Feeding your brain: Nutrients and Alzheimer´s disease

Alzheimer’s disease (AD) is the most common form of dementia; with dementia being defined as a series of conditions occurring when nerve cells or neurons in the brain die or no longer function as they should.  These changes will impair a person’s ability to carry out basic daily life activities such as bathing, dressing, eating, and even going to the bathroom by themselves; even more, AD will also affect one’s memory, behavior, and the ability to think clearly. (R)

 

The Alzheimer’s Association estimates that this brain condition affects almost 6 million people in the United States alone. It’s among the first six causes of death for US Americans older than 65 years old. However, Alzheimer’s is not just a disease of old age. There’s the so called the early or younger-onset Alzheimer’s disease, which is affecting a great proportion of people younger than 65. This hints at the fact that AD is not only caused by us getting older. (R) (R)

 

What causes Alzheimer´s disease?

 

Scientists still don’t know all the causes of AD. However, like many other chronic and degenerative diseases, this devastating disorder can be the result of multiple factors rather than a single one. As we mentioned above, aging would be the most obvious and important risk factor for some types of this disease, but we also know that lifestyle, family history and a person’s environment can be linked too.  (R)

 

What’s more, recent research has put into evidence that our genes play an important role as well.  So, let’s talk about the APOE family, which is an important compound for brain function produced by the APOE gene. Particularly, the apolipoprotein E (APOE) ε4, is believed to be the one which accounts for most of the genetic risk in your chances of developing Alzheimer’s disease. (R) (R) (R)

 

 The bad guy in the APOE family

Apolipoprotein E or APOE are the most prevalent brain lipoproteins. Part of their jobs are to carry cholesterol from our brains, to support lipid transport and to clear the beta-amyloid protein – Aβ –   in the brain, which is a component of plaque. (R) These complex particles come in several different forms, or alleles: APOE ε2, APOE ε3 and APOE ε4. All of us inherits a copy of some form of APOE from each parent and this combination will be what’s responsible for our likelihood of developing Alzheimer’s disease or not, and the rate of the resulting cognitive decline. (R) (R)

 

The APOE ε3 form is the most frequent in all populations and is believed to play a neutral role in the disease. Meaning if you inherit this gene, it doesn’t decrease nor increase your risk. Interestingly, APOE ε2 allele is protective, although it is relative rare, so if you are lucky enough to inherit this gene, you can likely give a sigh of relief. But if you inherit the ε4 allele gene, this is the one with the deepest impact and it’s strongly associated with increased risk for both early-onset and late-onset AD. (R)

 

According to several studies, those who inherit one copy of APOE ε4 have an increased risk of developing Alzheimer’s; but those who inherit two copies are at an even higher risk. This goes for the entire population, no matter your ethnicity, age or sex. (R) (R) (R) These groups of patients also go through a faster cognitive and functional decline following clinical disease onset. (R) (R)

 

Outside the brain, APOE ε4 is associated with hyperlipidemia and hypercholesterolemia, which lead to atherosclerosis, coronary heart disease and stroke, all of them comorbidities associated with cognitive impairment and dementia. (R) So, anyone inheriting this gene could indeed have some major issues to worry about developing.

 

However, in spite of this dark panorama, you should also know that not all ε4 carriers will develop AD, it just increases your chances. However, take note, as the odds can be reversed, which implies that just because we may have been dealt some bad genetic cards, it doesn’t mean we can’t reshuffle the deck by making some changes in some modifiable risk factors. (R) (R)

 

Eating right for your APO genotype

 

Several strategies have been proposed to help you to prevent, slow or stop the progression of Alzheimer’s disease. Nutrition is among these widely investigated approaches, suggesting an interaction between genes and nutrients in the development of the disease; hence, nutritional therapy is aimed to target specific nutrients depending on the APO genotype you have inherited. (R)

 

As we discussed earlier, the APOE protein carries cholesterol and other lipids through the blood; so, it’s easy to guess that if we follow a high-fat and high-cholesterol diet, our bodies will make more APOE. Usually, those who have the APOE ε4 genotype have hypercholesterolemia, which in turn can boost the production and accumulation of the toxic Aβ. (R) (R) (R)This means if you inherited it, you should take special care to follow a healthy diet.

Results have been controversial in this field, but most of them point out that some nutrients are associated with an increased risk of developing Alzheimer’s. Dietary factors include a moderate to high saturated fat intake and a low to moderate intake of polyunsaturated fats – PUFAS –, like the ones coming from fish oil.

If you fall into the APOE ε4 group, you are more vulnerable and have a bigger response to these dietary patterns too. (R) (R) Other findings suggest that changes in plasma cholesterol induced by your diet can lead to changes in brain APOE expression. (R) Plus, other groups of researchers also suggest that avoiding excess saturated fat and taking in enough PUFAS may decrease the risk or postpone the onset of dementia for this group. (R) (R)

 

Other lifestyles linked to this type of dementia and which interact with APOE genotype, includes physical activity, alcohol drinking and smoking. (R) For example, if you participate in daily exercise, it will help improve cognitive function and help to reduce the brain amyloid, especially among the APOE ε4 carriers (R) This data should be comforting for the genetically susceptible individuals; meaning that even though we can’t change our genetic markup, we can reduce our likelihood of disease by for example, preventing high cholesterol levels through dieting and adopting healthy lifestyle options. The greater benefit could be for an APOE ε4 allele carrier, who can reduce the risk close or equal to the ones who don’t carry this allele. (R) (R)

 

What else is out there?

 

Besides the possibilities resulting from the lipid profile from your diet, other nutrients and food patterns have been proposed to prevent, decrease risk or treat progression of AD. However, current evidence is not strong enough to give a verdict but rather can be used as a general guideline or recommendation to help you fight against AD.

 

Among the most studied eating patterns it’s worth mentioning The Mediterranean diet. This diet has provided to have favorable results in reducing the risk of Alzheimer’s, and it can improve cognitive function, and help you to prevent cognitive decline and dementia. (R) (R)

 

Foods rich in flavonoids and polyphenolic compounds – like fruits, vegetables and red wine –  will have a protective role due to their antioxidant and anti-inflammatory activity; vitamins from the B family and vitamin D will exert a benefit too. (R) However, these recommendations seem to be address especially those in the ε4 non-carriers groups; as these dietary interventions appear to be less effective if you are one of the ApoE4 carriers. (R)

 

All in all, genetics as well as diet are part of what could be a determining factor in whether or not you may get or can help yourself prevent Alzheimer’s disease and other forms of dementia.

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