Marc Joseph Nutrition - Blog

In a five-year study published in the top journal Neurology, researchers found that individuals who developed mild cognitive impairment (MCI) or Alzheimer’s disease had observable changes in brain structure long before the onset of cognitive decline.

Compared to the group that didn’t develop memory problems, the 23 people who developed MCI or Alzheimer’s disease had less gray matter in key memory processing areas of their brains even at the beginning of the study when they were cognitively normal.

“We found that changes in brain structure are present in clinically normal people an average of four years before MCI diagnosis,” said study author Charles D. Smith, MD, with the University of Kentucky Medical Center in Lexington and member of the American Academy of Neurology. “We knew that people with MCI or Alzheimer’s disease had less brain volume, but before now we didn’t know if these brain structure changes existed, and to what degree, before memory loss begins.”

The findings are definitely interesting, but not too surprising. As shown in the video below, it is known that exposing nerve cells to toxins may lead to damage consistent with that observed in Alzheimer’s disease:

How Mercury causes Neurodegeneration (brain degeneration)

Toxin exposure is, of course, not the only potential cause of cognitive decline. Nutritional deficiencies, stress, genetics, and other factors may also be involved.

Waiting Not a Good Option

As someone who experienced and recovered from MCI at a relatively young age, I can’t emphasize enough the importance of not ignoring minor cognitive changes (e.g., ability to think, focus, remember). MCI and Alzheimer’s disease are NOT a normal part of aging.

Each person has an internal reference point to their own cognitive abilities and usually is capable of recognizing changes in function long before friends, family, and co-workers may be aware there is an issue. It’s important to be self-aware and try to compare your current capabilities with where they’ve been and where you’d like them to be.

As this study suggests, if you suspect a decline in cognitive function, the time to act is now, as such change may be preceded by years of structural changes.

There are many preventive and therapeutic steps that may help prevent, slow, and possibly even help to reverse the development of conditions like MCI and AD. You can read an overview of my approach to helping people here. Diet, supplementation, lifestyle changes, and in some cases, low/frequent-dose chelation, may each play a role.

Cognitive decline is not inevitable. Don’t believe anyone who says it is.

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Discover How Nutrition Can Make a Difference in Your Life …

Marc Joseph Nutrition

From a recent US News & World Report cover story:

[P]erhaps as many as 640,000–under the age of 65…have dementia, the vicious thief of minds that steals memories, personality, relationships, language, and ultimately the ability to function as a human being.

“In the last five years, more younger people have been showing up at support group meetings and in doctors’ offices, asking for help, and we realized this is something we need to start taking seriously,” says neurologist Ronald Petersen, an Alzheimer’s and memory disorders specialist at the Mayo Clinic. It afflicts people in their 50s, their 40s, and even in their 30s. “Alzheimer’s is not just a disease that hits 80-year-olds in nursing homes,” says Dallas Anderson, a specialist in the epidemiology of dementia at the National Institute on Aging…

…”Nationally,” says Pierre Tariot, director of the Memory Disorders Clinic at the Banner Alzheimer’s Institute in Phoenix, “there’s not enough help for younger people with dementia–or older people.”

This growth in cases is clearly a significant challenge and a potential crisis, both in human and financial terms, if steps aren’t taken to proactively address it.

The official name for the early development of AD is “early-onset dementia.” The national Alzheimer’s Association acknowledged in a report earlier this year that it’s becoming a widespread problem:

Early Onset Dementia: A National Challenge, a Future Crisis

Younger afflicted individuals face complicated issues that older people don’t necessarily encounter:

In the years before they are diagnosed with the disease, younger people may fail at and lose their jobs, leaving their families in financial hardship and having to wait years before qualifying for disability or Social Security. After diagnosis, Schneider says, “friends and employers sometimes turn away from us, like they’re afraid they might catch the disease.”

The key questions are:

1. What is causing this increase in dementia cases among younger people?
2. What can be done to prevent the condition and/or slow its progression into AD?

Potential Causes

Regarding the first question, the answer is very complex, as there are likely multiple potential causes, both genetic and environmental. As noted in the US News article, however, the condition is likely more than genetics:

Scientists studying the genes of younger patients have found three mutations that seem to make some susceptible to the disease. But these genes don’t explain most of the cases, says John Morris, director of the Alzheimer’s Disease Research Center at Washington University in St. Louis.

What’s disappointing about the US News article is that it doesn’t emphasize the potential environmental factors, such as diet and environmental toxin exposure, that likely account for the majority of the increase in dementia cases.

Instead, the article paints a dire picture of a “progressive and incurable brain disease” that can currently primarily be treated with drugs that act as ineffective patches:

No one is truly happy with the current crop of drugs approved in the United States for the treatment of Alzheimer’s. Their names–Aricept, Cognex, Exelon, Razadyne, and Namenda–are familiar to anyone who cares for a dementia patient. “What all these drugs have in common is they act on the symptoms, not the underlying disease,” says John Morris, director of the Alzheimer’s Disease Research Center at Washington University in St. Louis. They boost chemicals that help the brain form memories, but “they don’t help a lot.”

The article does mention that new drugs are in development that may more directly address the condition. However, the drugs mentioned are focused on halting the development of beta-amyloid plaques. For years this area has been the primary focus of pharmaco AD research.

Now, though, the AD community is publicly acknowledging that there is likely much more to the picture. Many researchers have emphasized the importance of looking at potential upstream causes of plaque development, but have not gotten their ideas published. That focus may be changing, as this recent Wall Street Journal article noted:

[The] “there is more to” [AD than beta-amyloid plaques] statement. It is the focus of a paper in the October issue of the journal Alzheimer’s & Dementia reporting on a “research roundtable” convened by the private, nonprofit Alzheimer’s Association…

…[W]hen you think about it, concluding that B-amyloid and plaques cause Alzheimer’s is like believing a scab on your knee causes pain. The scab is the body’s response to an earlier injury. Similarly, there is evidence that amyloid plaques don’t cause Alzheimer’s.

To be fair, the online version of the US News article does include links to more about AD and potential treatments, and these links do mention the importance of pursuing diet and lifestyle habits that are good for the heart, as they are also likely helpful for brain health. But, the focus of the hardcopy article is on the drugs mentioned above, as well as on other palliative care steps, like using Post-It notes and computers to keep track of things.

Familiar Symptoms

It was interesting to read the story of one of the people with early-onset AD profiled in the article:

[H]e got weak and bedridden, sick with what turned out to be a wheat, or gluten, allergy. The next year, he was diagnosed with diabetes and started taking pills and insulin shots. But this was different. “My coordination and balance were off,” he says. “I had trouble hitting a light switch when I reached out for it. I found that I really had to concentrate on all my movements.” Over the next two years, memory troubles became more apparent…His major complaint is a lack of focus.

Wheat & gluten allergies? Poor blood sugar regulation? Coordination and balance problems? Progressive memory decline? Lack of focus?

And other AD symptoms from the US News story’s online resources:

• Problems with language.
• Disorientation and confusion.
• Inability to follow directions.
• Poor or decreased judgment.
• Problems with abstract thinking.
• Changes in mood and behavior.
• Changes in personality.
• Social withdrawal.

Gee, is there another condition with similar symptoms?

Hmmm, say one like…autism?

Could heavy metals, which are implicated in autism, also be playing a role in the development of dementia and Alzheimer’s disease?

Researchers have taken a look at the role of heavy metals in AD in a recent issue of the Journal of AD. Unfortunately, the focus of this research summary is on aluminum, iron, and metals other than mercury.

Yet, mercury poisoning symptoms closely mirror those of autism, mercury exposure produces brain lesions similar to those observed in AD, and mercury induces the formation of beta-amyloid and tau tangles (both commonly observed in AD) in neuroblastoma cells.

The question is: Why hasn’t more research been done to look at mercury as a potential contributory factor in the development of dementia and AD?

Could it be because the primary exposures to mercury are from amalgam fillings, vaccines, seafood, and emissions from coal power, chlorine, and cement plants? What role have interests representing these groups played in slowing and/or suppressing further research in this area?

What to Do

While we wait for answers to these questions, I think that anyone who is experiencing early-onset dementia would be making a big mistake to not explore whether heavy metals may be playing a role.

Unfortunately, there is no laboratory test for measuring heavy metals in the brain (if only it were so easy). Most doctors will run a blood or urine test to check for heavy metal poisoning. But knowledgeable practitioners know such tests are relatively worthless for measuring long-term, chronic exposure to heavy metals and current levels in various tissues of the body.

A hair test is the best bet for identifying potential heavy metal toxicities. And even this test, when done, is often interpreted incorrectly. (Hint: Low mercury levels don’t necessarily mean no toxicity. In fact, they could mean high toxicity.)

It’s important to work with someone who is familiar with:

• What test/s to run & how to correctly interpret them
• What to do if the test/s suggest metal toxicity, e.g.:
  • Safely remove existing exposures (e.g., amalgams)
  • Provide nutritional support
  • Safely reduce existing heavy metal levels using low, frequent-dose chelation.
  • Address existing chronic infections (e.g., fungal, viral)
  • Support endocrine function (thyroid, adrenals)

In my nutrition consulting practice, I am very familiar with this approach. In fact, I used it myself to fully recover from mercury poisoning and symptoms that, coincidentally, closely mirrored those of both autism and Alzheimer’s disease.

I was in my mid-30s when that occurred. The word “incurable” never entered my mind. If dementia begins to affect you or people you know, I hope that you won’t accept such a label and will instead work with a knowledgeable practitioner to take a close look as to whether heavy metal toxicity may be playing a role.

(Photos: Jeffrey MacMillan for US News & World Report)

New study (full text) out in the journal Archives of Internal Medicine that found that long-term supplementation of vitamin E in generally healthy older women did not significantly reduce the risk of cognitive decline.

But there may be more to the story.

Vitamin E is a powerful, fat-soluble antioxidant that helps to protect fatty substances in the body, such as cell membranes, nerve cells, lipoproteins, etc. Since oxidative stress is commonly observed in neurodegenerative diseases (e.g., Alzheimer’s) at even the earliest stages of the disease process, the thinking is that antioxidants such as vitamin E may help to reduce the onset and/or progression of the conditions.

There are actually eight forms of vitamin E: 4 tocopherols (alpha, beta, delta, gamma) and 4 tocotrienols (alpha, beta, delta, gamma). This study only used the alpha-tocopherol form of vitamin E. In earlier studies looking at vitamin E and cognitive decline, discussion regarding the type of vitamin E used has rarely been included. However, the authors of this study did raise this point (as did an editorial that accompanied the article):

It has been suggested that tocopherols such as {gamma}-tocopherol that is found in foods rather than in supplements* may be more important for delaying brain aging. Although {alpha}-tocopherol has stronger antioxidant properties, {gamma}-tocopherol has important additional anti-inflammatory effects that may enhance neuroprotection.

(* Broad-based vitamin E supplements containing gamma-tocopherol definitely are widely available. Well, at least the authors mentioned the issue.)

Also, recent research suggests that high amounts of alpha-tocopherol
may actually deplete gamma-tocopherol levels in the body. Given this potential, as well as gamma-tocopherol’s unique anti-inflammatory and antioxidant properties (e.g., its ability to inhibit cyclooxygenase and neutralize reactive nitrogen species — the latter especially relevant in protecting nervous system cells), it seems to make more sense to study the effects of a more balanced form of vitamin E on cognitive decline.

Other potential reasons why a beneficial result may have not been observed in this study:

• The dose given (600 IU, every other day) may have been too low.
• The supplements may not have been regularly taken with meals containing fat. Vitamin E is a fat-soluble vitamin and is not well absorbed unless taken with adequate amounts of fat.
• The timing of the initiation and length of the study may have been sub-optimal. Participants in this study were enrolled in their 60’s and given supplements for 10 years. Better results may have been observed if supplementation was started earlier in life and for a longer period.
• Approximately 1/4 of the study participants didn’t comply with the supplementation guidelines, and were thus excluded from the study results.

What would really be interesting to learn going forward is what neuroprotective effects may be offered by more balanced forms of vitamin E given to younger participants in moderate amounts and with meals containing fat. Such an interventional study would obviously take many years to perform in humans. Animal (e.g., mice) studies, although less conclusive, could be performed in the near-term.

Hopefully we’ll continue to see research done in this area, as early intervention is likely the best bet for heading off the progression of cognitive decline into more severe conditions such as Alzheimer’s disease.

A couple of more studies just released that again suggest omega fatty acids may be helpful in slowing cognitive decline:

Omega-3 fatty acid treatment in 174 patients with mild to moderate Alzheimer disease

This study found that patients with very mild Alzheimer’s disease (AD) who supplemented with omega-3 fatty acids (2.3 g/day)experienced significantly slower rates of decline in mental function. However, individuals with mild to moderate AD didn’t improve.

This result reinforces the importance of early intervention and prevention. Once damage to the brain is significant (as seen in moderate cases of AD), a single helpful nutrient like omega-3 fats, although not detrimental, is likely to not necessarily lead to great improvement.

Dietary supplementation of arachidonic and docosahexaenoic acids improves cognitive dysfunction.

Arachidonic acid is an omega-6 fat, while docosahexaenoic acid (or DHA) is an omega-3 fat. Most people get plenty of omega-6 fats in the diet, as they are found in high quantities in vegetable oils used in processed and restaurant-prepared foods. Arachidonic acid (ARA) is also found in high amounts in red meat and egg yolks. On the other hand, most people are deficient in omega-3 fats, such as DHA and eicosapentaenoic acid (EPA), which are found in fish oil.

This second study found that individuals with mild cognitive impairment who supplemented with only 240 mg of ARA and DHA experienced improvements in both immediate memory and attention scores. As in the earlier study, no improvement was seen in individuals who had already developed AD.

For omega-3 fats DHA & EPA, it’s important to make sure that the source (fish or supplements) is low in contaminants, such as heavy metals and PCBs. Tested fish oil supplements are your best bet there.

You can learn more about the important roles of omega-3 fats in disease prevention and treatment here.

And, you can learn more about ways to preserve and improve cognitive function here.

A recent study in the Journal of Gerontology took a look at the potential protective effect of beta-carotene in people with Alzheimer’s disease (AD). The researchers found that those individuals with a specific genotype known to be associated with greater risk of developing AD had a significantly reduced risk of cognitive decline if serum beta-carotene levels were kept high.

Earlier studies have identified that people who have blood lipoproteins of the apoE4 genetic type are at greater risk of developing early-onset AD. Lipoproteins are molecules that help transport fats and cholesterol through the blood. There are three types of these particular lipoproteins: apoE2, apoE3, and apoE4.

Each person has two copies of the gene that codes for this lipoprotein, one from the mother and one from the father. If both copies of the gene code for apoE4, then one is considered homozygous for that trait. If only one of the parents’ genes code for it, then one is considered heterozygous for that trait. Those at highest risk are individuals who are homozygous for apoE4.

More on the different gene types here:

• ApoE4 is associated with a higher risk of Alzheimer’s. About a quarter of the population inherits one copy of the ApoE4 gene, which increases their risk of developing Alzheimer’s disease by up to four times.
• Two per cent of the population get a ‘double dose’ of the ApoE4 gene, one from each parent. Their risk of developing Alzheimer’s disease is increased by about ten times.
• Sixty per cent of the population have a ‘double dose’ of the ApoE3 gene and are at ‘average risk’. About half of this group develop Alzheimer’s disease by their late 80s.
• ApoE2 is least associated with Alzheimer’s disease. One in six people carry it. People with one ApoE2 gene and one ApoE3 gene (11 per cent of the population) have a 50 per cent chance of getting Alzheimer’s disease when they reach their late 90s.
• One in 200 people inherit two copies of the ApoE2 gene and are at a lower risk of developing Alzheimer’s disease.

The researchers in the beta-carotene study found that in those individuals who were either hetero- or homozygous for apoE4, high serum levels of beta-carotene reduced the risk of cognitive decline by 89%. Little effect (11% risk reduction) was observed in people with no apoE4.

The researchers hypothesize that the beta-carotene may help to reduce the oxidative stress and resulting tissue damage that is observed with the build-up of beta-amyloid plaque deposits in AD brains. Also, there is research that suggests that people with the apoE4 form of the gene are less able to prevent the buildup of the plaque deposits observed in AD.

Another hypothesis as to why people with apoE4 are at higher risk is that a primary difference between the three lipoprotein types is the number of cysteine amino acids in the lipoprotein’s amino acid chain. apoE2 has two cysteine amino acids, apoE3 has one, and apoE4 has none. Cysteine is a sulfur-containing amino acid. Mercury has a high affinity for sulfur. The absence of cysteine in the apoE4 form of the lipoprotein may make individuals with this form less able to remove heavy metals from the bloodstream and more susceptible to toxin exposure.

Regardless of the mechanism, antioxidants such as beta-carotene, seem to play an important role in helping to manage the oxidative stress observed in AD.

An announcement that didn’t make the major newspaper headlines, but is nevertheless big news. Researchers at the Linus Pauling Institute at Oregon State University (OSU) have discovered a new technique that allows them to observe and accurately measure the level of a key oxidant (superoxide) in animal cells.

Prior to this, there was no direct and accurate way to measure superoxide or its origin from the two places that produce it, the cell’s cytosol or mitochondria. Now there is.

With the new system developed at OSU, researchers can use a fluorescent microscope, a fairly standard laboratory tool, to actually see levels of superoxide and observe changes as experiments are performed with living cells.

Oxidation is a process that occurs naturally in the body — for example, in cell energy production and some immune reactions. As a result of the process, unstable atoms and molecules (e.g., free radicals such as superoxide) can be formed.

The body produces substances (e.g., glutathione, superoxide dismutase, catalase) that help to stabilize these atoms and molecules and prevent excessive damage and inflammation. We also take in anti-oxidants through our diet, in the form of different nutrients such as vitamins C and E, that help to neutralize these free radicals.

When these free radicals accumulate, cell structures can be damaged. This damage is believed to play an important role in many degenerative diseases, including ALS, Parkinson’s, Alzheimer’s, heart disease, hypertension, diabetes, and more.

The discovery of this technique will help researchers better understand what’s really happening in cells, as well as the effects of different potential treatments, and should help to speed research in many diseases. It’s definitely good news.

A new review study to be published in an upcoming issue of The Lancet notes that there are over 200 industrial chemicals that may damage the human brain, yet most are neither examined for potential effects on the developing brain nor tightly regulated. With one out of every six children now affected by a developmental disorder, the stakes are high.

As one of the study’s authors notes: “We must make protection of the young brain a paramount goal of public health protection. You have only one chance to develop a brain.”

This article does a good job of summarizing the study’s important points:

Few chemicals are assessed for neurotoxicity in the developing brain:

The authors then examined the published literature on the only five substances on the list–lead, methylmercury, arsenic, PCBs and toluene–that had sufficient documentation of toxicity to the developing human brain in order to analyze how that toxicity had been first recognized and how it led to control of exposure…the number of chemicals that can cause neurotoxicity in laboratory animal tests exceeds 1,000

The toxicity issue is most critical for children:

A developing brain is much more susceptible to the toxic effects of chemicals than an adult brain. During development, the brain undergoes a highly complex series of processes at different stages. An interference–for example, from toxic substances–that disrupts those processes, can have permanent consequences. That vulnerability lasts from fetal development through infancy and childhood to adolescence. Research has shown that environmental toxicants, such as lead or mercury, at low levels of exposure can have subclinical effects–not clinically visible, but still important adverse effects, such as decreases in intelligence or changes in behavior.

The impact is significant, both in terms of people and dollars:

[Researchers] conclude that industrial chemicals are responsible for what they call a silent pandemic that has caused impaired brain development in millions of children worldwide. It is silent because the subclinical effects of individual toxic chemicals are not apparent in available health statistics. To point out the subclinical risk to large populations, the authors note that virtually all children born in industrialized countries between 1960 and 1980 were exposed to lead from petrol, which may have reduced IQ scores above 130 (considered superior intelligence) by more than half and increased the number of scores less than 70. Today, it’s estimated that the economic costs of lead poisoning in U.S. children are $43 billion annually; for methylmercury toxicity, $8.7 billion each year.

What can be done?

The study’s authors have four recommendations:

1. Document chemicals that have caused toxic effects on the nervous system in humans to facilitate targeted preventive action against releases of these chemicals;
2. Document human exposures to neurotoxic chemicals and identification of subgroups at risk due to residence, occupation, diet, and other factors;
3. Research the consequences of developmental exposures to neurotoxic chemicals to expand our understanding of the long-term consequences of such exposures; and
4. Screen for neurotoxicity of commonly used chemicals to identify those that may present a hazard to brain development.

But they mention that these actions are expensive and will likely not be taken soon.

In the meantime, there are steps that individuals can take to protect themselves and their own children, including:

• Drinking filtered water
• Avoiding produce that is high in pesticides
• Reducing the use of harmful cleaning products in the home
• Selecting safer personal care products
• Having your residence tested for lead if it was built prior to 1978, and having lead paint professionally sealed and/or replaced
• Avoiding mercury in fish, amalgams, and vaccines

And for people who suspect toxin exposure may be an issue for either themselves, their own children, or future planned children, there are also other actions that can be taken.

Curcumin, the yellow pigment found in tumeric, a common ingredient in curry, may help to protect against cognitive decline and slow the development of Alzheimer’s disease (AD).

There’s been quite a bit of research done the past few years regarding the potential connection. Two recent studies reinforce that link.

The first study looked cognitive performance and curry consumption in older, non-demented Asian individuals (aged 60-93 years). Researchers found that those who ate curry occasionally or frequently scored significantly better on a standardized mental health test. Those people who consumed curry often or very frequently had a 49% reduced risk of cognitive impairment, while those consuming it occasionally had a 38% decreased risk.

The study was observational, so cause and effect could not be determined (there may have been other factors playing a role — e.g., vegetable and fat intake), but the results are consistent with earlier experimental evidence on curry.

The second recent study found that immune system cells (macrophages) in blood drawn from AD patients were able to break down beta-amyloid plaques (found in the brains of AD patients) significantly better when treated with curcumin.

This study was a lab study (i.e., the test were done on the blood samples in petri dishes), but nevertheless the results were consistent with earlier research examining the effects of curcumin on immune system function.

Finally, this review study provides a good overview of curcumin’s suspected biochemical benefits in diseases such as AD, as well as for other conditions, such as cancer, heart disease, inflammatory digestive disorders, arthritis, and osteoporosis. In short, curcumin seems to have an excellent ability to regulate proteins, enzymes, and other factors that manage immune system response.

Curcumin certainly seems like a safe and important substance to potentially help prevent and treat many chronic conditions.

(Note: If you’re considering increasing tumeric intake by eating restaurant prepared curries, it’s important to consider the type and and amounts of fats used in their preparation. Restaurant-prepared curries can often be high in fats, especially saturated fats (like ghee, or clarified butter, and vegetable oil). In high amounts, these fats may counteract some of the curry’s beneficial effects by promoting elevated cholesterol and/or inflammation. Try to identify restaurants that use moderate amounts of these fats and/or other more healthy alternatives, such as olive oil.)

Calorie-restriction has been highlighted as a way to slow the aging process in general. Recent research looks at the potential for calorie-restriction to slow the progression of Alzheimer’s Disease (AD).

The researchers fed mice bred to develop AD a reduced-calorie diet (mostly through the reduction of carbohydrate intake), and found that the mice had fewer disease symptoms and better memories than the control group fed a regular-calorie diet.

In a separate study, the same researchers applied SIRT1, one of the sirtuin proteins with increased expression seen in calorie restriction and believed to play an important role in slowing aging, into the nerve cells affected by AD. They found that SIRT1 helped to prevent the cleavage of beta-amyloid precursor molecules, which, in turn, slowed the formation of plaques.

So, calorie-restriction (with adequate nutrition) may be one way to help slow the progression of aging and cognitive decline. Other potential approaches to preserving cognitive function are discussed here.

This recent NY Times article discusses the increasing evidence of a greater risk of Alzheimer’s disease (AD), perhaps as much as double, for individuals with diabetes.

The relationship may be related to vascular damage observed in each condition. Other similarities and factors, such as:

• the build-up of amyloid plaque in both the brain in AD and the pancreas (which secretes insulin to manage blood sugar levels) in diabetes
• higher insulin levels leading to inflammation in the blood vessels & brain, and possibly even contributing to increased amyloid plaque formation

As summarized by the Alzheimer’s Association, the numbers and potential impact on society are breathtaking:

Alzheimer’s affects 1 in 10 people over age 65, and nearly half of people over 85. About 4.5 million Americans have it, and taking care of them costs $100 billion a year, according to the association. The number of patients is expected to grow, possibly reaching 11.3 million to 16 million by 2050, the association said.

And those numbers don’t include the potential increase from diabetes.

With diabetes rates skyrocketing:

• ~20M people with Type 2 diabetes in the U.S. — double the number of ten years ago
• ~40M people in the U.S. with “pre-diabetes,” or elevated blood sugar
• ~230M people worldwide with Type 2 diabetes — up from 20M twenty years ago

it’s easy to see why a neurology professor quoted in the article says, “Alzheimer’s is going to swamp the health care system.”

Whether cognitive decline is brought on by Alzheimer’s, vascular disease, diabetes, environmental toxicity, or a combination of the conditions, what is clear is the importance of preventive measures and acting early to head off potential problems. The links above provide overviews of actions that can be taken to do just that.