Cooperative Study. N Engl J Med. 1997 Apr 24;336(17):1216-22.
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Mangialasche F, Westman E, Kivipelto M, Muehlboeck JS, Cecchetti R, Baglioni M, Tarducci R, Gobbi G, Floridi P, Soininen H, Kłoszewska I, Tsolaki M, Vellas B, Spenger C, Lovestone S, Wahlund LO, Simmons A, Mecocci P; AddNeuroMed consortium. Classification and prediction of clinical diagnosis of Alzheimer’s disease based on MRI and plasma measures of α-/γ-tocotrienols and γ-tocopherol. J Intern Med. 2013 Jun;273(6):602-21. doi: 10.1111/joim.12037.
Mangialasche F, Solomon A, Kåreholt I, Hooshmand B, Cecchetti R, Fratiglioni L, Soininen H, Laatikainen T, Mecocci P, Kivipelto M. Serum levels of vitamin E forms and risk of cognitive impairment in a Finnish cohort of older adults. Exp Gerontol. 2013 Dec;48(12):1428-35. doi: 10.1016/j.exger.2013.09.006.
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