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Alzheimer’s Disease and Nutrition

March 28, 2009 Written by JP       [Font too small?]

Alzheimer’s disease (AD). Those two words often provoke a fearful and visceral reaction in many people. I think part of the reason is that when AD strikes there’s really nothing much that can be done to strike back. Today’s blog reports on a new “medical food” that may help those diagnosed with AD to regain some control over their destiny.

Nutrition for the Brain

A few years ago, a product was developed in collaboration with Dr. Richard Wurtman of M.I.T.’s Department of Brain and Cognitive Sciences. The formulation of this nutritional cocktail was intended to provide support for those suffering the beginning stages of AD. It was given the name: Souvenaid. Souvenaid is a milk-based beverage that contains therapeutic levels of nutrients such as antioxidants, B vitamins, choline, fish oil, phospholipids (like those found in lecithin) and uridine-5-monophosphate (a building block of RNA and DNA commonly found in mother’s milk and molasses).

Alzheimer's Disease in the US

This past week a presentation was given at the 24th Conference of Alzheimer’s Disease International that examined the results of a new trial involving Souvenaid in early AD patients. Here’s how the study was designed:

  • A total of 160 patients with AD were either given a 4 oz. serving of Souvenaid once daily or a placebo for 24 weeks.
  • At the beginning of the trial and at the 12 week mark, all of the patients were asked to participate in a mental test that measured verbal memory.
  • Side effect tracking was put in place to monitor any adverse reactions.

The results of the study were promising, though not miraculous. The specific findings were as follows:

  • There was a statistically significant improvement in verbal memory in those receiving the Souvenaid, but not in those drinking the placebo.
  • The Souvenaid users demonstrated higher blood levels of DHA ( the omega-3 fatty acid) and lower levels of homocysteine. Both changes are considered desirable in cases relating to dementia and AD.
  • Both beverages were equally well tolerated with no adverse effects reported.
Alzheimer's Brain

One of the lead researchers involved in the study, Dr. Patrick Kamphuis, explained that, “The medical food contains uridine-5′-monophosphate, omega-3 fatty acids, choline/phospholipids, B vitamins, and antioxidants, and has been designed to improve the formation of synapses”. Dr. Kamphuis went on to say that, “Several preclinical studies have demonstrated that specific combinations of these agents may stimulate synapse formation.” Without adequate synapse activity, cells in the brain cannot properly communicate with each other. This can obviously interfere with normal brain functioning and the ability to recall information.

The results of this current trial confirm prior research that was presented at the 2008 Alzheimer’s Association International Conference on Alzheimer’s Disease. The 2008 study (PDF) demonstrated similar benefits for those using Souvenaid with regard to their “delayed verbal memory task” abilities. This indicates an improvement in cognition, which was not (again) present in the placebo portion of volunteers.

Souvenaid is currently considered to be an experimental supplement. It hasn’t yet made it to the commercial market. The reason I decided to feature it is because foods and supplements with the similar ingredients are available right now. It may not be necessary to use this particular product in order to derive the benefits noted in today’s referenced research.

In closing, I’d like to direct you to several links from prior blogs where I’ve described other approaches that may help promote optimal brain performance. Ideally, we shouldn’t put all our hope in one single approach, but it’s best to address any condition from a more holistic perspective. In the case of AD or other forms of memory related conditions, an antioxidant and nutrient rich diet, exercising the body and mind, managing stress and incorporating mind-body techniques are all tools that should not be overlooked.

Note: Please check out the “Comments & Updates” section of this blog – at the bottom of the page. You can find the latest research about this topic there!

Be well!

JP

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9 Comments & Updates to “Alzheimer’s Disease and Nutrition”

  1. Iggy Dalrymple Says:

    This article shows that Alzheimer’s improves with supplementation of vitamin D and turmeric. The author describes the turmeric supplement as synthetic curcuminoids. What is that?
    http://tinyurl.com/VitD-Turmeric-Alzheimers

  2. JP Says:

    They *may* have chemically modified the curcuminoids in order to enhance their activity. The concern with this class of phytochemicals is their relatively poor absorption. Perhaps the synthetic form aims to address that.

    Be well!

    JP

  3. Iggy Dalrymple Says:

    “For years we thought that A-beta was just metabolic garbage produced as a byproduct of other processes within the brain, but these data suggest it is a normal component of the brain’s innate immune system.” says Rudolph Tanzi, PhD, director of the Genetics and Aging Unit in the MassGeneral Institute for Neurodegenerative Disease (MGH-MIND), co-senior author of the PLoS One report. “It looks like factors that trigger hyperactivity of the innate immune system – not only infection but also traumatic brain injury and stroke, which are already known to increase the risk for Alzheimer’s – could cause excessive deposition of A-beta.” http://www.physorg.com/news186816587.html
    ~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
    “Is there any connection between toxins in the environment and Alzheimer’s?

    Schiffer says no. The old aluminum theory originated by Linus Pauling over 30 years ago is history. Turns out that yes, there is increased aluminum in some of the plaques and tangles of the Alzheimer’s brain–but now we know that aluminum just “goes into areas of injury”. It isn’t the cause of the injury. It also appears in the brains of stroke patients, and in brain tumors.

    Schiffer also doesn’t think it’s likely that BPA from plastics is a player in Alzheimer’s. I have heard Alzheimer’s expert Dr. Peter Whitehouse propose the theory of lead as a cause of Alzheimer’s, and the research is compelling. Click here to read more.

    What about the “plaques and tangles” theory of Alzheimer’s? Isn’t that the cause of dementia?

    Yes, plaques and tangles were the oldest objective evidence that Alzheimer’s was a neurological disease, and they’ve seen for years. But, even though they are a partial marker of “risk” for Alzheimer’s–here’s the problem with the “plaque-and-tangle” theory. Many people will die and have a brain full of plaques and tangles, and still have normal cognition. Some people will have full-blown Alzheimer’s and have very few plaques and tangles. According to Schiffer, the relationship between those traditional Alzheimer neuro-pathologies and the clinical disease is not very strong.”

    Concerned About Brain Health, Alzheimer’s or Dementia?

  4. JP Says:

    Thanks, Iggy. Interesting info!

    Be well!

    JP

  5. Alex Says:

    this website is great for wat i needed

  6. JP Says:

    Update: Ashwaghanda, a traditional Ayurvedic herbal remedy, may offer new hope in the near future …

    http://msutoday.msu.edu/news/2015/promising-alzheimers-treatment-moves-toward-clinical-trials/

    “While plants cannot be patented, compounds from them can. MSU holds the patent for withanamides, and earlier research revealed that the compound, found in the plants’ seeds, proved to be a powerful anti-oxidant – double the strength of what’s on today’s market. The potent compound has shown that it can protect cells against damaging attacks by a rogue protein ­– the earliest stage of Alzheimer’s.

    Alzheimer’s begins when a specific protein starts breaking, or cleaving, at the wrong place to produce an unwanted fragment. This bad fragment, called BAP, stresses cells’ membranes, sparks plaque formation and eventually kills the cells. This attack begins in the frontal lobe, erasing memories and continuing its unrelenting assault deeper into the brain.

    A complicating factor is that the majority of protein cleaving is a natural, healthy process. Pharmaceutical companies, however, have focused their efforts on blocking the tiny faction of bad cleaving of the protein producing BAP.

    ‘Rather than trying to stop only the malevolent cleaving, our compound keeps the bad protein from entering the cell where it does its damage,’ said Nair, who’s in the horticulture department. ‘Our studies have shown that withanamides effectively protect the brain cells by neutralizing the effect of BAP.’”

    Be well!

    JP

  7. JP Says:

    Update 06/30/15:

    http://www.fasebj.org/content/29/7/2681

    FASEB J. 2015 Mar 24. pii: fj.14-264218.

    ω-3 Supplementation increases amyloid-β phagocytosis and resolvin D1 in patients with minor cognitive impairment.

    We investigated the effects of 4-17 month supplementation with ω-3 fatty acids and antioxidants (Smartfish drink; Smartfish AS, Oslo, Norway) in 12 patients with minor cognitive impairment (MCI) [minimental state examination (MMSE) ≥19], 2 patient with pre-MCI s (normal MMSE), and 7 patients with Alzheimer disease (AD) (MMSE <19). We measured the phagocytosis of amyloid-β 1-42 (Aβ) by flow cytometry and microscopy, the transcription of inflammatory genes by RT-PCR, the production of resolvin D1 (RvD1) by enzyme immunoassay, and the cognitive status by MMSE. In patients with MCI and pre-MCI, phagocytosis of Aβ by monocytes increased from 530 to 1306 mean fluorescence intensity units (P = 0.016). The increase in patients with AD was not significant (N.S.). The lipidic mediator RvD1, which stimulates Aβ phagocytosis in vitro, increased in macrophages in 80% of patients with MCI and pre-MCI (mean increase 9.95 pg/ml) (N.S.). Transcription of inflammatory genes’ mRNAs was increased in a subgroup of patients with low transcription at baseline, whereas it was not significantly changed in patients with high transcription at baseline. The mean MMSE score of patients with MCI and pre-MCI was 25.9 at baseline and 25.7 after 4-17 months (N.S.). Our study is the first to show significant immune and biochemical effects of ω-3 fatty acids with antioxidants in patients with MCI. Cognitive benefits of ω-3 supplementation in patients with MCI should be tested in a clinical trial.-Fiala, M., Halder, R. C., Sagong, B., Ross, O., Sayre, J., Porter, V., Bredesen, D. E. ω-3 supplementation increases amyloid-β phagocytosis and resolvin D1 in patients with minor cognitive impairment.

    Be well!

    JP

  8. JP Says:

    Updated 09/28/15:

    http://content.iospress.com/articles/journal-of-alzheimers-disease/jad150102

    J Alzheimers Dis. 2015 Sep 4.

    Plasma Fatty Acid Profiles in Relation to Cognition and Gender in Alzheimer’s Disease Patients During Oral Omega-3 Fatty Acid Supplementation: The OmegAD Study.

    BACKGROUND: ω3 fatty acids (ω3 FAs) may slow the rate of decline in cognitive performance in mild forms of cognitive impairment and Alzheimer’s disease (AD). However, the relationship between changes of plasma ω3 FA levels and cognitive performance, as well as effects of gender, are poorly known.

    OBJECTIVE: To study the effect of 6-month administration of DHA-rich ω3 FA supplementation on plasma FA profiles in patients with mild to moderate AD in relation to cognitive performance and gender. This investigation is part of the OmegAD Study.

    METHODS: 174 AD patients (74 ± 9 years) were randomized to a daily intake of 2.3 g ω3 FA or placebo for 6 months; subsequently all received the ω3 FA preparation for the next 6 months. Baseline as well as changes in plasma levels of the main ω3 FAs in 165 patients, while receiving ω3 FA supplementation for 6 months, were analyzed for association to cognitive performance (assessed by ADAS-cog and MMSE scores) as well as to gender.

    RESULTS: Preservation of cognitive functioning, assessed by ADAS-cog or its sub-items (but not MMSE) scores, was significantly associated to increasing plasma ω3 FA levels over time. Thus, the higher ω3 FA plasma levels rose, the lower was the rate of cognitive deterioration. This effect was not related to gender; since although females displayed higher ω3 FA plasma levels than did males after 6 months of supplementation, this difference disappeared when adjusted for body weight.

    CONCLUSIONS: Since our study suggests dose-response relationships between plasma levels of ω3 FA and preservation of cognition, future ω3 FA trials in patients with mild AD should consider exploring graded (and body weight adjusted) doses of ω3 FA.

    Be well!

    JP

  9. JP Says:

    Updated 12/17/15:

    http://www.ncbi.nlm.nih.gov/pubmed/26667739

    Nutr Hosp. 2015 Dec 1;32(n06):2822-2827.

    [COCONUT OIL: NON-ALTERNATIVE DRUG TREATMENT AGAINST ALZHEIMER´S DISEASE].

    BACKGROUND: Alzheimer’s dementia is the most prevalent nowadays. As for treatment, there is no definitive cure drug, thus new therapies are needed. In this regard the medium chain triglycerides are a direct source of cellular energy and can be a nonpharmacological alternative to the neuronal death for lack of it, that occurs in Alzheimer patients.

    OBJECTIVE: To evaluate the impact of coconut oil in the development of Alzheimer’s dementia, in any degree of dementia. Also determine whether this improvement influences within variables such as sex and suffering or not Type II Diabetes Mellitus.

    MATERIAL AND METHODS: A prospective study was conducted in patients with Alzheimer’s dementia, with a control and an intervention group which was administered 40 ml/day of extra virgin coconut oil. The parameters evaluated were the mini test scores Lobo cognitive test, pre and post intervention in both groups.

    RESULTS: It was observed in subjects taking the product, a statistically significant increase in test score MECWOLF and therefore an improvement in cognitive status, improving especially women’s, those without diabetes mellitus type II, and severe patients.

    CONCLUSION: This study, although preliminary, demonstrated the positive influence of coconut oil at the cognitive level of patients with Alzheimer’s, this improvement being dependent on sex, presence or absence of diabetes and degree of dementia.

    Be well!

    JP

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