The Key to Preventing Alzheimer’s May Be a Trip to the Grocery Store

A new study just hit my desk: The Journal of the American Medical Association (JAMA) reports that high levels of leptin are associated with lower rates of dementia and Alzheimer’s disease.₂

The 12-year study found that people with the lowest leptin levels were approximately four times more likely to develop dementia and Alzheimer’s disease than people with the highest levels.

This raises the possibility that leptin may have a protective role in the brain and may even be a contributing factor to memory.

Dementia Hits Harder and More Often Than You Think… As you age, it’s pretty common to forget things. You see someone you know, and his name escapes you. You can’t remember where you put your car keys. You miss appointments if you don’t write them down. Sound familiar? For some people, it’s more than just an embarrassing moment that passes. It’s the beginning of dementia. Developing dementia is a terrifying thought to most people. Part of the fear comes from the fact that people (not to mention most doctors) have no idea what to do to prevent it. Here are a few facts you need to know about dementia: The chance of developing dementia doubles every five years after the age of 60. In some communities, almost half the population over the age of 85 has it. As many as 6.8 million people in the United States have some form of dementia. Alzheimer’s disease is the most common cause, affecting one out of 10 people over the age of 65.1 Alzheimer’s disease is characterized by the development of abnormal proteins, called plaques, and tangles that prevent nerve cells from communicating with one another and eventually causes them to die.

So, what is leptin and how do you get some of it?

The word “leptin” comes from the

Greek word leptos, which means “thin.” Leptin is a hormone (made primarily in fat cells) that regulates the way your body uses energy. Your appetite, your metabolism, and whether or not you store fat on your body all are affected by leptin.

It’s a delicate balance. As you begin to store fat, leptin is released, signaling you to eat less.

• If you starve yourself, your body produces less leptin, so you have less control to stop eating.
• If you eat too much and become too overweight, it sets up inflammation in your body, and you become leptin-resistant – which also means you have less control to stop eating.

Now, for just a moment, consider another recent study that looked at obesity and dementia over the course of 36 years and found three times the risk of developing dementia if you were obese! And the bigger your waistline, the bigger the risk!₃

So what does this mean to you?

The best way to increase and maintain your leptin levels is to avoid the root cause of leptin resistance: inflammation.

Chronic inflammation prevents leptin from crossing the blood-brain barrier. That means leptin has no communication with the part of the brain that controls weight gain and cognitive function. This lack of communication in the brain is what sets up obesity and dementia.

The worst offenders include sugar, artificial sweeteners, vegetable oils, and farm-raised fish, especially salmon.

So stay away from high-fructose corn syrup, processed foods, and fried foods. And eat only wild-caught fish.

You can also follow a low-inflammation diet.

It’s easier than you think. You can often tell if a food is inflammatory by the effect it has on your breathing.

A Stuffy Nose Can Tell You
Which Foods to Avoid

Ever had a crème-filed donut or pizza and soda – only to find that a few minutes later it’s harder to breathe through your nose? That’s probably evidence of an immediate inflammation response.

The tissue and blood vessels in your nose are very sensitive, so it’s easy to tell when a certain food triggers that kind of inflammation. But when inflammation happens elsewhere in your body over time, the symptoms may be harder to pinpoint – and their results can be more severe – like the leptin resistance that leads to obesity and Alzheimer’s.

Your cells make both inflammatory and anti-inflammatory chemicals. How much of the various compounds are produced depends a lot on the foods you eat.

Certain foods lead your body to produce more compounds that are inflammatory. Other foods lead your body to generate anti-inflammatory compounds. When you know which foods are which, you can use this to your advantage.

Foods that promote inflammation	Replacements to reduce inflammation
Refined carbohydrates. These include anything made with flour or sugar (white bread, pasta, rolls, pastry, cakes, cookies, sweets, candy, soda and juice drinks, breakfast cereals, etc.).	Natural carbohydrates, such as fruits, vegetables and legumes.
Saturated fats, including fatty cuts of grain-fed meat, and commercial dairy products.	Mono-unsaturated fats, including olive oil and canola oil.
Trans fats, which are found in fried foods, snacks, margarine, mayonnaise, and any packaged food that contains “hydrogenated” or “partially hydrogenated” oils.	Foods that contain omega-3 fatty acids, such as wild-caught salmon, tuna, herring, sardines, and mackerel.
White produce and processed foods, which tend to be antioxidant-poor.	Brightly colored vegetables and fruits, which tend to be high in antioxidants.

The IF (Inflammation Factor) Rating system is a tool created by noted nutritional researcher Monica Reinagel. This system, which evaluates 20 different nutritional factors that have an impact on inflammation, makes it easy to stay on an anti-inflammatory diet.

Foods with a negative rating are inflammatory, and foods with a positive rating are anti-inflammatory. The higher the number, the stronger the effect.

The following table shows some of the best-rated foods:

1. Dementia” accessed 12/23/09 http://www.medicinenet.com/script/main/art.asp?articlekey=9090
2. Lieb, W., Beiser, A. “Association of Plasma Leptin Levels With Incident Alzheimer Disease and MRI Measures of Brain Aging.” JAMA. 2009;302(23):2565-2572.
3. Whitmer, R. A., Gustafson, D. R., et. al. “Central obesity and increased risk of dementia more than three decades later” NEUROLOGY 2008;71:1057-1064