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Curcumin is the most practical supplement to include in any nutritional program for preventing or treating Alzheimer’s disease. It is a must for any nutritional program for stopping the progression of the new diagnostic category, mild cognitive impairment, also known as pre-Alzheimer’s disease. at least slows down the progression of full-blown Alzheimer’s disease, but it is always better to use curcumin as a preventive rather than as a treatment.

If you have not been dealing with Alzheimer’s disease in your life or the life of a loved one very long, the new terminology for the different phases of the disease is probably unfamiliar. It is important to know the distinctions because different natural health practices support brain health at different stages of the disease. Let’s start with the new vocabulary of Alzheimer’s disease, preclinical Alzheimer’s disease, and mild cognitive impairment, confusingly but commonly termed “pre-Alzheimer’s disease”.

Alzheimer’s, Preclinical Alzheimer’s, and Mild Cognitive Impairment

We all have an idea of what Alzheimer’s is. As some people get older, their mental abilities deteriorate. People have memory problems. Then they start making errors in judgment. Then they begin to display symptoms of dementia, a condition of being in “another world”. Finally they lose their ability to feed themselves, dress themselves, go to the toilet, and walk, and a combination of factors the coroner usually calls “failure to thrive” sets in. An avalanche of small problems converge at the end of a very difficult life.

In 2011, the medical profession in the United States created a new diagnostic category for people with age-related brain decline called mild cognitive impairment. This is the condition often called “pre-Alzheimer’s disease,” but it is not the same as the other new diagnosis, pre-clinical Alzheimer’s disease. The idea behind creating the new diagnostic categories was to enable patients to get treatment sooner to maintain quality of life.

Mild cognitive impairment is diagnosed when:

1. The patient, a member of the patient’s family, a friend or neighbor, or the doctor becomes concerned that the patient’s ability to make good judgments about life concerns (“executive function”), the ability to communicate with words, eye-hand coordination, or muscle coordination, or all of these abilities, have become seriously impaired, impaired enough to interfere with daily life.
2. These observations are confirmed by an objective evaluation, such as a neurological examination or a psychological test, but
3. There are no signs of dementia (yet) and it is still possible for the patient to carry out the normal routine of daily life without assistance.

The American Psychiatric Association created this new diagnosis specifically to get insurance codes and Medicare reimbursement codes that would allow people to get help with their condition. For that reason, it’s a specifically American diagnosis. If you live in Canada or Australia or New Zealand or the UK or the rest of the EU, you won’t be diagnosed with mild cognitive impairment. You won’t have a diagnosis until you have full-blown Alzheimer’s, when it is late to make the lifestyle changes that may extend the good years of your life.

What happens after someone is diagnosed with mild cognitive impairment? It is to be hoped, nothing, but doctors will be on the lookout for signs of worsening mental condition.

In the United States, after there is a diagnosis of mild cognitive impairment, then the doctor would probably order a kind of brain scan called positron emission spectroscopy, or PET¹. The doctor could possibly order a much less expensive kind of brain scan called single-photon emission computerized tomography , or SPECT. The doctor might also perform a spinal tap to test cerebrospinal fluid. At that point, if there is evidence from PET or SPECT that parts of the brain are not using energy as they should, or if there is a certain kind of tangled protein in the spinal fluid, the diagnosis would be pre-clinical Alzheimer’s disease. This means that the patient still has enough mental function to keep charge of his or her own decisions, but full-fledged Alzheimer’s disease is likely a few years away.

After this initial diagnosis, handling of the patient’s fate is subjective. As long as it is possible for the patient to live at home with a minimum of assistance, the diagnosis is preclinical Alzheimer’s disease. But when it is just impossible for the patient to live independently, that’s the point at which a diagnosis of Alzheimer’s is made.

Many Diseases Imitate Alzheimer’s

If that sounds potentially unfair, it is. Reasonable people may disagree whether someone has progressed to full-blown Alzheimer’s disease (and many families are torn apart over disagreements about Alzheimer’s care). Moreover, Alzheimer’s disease and depression have many symptoms that overlap. And a dizzying variety of diseases can be misdiagnosed as Alzheimer’s, including:

• Alcohol abuse
• Bladder infections
• Cerebrovascular disease, either causing “low flow” of blood to the brain or accumulated brain damage caused by “mini-strokes” throughout the brain
• Chronic traumatic encephalopathy, caused by multiple blows to the head in sports
• Dehydration
• Excessive salt/sodium consumption
• Hyperthyroidism
• Hypothyroidism
• Medication interactions
• Parkinson’s disease
• Social isolation and/or poverty
• Street drug abuse
• Stroke
• Undetected eyesight problems
• Undetected hearing problems
• Vitamin B12 deficiency

If these conditions, are ruled out, then Alzheimer’s may have to be ruled in. Ultimately, the diagnosis of Alzheimer’s disease is made on the basis of behavior, not brain scans. Until very recently, the brain changes of Alzheimer’s really couldn’t be confirmed without autopsy. But there is a point that the symptoms are so bad that the exact diagnosis doesn’t make a difference.

You don’t want to the disease to get that far. And the two things that help most to prevent the progression to Alzheimer’s disease or the progression of Alzheimer’s disease once it has occurred are diet and curcumin. Let’s look at diet first.

Diet Makes a Difference for Alzheimer’s Disease

Diet makes a difference in Alzheimer’s disease. Diet is almost never mentioned as a preventive measure or treatment for Alzheimer’s, since nobody gets to sell a product or bill for it. But because diet for Alzheimer’s can make such a major difference in the disease it really doesn’t make sense to take any supplements if you aren’t making a basic change in diet first.

The most important dietary change for preventing the progression of mild cognitive impairment to pre-clinical Alzheimer’s disease and the progression of pre-clinical Alzheimer’s disease to full-blown Alzheimer’s disease is calorie restriction.

What you eat doesn’t make a big difference in whether you develop Alzheimer’s disease. It’s more about what you don’t eat. Changing your diet is not an absolute guarantee you won’t develop Alzheimer’s disease, but diet can make a major difference in your chances of maintaining brain health throughout your later years. And one of the most important things diet can do for you is helping you limit insulin resistance.

Insulin Resistance in “Type 3 Diabetes”

The best understood contributing factor for Alzheimer’s disease is a condition called insulin resistance. Insulin resistance is usually explained with a circular definition on the lines of “Insulin resistance is resistance to insulin. ” A more helpful way to understand it is as a downward spiral in the ability of most of the cells of the body to use insulin to receive glucose from the bloodstream.

Insulin acts as a sort of key that unlocks cellular doors that allow sugar to come inside. Cells use glucose very efficiently to make energy. They can also use fatty acids. Insulin transports both, but at different sites.

Energy is mostly a good thing, but when cells receive too much sugar, they make too much energy. The process of making energy requires oxygen, and using oxygen creates trillions of free radicals every second. These free radicals can destroy DNA or the structure of the cell itself, but as long as there is not too much sugar coming in, the cell can prevent the damage.

There is only a problem when too much sugar enters the cell, and the cell deals with this by “bolting the door” at the receptor sites that respond to insulin. That saves the cell, but it leaves sugar in the bloodstream. The pancreas senses excess sugar in the bloodstream, and releases more insulin.

Cells then shut down even more receptor sites, leaving even more sugar in the bloodstream, forcing the pancreas to make more insulin. A condition called type 2 diabetes can result, in which cells in the liver and skeletal muscles (the muscles you mentally control) become permanently insulin resistant.

The brain also burns glucose from the bloodstream. Brain cells can also become insulin resistant, but they still need insulin, like the rest of the body. When insulin resistance goes on so long that the insulin-making cells of the pancreas begin to “burn out,” the brain is left both insulin-resistant and insulin-deficient. The result is brain cells don’t receive enough sugar to function properly, and they are also unable to repair themselves.

The result is the formation of lacunae, which are literal holes in your head². These holes in your brain don’t cause Alzheimer’s disease, but they make it much more difficult for surviving brain tissue to compensate for it. Insulin resistance is one of the factors that makes Alzheimer’s worse, faster. And what is the one sure way to prevent the ill effects of insulin resistance? Eat less!. But insulin resistance isn’t the only factor that can be corrected by the same diet.

The APOE-4 Gene in Alzheimer’s Disease

Good diet can compensate for bad genes in Alzheimer’s disease, especially for the APOE-4 gene. And it’s possible to “turn off” the APOE-4 gene by eating less—but eating less in the right way.

APOE is short for “apolipoprotein E”. It is a molecule made in the liver, in the kidneys, and in the glial cells of the brain. Just as neurons in the brain have special receptor sites for insulin, they also have special receptor sites for APOE. This specialized chemical helps them receive proteins and cholesterol (cholesterol in this case being a good thing, forming the protective lining of each cell). APOE transports the proteins that the brain uses to build its framework that holds tissues together.

The problem arises when the gene that codes APOE is a variation called APOE-4. This gene is associated with the formation of tangles of protein that literally strangle brain cells, eventually leading to holes in the brain similar to the lacunae caused by insulin resistance. In a study conducted in Japan, people who had one or more copies of the APOE-4 gene (it’s possible to inherit one copy, or none, of the gene from either parent), were up to 30 times more likely to develop late-onset (after age 65)³ Alzheimer’s disease than people who did not have the gene.

Having this gene, however, does not necessarily doom someone to developing Alzheimer’s disease. American researchers have found that some people have the maximum two copies of the gene in their DNA and live into their 90′s without ever losing brain function. The difference, a researcher named Luchsinger found out, is eating less, actually not eating at all for one or two evenings or mornings each week.

A Brain-Saving Diet That Works, Usually

Dr. José A. Luchsinger is a senior fellow at the Taub Institute for Research in Alzheimer’s Disease and the Aging Brain at Columbia University in New York City. For 20 years, he has studied thousands of people to find the connections between diet and Alzheimer’s prevention. In 2001, Luchsinger and his colleagues conducted a study to determine if simply eating less could prevent Alzheimer’s disease.

Luchsinger’s research team found that sometimes it does, and sometimes it doesn’t.

The bad news was that among people who didn’t have the APOE-4 gene, the researchers found in their four-year study, eating less didn’t reduce the risk of Alzheimer’s disease significantly. The good news was that people who don’t have this gene already are less likely to get the condition anyway. In people who did have the APOE-4 gene, eating less reduced the risk of developing Alzheimer’s by over 60%.

How do you eat less? It turns out that it isn’t hard. Simply skip a meal every other day, giving your brain a break from food for at least 18 hours.

Why should something as simple as intermittent fasting make such a big difference in Alzheimer’s disease?

If you eat all the time, even if it’s just tiny snacks, your brain has to deal with a steady stream of glucose and fatty acids. If the brain is insulin-resistant or insulin-deficient, even if your blood sugar levels test normal, the brain simply can’t process all the nutrients. They tend to become tangles, and the tangles solidify and kill brain tissue.

If you simply skip a meal every other day, even if you more than make up for it later, at least you gave your brain a break from dealing with insulin resistance and insulin deficiency. This allows it to generate the substances that remove tangles and plaques and keep neurons functional.

Simply skipping a meal—entirely, not eating even a snack—has other surprising advantages. Intermittent fasting, Luchsinger and associates discovered:

• Reduces body fat.
• Reduces blood pressure.
• Increases the “good” cholesterol known as HDL.
• Helps the brain produce an antioxidant chemical known as beta-hydroxybutyrate.

In fact, fasting occasionally produces more of the brain-protective chemical that dieting all the time. Moreover, since the body has to use some calories to digest food, eating extra after your “mini-fast” or 12 to 18 hours takes off extra weight just as efficiently as forcing yourself to eat less at every meal, although most people only lose 10 or 12 pounds (4 or 5 kilos) this way.

Luchsinger and colleagues also found that what you eat makes a difference:

Getting more omega-3 essential fatty acids, such as those found in flaxseed oil and fish oil, slows the progression of Alzheimer’s.
Following a Mediterranean diet⁴ for 4 years (more fish, olive oil, vegetables, and dried fruit, and less organ meat, red meat, and butter) was linked to nearly 60% lower risk of developing Alzheimer’s, without regard to genetics.
Following a Mediterranean diet for 1 to 16 years was associated with up to 90% lower risk of developing mild cognitive impairment, the condition often called pre-Alzheimer’s.
Controlling blood sugar levels with insulin, even if they aren’t controlled very well, lowers the risk of developing “type 3” diabetes⁵ if you already have type 2 diabetes.

These aren’t difficult suggestions. To slow down or stop Alzheimer’s, sometimes you eat, and sometimes you don’t. Take a break from eating all the time by skipping a meal and snacks for at least 18 hours twice a week. (For an excellent discussion of this technique, see The 5: 2 Diet Book: Feast for 5 Days a Week and Fast for 2 to Lose Weight, Boost Your Brain and Transform Your Health by Kate Harrison).

Don’t eat lots of red meat. Don’t eat lots of butter. Don’t eat all the time. If you can’t fast completely, eat lightly—but many people find it easier simply to eat nothing at all than to try to be satisfied with nibbles. Eat some fish a few times a week or take a fish oil supplement every day These simple dietary changes increase the brain’s production of its preferred antioxidant, beta-hydroxybutyrate, and they make a bigger difference than taking any supplement—except curcumin. The usual advice to take a lot of antioxidant supplements really isn’t a good idea.

Wouldn’t It Be Easier Just to Take Antioxidant Supplements?

It is not unusual for people who have been diagnosed with pre-clinical Alzheimer’s or early clinical Alzheimer’s to take 20, 50, and sometimes even 100 different supplements every day. The cost of buying up to 100 supplements every month becomes quite significant. The sheer mass of gelatin from all the capsules begins to interfere with digestion.

And it’s not necessarily even a good idea to take multiple antioxidant supplements, because they can interfere with each other. Here are some examples:

• Beta-carotene is a great antioxidant, but it only works when there is a relatively good oxygen supply in the bloodstream. In people who smoke, or in people who have circulatory problems in the brain, it may even act as a pro-oxidant, causing the damage it is meant to prevent.
• Vitamin E is an effective antioxidant that has demonstrable benefits, at least in the laboratory, in protecting brain tissue. But if you don’t get enough vitamin C at the right time, vitamin E tends to break down in your bloodstream after 10 to 12 hours. And if you get too much vitamin C, the vitamin C not only doesn’t recharge vitamin E, it destroys it.
• All the other antioxidants you might take in a brain health program have limited availability in the brain itself, because it is hard for them to pass the blood-brain barrier, an anatomical feature that keeps microorganisms out of the brain by surrounding blood vessels with tough tissue known as basement membrane. Only fat-soluble antioxidants pass easily into the brain, but these antioxidants don’t travel well through the watery bloodstream. You can take lots of antioxidants, but very little will actually reach the brain. Except, it turns out, for an antioxidant called curcumin. It is one of the few antioxidant supplements that actually has an helpful effect on the brain changes that lead to Alzheimer’s disease.

What Curcumin Does for the Brain

Curcumin is the antioxidant pigment that gives turmeric powder its distinctive orange color. It has such a bright color that just a pinch of turmeric makes curry powder orange, and in turn, makes curries orange. Curcumin is also an especially strong antioxidant.

Scientists did not start off with the idea that curcumin could stabilize brain health. They began with the observation that countries where lots of curry is eaten tend to have relatively low rates of Alzheimer’s disease. There was a long research process that determined that it was the turmeric in curry that makes the difference in brain health, and more specifically it is the curcumin in the curry that actually reaches the brain and helps protect neurons from being coated with tangles of protein plaques.

Keep in mind that curcumin has a lot less to do if the brain at least occasionally gets a break from any overload of sugar and fatty acids through dietary restraint. But this is how curcumin works:

Tests with healthy volunteers have found that curcumin dissolves the proteins (known as beta-amyloid)⁶ that form tangles on neurons in the brain. The effect isn’t immediate, but in otherwise healthy people, taking 80 mg of “free” curcumin for 30 days dissolves on average 8% of the brain-destructive protein.
Taking curcumin for 30 days also lowers production of stress hormones (measured with a saliva test for an enzyme called salivary amylase). When there is less stress on the brain, it has more energy to repair itself.
In studies with mice (with which it is possible directly to observe changes in brain tissue after curcumin treatment), giving curcumin increased the brain’s production of an enzyme called synaptophysin. This enzyme helps the neurons in the brain form connections, allowing the brain to wire itself so that if one neuron is lost, another can take its place. Literally hundreds of billions of new connections can be formed in just weeks.
Also in studies with mice, curcumin stimulates activity in the glial cells, which break down the proteins that form the tangles that strangle neurons.

No one has run a clinical trial with hundreds of Alzheimer’s patients over a 3- or 4-year period to establish the usefulness of curcumin in the way that Dr. Luchsinger’s team has established the usefulness of dietary changes. But that is largely because scientists know from over 200 studies of curcumin in other clinical applications that there isn’t a downside to taking curcumin. It’s inexpensive, it almost never causes any side effects and those side effects are minor, and there is very clear understanding of how it can work.

How to Use Curcumin for Supporting Brain Health

The the question becomes, how much curcumin is enough, and what kind. In countries where curry is an everyday part of the diet, the turmeric in the curry sauce provides an average of 80 mg of curcumin per day. That’s the dosage that has been tested in clinical trials that found beneficial brain changes in human volunteers. It only takes a tiny amount of curcumin to make a big difference in brain health.

The makers of some curcumin products argue, with good reason, that the 80 mg of curcumin you take for brain health should be a specialized form that crosses the blood-brain barrier easily. However, the curcumin that hundreds of millions of people get from their curry every day also protects brain health, and it isn’t a special chemical known as “free” curcumin like the expensive brand promoted for brain health. But let’s suppose the makers of the specialized curcumin products have a point.

“Free” curcumin is simply curcumin that has not been chemically transformed by the liver. A percentage of curcumin from any product is always free. So instead of taking 80 mg of “free” curcumin per day, simply take 3,000 to 4,000 mg of any curcumin product per day. You will get the same result.

Just start taking curcumin now. The changes in the brain that eventually lead to Alzheimer’s, researchers believe, occur over a period of about 20 years. That gives you a very long lead time to do something positive for your brain. Dietary restraint, simply giving your brain a break from food at least twice a week (even if you eat extra after you skip those meals), makes a big difference. It enables your brain to make its own antioxidants. Then taking curcumin every day adds to the effect.

A clinical study of the safety of curcumin supplements⁷ conducted at the David Geffen School of Medicine at the University of California at Los Angeles found no ill effects when curcumin was taken for up to 24 weeks, except in 8% of volunteers who reported minor stomach upset and loose stools. Of course, whether loosening the stools is a problem or a benefit depends on the individual.

One Alzheimer’s disease has set in, research suggests, it may be possible to stop the formation of new plaques, but it is highly unlikely the brain will be able to grow new neurons. Once the damage has been done, curcumin and dietary restraint are likely just to slow down the disease or possibly stabilize it. The time to take curcumin is NOW, to protect your brain to keep your cognitive faculties the rest of your life.

If You Want An Added Layer of Protection

Would you feel better if you took something in addition to curcumin? The best evidence is for taking fish oil and resveratrol.

Fish oil is anti-inflammatory, but in preventing the progression of Alzheimer’s disease its main use if in controlling triglycerides. These are the storage form of excess calories from either sugars or fat, which form a literal “goo” on neurons in the brain. The omega-3 essential fatty acids in fish oil lower triglyceride concentrations in the bloodstream. As little as 360 mg of omega-3′s (typically found in about 1,000 mg of fish oil) per day is enough to make a difference.

The other helpful supplement is resveratrol. Despite the enthusiasm about resveratrol, it has not been as well tested as curcumin. However, scientists know that it amplifies the anti-plaque effects of curcumin and many believe that it amplifies the effects of curcumin for keeping the brain young. An appropriate dosage is at least 20 mg up to 250 mg per day. Resveratrol is found in red wine, but you can’t drink enough red wine to get enough resveratrol to make a difference. You have to take the supplement.

Still want to do more? Dr. Luchsinger’s latest line of research has investigated the role of exercise in slowing down Alzheimer’s. Getting even light exercise, the equivalent of walking 10 minutes a day, Luchsinger and associates have found, extends life an average of 5. 5 years. Getting 30 minutes of easy exercise every day, the equivalent of walking slowly for a mile (about 1-1/2 km), slows down the disease by an average of 8 years.

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