DNC News

Juice protects against Alzheimer's Disease

Jacob Schor, ND

September 6, 2006



Drinking a couple of glasses of juice each week lowers one's risk of getting Alzheimer's disease by 76%. At least that's the conclusion of the study published a few days back in the September issue of the American Journal of Medicine. The journal report was written by scientists who had monitored 1836 older Japanese Americans in King County , Washington , for a decade. They found that those individuals who drank fruit and/or vegetable juice at least three times a week had a 76% lower chance of developing Alzheimer's Disease compared to people who drank juice once a week or less.

The amount of juice people drank was determined from self-administered questionnaires. Cognitive function was measured by trained interviewers using standardized tests. [i]

As striking as these results seem, they are not coming out of the blue; prior studies have suggested chemicals in fruits offered brain protection, though the magnitude of the protection offered still comes as a surprise. A March, 2005 study on mice showed that apple juice slowed oxidative damage to the brain and prevented cognitive decline. [ii] Earlier this summer we saw an article on Mediterranean-like Diets decreasing Alzheimer's incidence by 40%. [iii] Over the last few years several studies have shown that blueberries can both slow brain aging and improve cognitive function. [iv] [v] A study from 1998 compared spinach, strawberries and vitamin E for protective effects against brain deterioration. [vi] The idea that particular foods might be protective against certain diseases of course isn't a new idea, it's just that few would have predicted they would work so well.


While evidence has mounted validating the protection provided by foods, there has been a steady erosion for the health claims ascribed to the vitamin pills.


Life, it seems, is more complicated than we thought. At one time scientists thought that the health benefits of a particular food could be attributed to a particular vitamin found in that food. Rather than having to eat the food, people could, in theory, get the same benefit from taking the vitamin. You've got to remember that many of the scientists who came up with these ideas are from the generation that thought Tang was an adequate substitute for orange juice.


Betacarotene was the first vitamin to disappoint us. Carrots are good for people so the easy assumption was that these benefits were all derived from betacarotene because carrots are loaded with it; it's what makes them orange.


Betacarotene was once recommended to smokers to protect them from lung cancer. Carrots provide protection, so should betacarotene. The logic is simple enough. The one thing we should have learned by now is that biology isn't simple or neat; it's a messy business.


Unfortunately, it didn't work that way. In 1992 researchers at the US National Cancer Institute began testing betacarotene's protective effect. They recruited more than 18,000 people at high risk of developing lung cancer, either because they smoked or had been exposed to asbestos, and gave around half of them beta carotene supplements. The trial was supposed to run for six years, but the researchers called it quits after four years; people taking betacarotene were doing worse than the controls. Their lung cancer rate was 28 per cent higher, and the overall death rate was up 17 per cent.

Further trials have only strengthened the evidence that beta carotene supplements not only fail to protect people against cancer but can also increase the risk of lung cancer in smokers. [vii]

Vitamin E has been something of a disappointment of late. Vitamin E shot to stardom in the early 1990s, after two large studies found that those with a diet high in vitamin E were significantly less likely to develop cardiovascular disease. The first study followed 87,245 female nurses for eight years and found that the top 20 per cent with respect to vitamin E consumption had a 41 per cent lower incidence of cardiovascular disease than the bottom 20 per cent. [viii] The second study, involving 39,910 male health professionals, found a similar reduction in heart disease risk. [ix]

Having seen these positive results, other researchers set up large studies using vitamin E supplements. The results, however, have been disappointing. Only one experiment - the Cambridge heart antioxidant study (CHAOS) - found a positive effect, a 77 per cent reduced risk of heart attack. Several others found no protective effect and one even concluded that vitamin E increased the risk of heart failure.

Other trials designed to test whether vitamin E supplements could prevent cancers, such as the ATBC study in Finland , also came in negative. And relevant to this juice study, Vitamin E also did nothing to halt the progression to Alzheimer's disease.

Despite good evidence that vitamin E is a powerful antioxidant in the test tube, there is now doubt that it acts the same way in the body

There's a new and intriguing explanation that is being tossed about.

Take tea and coffee as an example. Tea and coffee are often touted as the leading antioxidants in our diets. Evidence abounds linking green tea with reduced risk of cancer and cardiovascular disease. There is growing evidence that coffee protects against liver cancer. Yet for all our talk of tea and coffee being antioxidants, in actuality they are full of reactive oxygen species in the form of hydrogen peroxide. They may act as antioxidants in the body but not in a test tube.

Why would drinking cup after cup of free radical beverages be good for us? One possibility is that they trigger our own internal antioxidant systems to work better. If it turns out that antioxidants in food work because they actually generate free radicals, that would be one big change of perspective. [x] It would certainly go along way to explain why vitamin pills fail to protect against disease while juice can. Whatever the final explanation will be, our old understanding of free radicals and antioxidants is outdated and needs to be revised.


In the meantime, the important thing current research is telling us is that we ought to pay a lot less attention to the vitamin pills we take and a lot more attention to the foods we consume. In the case of this most recent study, drinking juice, vegetable or fruit, three times a week provided more protection against Alzheimer's disease than any combination of vitamins has ever done.


[i] Am J Med. 2006 Sep;119(9):751-9.

Fruit and vegetable juices and Alzheimer's disease: the Kame Project.

  Dai Q,

  Borenstein AR,

  Wu Y,

  Jackson JC,

  Larson EB.

Department of Medicine, Division of General Internal Medicine and Public Health, Vanderbilt Center for Health Services Research, Vanderbilt-Ingram Cancer Center, Vanderbilt School of Medicine, Nashville, Tenn, USA. qi.dai@vanderbilt.edu

BACKGROUND: Growing evidence suggests that oxidative damage caused by the beta-amyloid peptide in the pathogenesis of Alzheimer's disease may be hydrogen peroxide mediated. Many polyphenols, the most abundant dietary antioxidants, possess stronger neuroprotection against hydrogen peroxide than antioxidant vitamins. METHODS: We tested whether consumption of fruit and vegetable juices, containing a high concentration of polyphenols, decreases the risk of incident probable Alzheimer's disease in the Kame Project cohort, a population-based prospective study of 1836 Japanese Americans in King County, Washington, who were dementia-free at baseline (1992-1994) and were followed through 2001. RESULTS: After adjustment for potential confounders, the hazard ratio for probable Alzheimer's disease was 0.24 (95% confidence interval [CI], 0.09-0.61) comparing subjects who drank juices at least 3 times per week with those who drank less often than once per week with a hazard ratio of 0.84 (95% CI, 0.31-2.29) for those drinking juices 1 to 2 times per week (P for trend < .01). This inverse association tended to be more pronounced among those with an apolipoprotein Eepsilon-4 allele and those who were not physically active. Conversely, no association was observed for dietary intake of vitamins E, C, or beta-carotene or tea consumption. CONCLUSIONS: Fruit and vegetable juices may play an important role in delaying the onset of Alzheimer's disease, particularly among those who are at high risk for the disease. These results may lead to a new avenue of inquiry in the prevention of Alzheimer's disease.


[ii] Journal of Alzheimer's Disease

  Issue:   Volume 8, Number 3 / 2005

  Pages:   283 - 287

Apple juice concentrate prevents oxidative damage and impaired maze performance in aged mice


Flaubert Tchantchou A1, Amy Chan A1, Lydia Kifle A1, Daniela Ortiz A1, Thomas B. Shea A1


A1 Center for Cellular Neurobiology and Neurodegeneration Research, Department of Biological Sciences, University of Massachusetts Lowell, Lowell, MA 01854, USA


Oxidative stress contributes to age-related cognitive decline. In some instances, consumption of fruits and vegetables rich in antioxidant can provide superior protection than supplementation with purified antioxidants. Our prior studies have shown that supplementation with apple juice concentrate (AJC) alleviates oxidative damage and cognitive decline in a transgenic murine model compromised in endogenous antioxidant potential when challenged with a vitamin-deficient, oxidative stress-promoting diet. Herein, we demonstrate that AJC, administered in drinking water, is neuroprotective in normal, aged mice. Normal mice aged either 9-10 months or 2-2.5 years were maintained for 1 month on a complete diet or a diet lacking folate and vitamin E and containing iron as a pro-oxidant, after which oxidative damage was assayed by thiobarbituric acid-reactive substances and cognitive decline as assayed by performance in a standard Y-maze. Mice 9-12 months of age were unaffected by the deficient diet, while older mice demonstrated statistically-increased oxidative damage and poorer performance in a Y maze test. Supplementation with AJC prevented these neurodegenerative effects. These data are consistent with normal aged individuals being susceptible to neurodegeneration following dietary compromise such as folate deficiency, and a hastened onset of neurodegeneration in those individuals harboring a genetic risk factor such as ApoE deficiency. These findings also support the efficacy of antioxidant supplementation, including consumption of antioxidant-rich foods such as apples, in preventing the decline in cognitive performance that accompanies normal aging.




[iii] Ann Neurol. 2006 Jun;59(6):912-21.


Mediterranean diet and risk for Alzheimer's disease.


* Scarmeas N,

* Stern Y,

* Tang MX,

* Mayeux R,

* Luchsinger JA.


Taub Institute for Research in Alzheimer's Disease and the Aging Brain, New York , NY 10032 , USA . ns257@columbia.edu


OBJECTIVE: Previous research in Alzheimer's disease (AD) has focused on individual dietary components. There is converging evidence that composite dietary patterns such as the Mediterranean diet (MeDi) is related to lower risk for cardiovascular disease, several forms of cancer, and overall mortality. We sought to investigate the association between MeDi and risk for AD. METHODS: A total of 2,258 community-based nondemented individuals in New York were prospectively evaluated every 1.5 years. Adherence to the MeDi (zero- to nine-point scale with higher scores indicating higher adherence) was the main predictor in models that were adjusted for cohort, age, sex, ethnicity, education, apolipoprotein E genotype, caloric intake, smoking, medical comorbidity index, and body mass index. RESULTS: There were 262 incident AD cases during the course of 4 (+/-3.0; range, 0.2-13.9) years of follow-up. Higher adherence to the MeDi was associated with lower risk for AD (hazard ratio, 0.91; 95% confidence interval, 0.83-0.98; p=0.015). Compared with subjects in the lowest MeDi tertile, subjects in the middle MeDi tertile had a hazard ratio of 0.85 (95% confidence interval, 0.63-1.16) and those at the highest tertile had a hazard ratio of 0.60 (95% confidence interval, 0.42-0.87) for AD (p for trend=0.007). INTERPRETATION: We conclude that higher adherence to the MeDi is associated with a reduction in risk for AD. Ann Neurol 2006.


PMID: 16622828 [PubMed - indexed for MEDLINE]


[iv] Ann N Y Acad Sci. 2002 Apr;959:128-32.

Fruit polyphenolics and brain aging: nutritional interventions targeting age-related neuronal and behavioral deficits.


* Galli RL,

* Shukitt-Hale B,

* Youdim KA,

* Joseph JA.


USDA-ARS, HNRCA at Tufts University , Boston , Massachusetts 02111 , USA . rachel.galli@simmons.edu


Nutritional interventions, in this case, increasing dietary intake of fruits and vegetables, can retard and even reverse age-related declines in brain function and in cognitive and motor performance in rats. Our lab has shown that as Fischer 344 rats age their brains are increasingly vulnerable to oxidative stress. Dietary supplementation with fruit or vegetable extracts high in antioxidants (e.g., blueberry, BB, spinach, respectively) can decrease this vulnerability to oxidative stress as assessed in vivo by examining reductions in neuronal signaling and behavioral deficits and in vitro via H2O2-induced decrements in striatal synaptosomal calcium buffering. Examinations have also revealed that BB supplementations are effective in antagonizing other age-related changes in brain and behavior, as well as decreasing indices of inflammation and oxidative stress in gastrocnemius and quadriceps muscles. In ongoing studies we are attempting to determine the most effective BB polyphenolic components. To date, the anthocyanins show the most efficacy in penetrating the cell membrane and in providing antioxidant protection. In sum, our results indicate that increasing dietary intake of fruits and vegetables high in antioxidant activity may be an important component of a healthy living strategy designed to maximize neuronal and cognitive functioning into old age.


PMID: 11976192 [PubMed - indexed for MEDLINE]


[v] Neurobiol Aging. 2005 Dec;26 Suppl 1:128-32. Epub 2005 Sep 27.

The beneficial effects of fruit polyphenols on brain aging.


* Lau FC,

* Shukitt-Hale B,

* Joseph JA.


Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University , Boston , MA 02111 , USA .


Brain aging is characterized by the continual concession to battle against insults accumulated over the years. One of the major insults is oxidative stress, which is the inability to balance and to defend against the cellular generation of reactive oxygen species (ROS). These ROS cause oxidative damage to nucleic acid, carbohydrate, protein, and lipids. Oxidative damage is particularly detrimental to the brain, where the neuronal cells are largely post-mitotic. Therefore, damaged neurons cannot be replaced readily via mitosis. During normal aging, the brain undergoes morphological and functional modifications resulting in the observed behavioral declines such as decrements in motor and cognitive performance. These declines are augmented by neurodegenerative diseases including amyotrophic lateral sclerosis (ALS), Alzheimer's disease (AD), and Parkinson's disease (PD). Research from our laboratory has shown that nutritional antioxidants, such as the polyphenols found in blueberries, can reverse age-related declines in neuronal signal transduction as well as cognitive and motor deficits. Furthermore, we have shown that short-term blueberry (BB) supplementation increases hippocampal plasticity. These findings are briefly reviewed in this paper.


PMID: 16194581 [PubMed - indexed for MEDLINE]


[vi] J Neurosci. 1998 Oct 1;18(19):8047-55.

Long-term dietary strawberry, spinach, or vitamin E supplementation retards the onset of age-related neuronal signal-transduction and cognitive behavioral deficits.


* Joseph JA,

* Shukitt-Hale B,

* Denisova NA,

* Prior RL,

* Cao G,

* Martin A,

* Taglialatela G,

* Bickford PC.


United States Department of Agriculture Human Nutrition Research Center on Aging at Tufts, Boston , Massachusetts 02111 , USA .


Recent research has indicated that increased vulnerability to oxidative stress may be the major factor involved in CNS functional declines in aging and age-related neurodegenerative diseases, and that antioxidants, e.g., vitamin E, may ameliorate or prevent these declines. Present studies examined whether long-term feeding of Fischer 344 rats, beginning when the rats were 6 months of age and continuing for 8 months, with diets supplemented with a fruit or vegetable extract identified as being high in antioxidant activity, could prevent the age-related induction of receptor-mediated signal transduction deficits that might have a behavioral component. Thus, the following parameters were examined: (1) oxotremorine-enhanced striatal dopamine release (OX-K+-ERDA), (2) cerebellar beta receptor augmentation of GABA responding, (3) striatal synaptosomal 45Ca2+ clearance, (4) carbachol-stimulated GTPase activity, and (5) Morris water maze performance. The rats were given control diets or those supplemented with strawberry extracts (SE), 9.5 gm/kg dried aqueous extract (DAE), spinach (SPN 6.4 gm/kg DAE), or vitamin E (500 IU/kg). Results indicated that SPN-fed rats demonstrated the greatest retardation of age-effects on all parameters except GTPase activity, on which SE had the greatest effect, whereas SE and vitamin E showed significant but equal protection against these age-induced deficits on the other parameters. For example, OX-K+-ERDA enhancement was four times greater in the SPN group than in controls. Thus, phytochemicals present in antioxidant-rich foods such as spinach may be beneficial in retarding functional age-related CNS and cognitive behavioral deficits and, perhaps, may have some benefit in neurodegenerative disease.


PMID: 9742171 [PubMed - indexed for MEDLINE]


[vii] J Nutr. 2004 Jan;134(1):225S-230S.

From 1989 to 2001: what have we learned about the "biological actions of beta-carotene"?


* Bendich A.


Medical Affairs, GlaxoSmithKline, 1500 Littleton Rd, Parsippany , NJ 07054 , USA . Adrianne.4.Bendich@gsk.com


Dr. James Allen Olson helped us to define the role of beta-carotene in human health by categorizing these as "functions, actions and associations." In the last decade, significant research has shown that beta-carotene acts as an antioxidant in biologically relevant systems, affects several aspects of human immune function and higher intake/serum levels are associated with improvements in certain physiological functions such as lung function. The unexpected findings of increased lung cancer in beta-carotene supplemented smokers in the ATBC and CARET intervention studies have resulted in the need for expanded research efforts to define the mechanism(s) of action of beta-carotene. Recent survey data as well as laboratory animal studies continue to find an inverse association between beta-carotene and cancer risk. Because beta-carotene is the major source of vitamin A for the majority of the world's population, it is critical to define the safe levels of intake from foods and supplements.


PMID: 14704324 [PubMed - indexed for MEDLINE]


[viii] New England Journal of Medicine , vol 328, p 1444


[ix] ( New England Journal of Medicine , vol 328, p 1450)


[x] New Scientist magazine, 05 August 2006 , page 40-43

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