Alzheimer’s: Assessing and Reversing Your Risk

Alzheimer’s disease has no single cause but many contributory factors at least half of which you can prevent. That’s the conclusion of a statement made by 113 of the world’s leading experts on dementia. These researchers agree on the idea that it is a degenerative disease that develops largely due to the long-term consequence of faulty nutrition, lack of exercise and social stimulation, much like cardiovascular disease, and that multiple factors have to be in place for the condition to develop.

How do you know what these factors are so you can reduce your total risk?

Since the majority are related to what you put in your mouth, any long-term solution must involve fundamental changes to your diet.

The contributory factors include:

  • A genetic predisposition
  • Inflammation
  • Lack of antioxidant nutrients
  • Lack of omega-3 fats
  • Excessive stress and elevated cortisol
  • Poor blood sugar control and excess carbs
  • Raised homocysteine
  • Lack of B vitamins
  • Indigestion and/or malabsorption
  • Poor circulation.

Aside from a genetic predisposition, each of these can be prevented and these prevention steps form the basis of my Alzheimer’s Prevention Diet. But be aware that having a genetic predisposition, such as having the ApoE4 gene, on its own is not enough to cause the disease. Only one in a hundred cases of Alzheimer’s are ‘caused’ by the extremely rare familial pre-senilin genes causing very early onset Alzheimer’s.

An inflammatory issue?

It is highly likely that both cardiovascular disease and Alzheimer’s result at least in part from the same or a similar disease process. In cardiovascular disease the arteries become inflamed and damaged. A similar process occurs in the brain in Alzheimer’s disease. Often, the two diseases occur together. A review carried out at New York University’s neurology department highlights the fact that at least a third of patients with Alzheimer’s also have some degree of vascular disease. Not only does the presence of cardiovascular disease greatly increase the chances of getting Alzheimer’s, especially if you happen to have the ApoE4 gene,1 but many causative factors apply to both conditions.

It’s one of those chicken or egg situations. For example, having vascular disease tends to speed up the memory loss associated with Alzheimer’s. Once cardiovascular disease is present, blockages in arteries may lead to a poor supply of key nutrients to the brain – a condition known as cerebrovascular disease. And without a good supply of antioxidants, brain cells become more vulnerable to damage from free radicals, rogue molecules produced by combustion, for example from frying foods or smoking. So cerebrovascular disease is intimately linked to both a lack of antioxidants and excess exposure to oxidants. Antioxidant nutrients such as vitamins C and E have been shown to help both conditions – not only to mop up these brain pollutants, but also to reduce inflammation.

Cerebrovascular disease is also strongly linked to having a high homocysteine level. Based on an analysis of all current research, having a high homocysteine level makes you more than twice as likely to develop Alzheimer’s as having cerebrovascular disease. A high H score also makes you much more likely to develop cerebrovascular disease. So, whichever way you cut it, keeping your homocysteine level low is essential.

All of these factors – a lack of antioxidants, too many brain pollutants, the presence of cardiovascular or cerebrovascular disease – tend to increase the risk and severity of Alzheimer’s, with the critical link being inflammation. Now, let’s explore how this inflammation occurs, and how to prevent it.

The presence of beta-amyloid plaques or remains of dead cells and other waste material in the brain distinguish Alzheimer’s from other forms of dementia. Beta-amyloid is an abnormal protein that is also found in the plaques of arterial deposits. It is a toxic invader that arises when the body is in ‘emergency mode’, as can happen when a person’s total environmental overload exceeds their genetic capacity to adapt. In such cases, the person’s immune system can become over-reactive and trigger inflammation. In fact, most major diseases involve inflammation. That includes cardiovascular disease, diabetes, cancer, and any that end in ‘itis’ – colitis, arthritis, bronchitis and sinusitis, for instance.

So, looked at in this way, the presence of the ApoE4 gene simply means a person has less genetic capacity to adapt to the insults of today’s diets and lifestyles. But this weakness can be countered by optimum nutrition, which endows us with more adaptive capacity by giving the brain and body a less toxic chemical environment. Inflammation, in this model, is the alarm bell. It’s your body telling you something is wrong.

To get rid of inflammation you have to get to the root cause, and in my book The Alzheimer’s Prevention Plan you can find out how digestive problems, too much sugar and stress, a lack of antioxidants and too much homocysteine can all lead to inflammation.

Looking at Alzheimer’s as an inflammatory disease also explains why taking anti-inflammatory drugs offers some protection from it, which is consistent with the hypothesis that the damage that occurs to brain cells is part of an overall inflammatory reaction. But unfortunately many of these drugs end up encouraging inflammation and in the long run by damaging the gut, which leads to more inflammation!

Luckily, there are natural anti-inflammatory nutrients that don’t harm the digestive tract, and these may prove to be more effective, both in the long run and in preventing inflammation. Antioxidants and omega-3 fats are effective anti-inflammatories. There are also some very powerful antiinflammatory herbs, such as turmeric.

You can check out your own risk of developing Alzheimer’s or dementia in the Alzheimer’s Risk Factors Check below but far better is to complete Food for the Brain’s free online Cognitive Function Test (www.foodforthebrain.org) which calculates your risk and gives you a perosnalised strategy to reduce it.

Alzheimer’s Risk Factors Check List

  • Do you forget the name of your friends?
  • Do you forget where you put things more than once a week?
  • Do you forget the word that you are looking for more than once a week?
  • Do you lose your way outside your own neighbourhood?
  • Would anyone in your family or close friends think that your memory is worse than it used to be?
  • Are you overweight?
  • Do you eat oily fish such as mackerel or sardines less than once a week?
  • Do you rarely eat seeds?
  • Do you smoke?
  • Do you have high blood pressure?
  • Have you had a heart attack or stroke, or do you suffer from angina or thrombosis?
  • Are you currently taking anti-inflammatory drugs such as cortisone or NSAIDS?
  • Do you eat fewer than four servings of fruit and vegetables a day?
  • Do you have a family history of dementia or Alzheimer’s?
  • Do you have digestive problems?
  • Do you eat something fried most days?
  • Do you drink more than 10 units of alcohol a week?
  • Do you have more than one coffee or tea every day?
  • Are you often stressed?
  • Do you rarely take B vitamin supplements?
  • Do you rarely take antioxidant supplements, including vitamins C and E?
  • If you’ve had a homocysteine test, was your score above 10?
  • If you’ve had a homocysteine test, was your score above 15?
  • If you gave more than 6 ‘yes’ answers you have probably increased your risk by half.
  • If you gave more than 12 ‘yes’ answers you may have doubled your risk.
  • If you gave more than 16 ‘yes’ answers you may have quadrupled your risk.

But don’t worry. Instead, put your energy into turning all ‘yes’ answers into ‘no’s by making simple changes to your diet and lifestyle. See my report ‘Alzheimer’s Prevention Steps’.

Food for the Brain’s Cognitive Function Test will give you an accurate score for your cognitive function as well as a personalised prevention plan. Use this to track your progress as you address your weakest areas.

References

  1. Hoffman A. et al., letter in Lancet, 349:151 (1997).