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Omega-3 Displays More Alzheimer’s-Deterring Effects
6/25/2007
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Omega-3/Omega-6 dietary ratio found a key factor; excess omega-6 fats reduce the brain-protective benefits of omega-3 DHA
by Craig Weatherby


The clever mouse at left was smart enough to seek refuge from an Indian flood on the back of a remarkably placid frog.

And perhaps a diet high in omega-3-rich aquatic plants gave the riverine rodent the smarts to rescue itself on the amiable amphibian.

Animal and cell studies indicate that omega-3s from fish can help deter age-related mental declines and Alzheimer’s by impacting brain and memory function in fundamentally beneficial ways.

And a few studies in people indicate that omega-3 DHA may exert therapeutic effects in Alzheimer’s patients (see the “Fish really is brain food” sidebar, below).

(The same is true of antioxidants in turmeric, berries, and other zesty, colorful fruits, vegetables, and herbs... we'll report new evidence on that in our next issue.)

A 2005 study from UCLA showed that omega-3 DHA appears to prevent the beta-amyloid protein “plaque” that causes

Fish really is brain food
A fast-growing body of epidemiological, laboratory, and clinical research affirms the folk reputation of fish as brain food.

To learn more search our newsletter archive for “brain” and “Alzheimer”.

We reviewed five of the most compelling studies in these articles:
lesions in Alzheimer's patients’ brains (see “Research Reveals How Fish Oil Deters Alzheimer’s Disease”).

New findings extend DHA’s protective potential to "tau" tangles
Now, researchers at the University of California, Irvine report that in addition to blocking formation of beta-amyloid plaque, omega-3 DHA also slows accumulation of a protein called “tau” in mice bred to develop Alzheimer’s disease.

This tau-blocking effect prevents the formation of the brain-damaging nerve “tangles” characteristic of Alzheimer's, which add more lesions to ones caused by build up of beta-amyloid protein plaque (Green KN et al 2007).

The UC-Irvine group also revealed that DHA lowers brain levels of beta amyloid protein by reducing brain levels of an enzyme called presenilin, without which beta amyloid cannot accumulate quickly.

Omega-6 excess proves bad for mouse brains
Just as important, the UC-Irvine researchers tested the effects of giving the test mice various ratios of omega-3 and omega-6 fatty acids in their diets.

And the results confirm everything we’ve reported about the unhealthful effects of the omega-6 overload in Americans’ diets, which stem in part from their generally pro-inflammatory influence. (See “Omega-6 excess proves bad for mouse brains”, below.)

Omega-6 fatty acids are abundant in corn, soy, canola, peanut, cottonseed, safflower, and sunflower oils and therefore in most packaged and prepared/restaurant foods.

The UC-Irvine team, led by Professor Frank LaFerla, Ph.D., studied the effects of feeding Alzheimer’s-prone mice omega-3 DHA and omega-6 fatty acids in various ratios.

The UC team divided their mice into four groups: one "control" and three "test" groups.

The mice in the control group were given mouse food containing 10 parts omega-6 fatty acids to one part omega-3s: the ratio typical of most Americans’ diets.

(The ideal ratio for human diets is more like three omega-6s to every omega-3 molecule, but many Americans’ diets range as high as 30 to one.)

Each of three test groups were given a “fat-neutral” mouse chow providing equal amounts of omega-6 and omega-3 fatty acids: that is, a one to one ratio.

In addition to the fat-neutral chow:
  • One of the three test groups received supplemental DHA.

  • The other two test groups received supplemental DHA + supplemental omega-6 fatty acids: one omega-6 group got lower and one higher total amounts (as omega-6 arachidonic acid or docosapentaenoic acid).
And these were the encouraging findings:
  • After three months, the mice in all of the test groups had lower levels of damaging beta amyloid and tau proteins than mice in the control group. This was due, no doubt, to the healthier omega-6/omega-3 balance in all three test groups' chow (1:1 ratio instead of 10:1 in the control group).

  • After nine months, only the mice that received supplemental omega-3 DHA without any additional omega-6s had lower levels of both harmful brain proteins.
These results confirm two things suggested by prior research:
  1. Dietary omega-3s – specifically DHA – fight formation of the beta amyloid and tau proteins that cause brain lesions in Alzheimer’s patients.

  2. The excessive intake of omega-6 fatty acids typical of American diets promote formation of these lesion-inducing proteins.
The lesson seems clear: people should replace standard vegetable oils with olive oil or other low-omega-6 oils (e.g., macadamia nut oil or hi-oleic safflower oil) minimize consumption of packaged and prepared foods, and eat plenty of plant foods and fish.


Sources
  • Green KN, Martinez-Coria H, Khashwji H, Hall EB, Yurko-Mauro KA, Ellis L, LaFerla FM. Dietary docosahexaenoic acid and docosapentaenoic acid ameliorate amyloid-beta and tau pathology via a mechanism involving presenilin 1 levels. J Neurosci. 2007 Apr 18;27(16):4385-95.

  • Lim GP, Calon F, Morihara T, Yang F, Teter B, Ubeda O, Salem N Jr, Frautschy SA, Cole GM. A diet enriched with the omega-3 fatty acid docosahexaenoic acid reduces amyloid burden in an aged Alzheimer mouse model. J Neurosci. 2005 Mar 23;25(12):3032-40.

  • UC-Irvine. Omega-3 fatty acid may help prevent Alzheimer's brain lesions: Study suggests DHA-rich diet can curb onset of the disease. Accessed online June 18 at http://today.uci.edu/news/release_detail.asp?key=1594

  • Billings LM, Green KN, McGaugh JL, LaFerla FM. Learning decreases A beta*56 and tau pathology and ameliorates behavioral decline in 3xTg-AD mice. J Neurosci. 2007 Jan 24;27(4):751-61.

  • Rosario ER, Carroll JC, Oddo S, LaFerla FM, Pike CJ. Androgens regulate the development of neuropathology in a triple transgenic mouse model of Alzheimer's disease. J Neurosci. 2006 Dec 20;26(51):13384-9.

  • Green KN, Billings LM, Roozendaal B, McGaugh JL, LaFerla FM. Glucocorticoids increase amyloid-beta and tau pathology in a mouse model of Alzheimer's disease. J Neurosci. 2006 Aug 30;26(35):9047-56.

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