By Dr. Mercola
According to the U.S. Centers for Disease Control and Prevention (CDC),1 an estimated 5.4 million Americans are living with Alzheimer’s disease, the incidence of which increases as you age and doubles every five years beyond age 65. The National Institute on Aging2,3 suggests Alzheimer’s is the third leading cause of death for older people, falling behind heart disease and cancer. Currently, there is no cure for this irreversible, progressive brain condition.
Due to the seriousness of Alzheimer’s, you’d be wise to proactively address any areas that may be putting you at risk for developing the disease. I’d like to discuss several lifestyle factors that have been linked to this condition, as well as share some healthy prevention tips, in hopes you will take action now to ensure you or someone you love will not become an Alzheimer’s statistic. First, let’s take a look at some genetic links to the disease and recent news on gene research.
The Genetic Links to Alzheimer’s Disease
In the featured video, Dr. Dale Bredesen, director of neurodegenerative disease research at the University of California, Los Angeles (UCLA) School of Medicine, and author of “The End of Alzheimer’s: The First Program to Prevent and Reverse Cognitive Decline,” suggests Alzheimer’s is a trillion-dollar global health problem that strikes about 15 percent of the population, making it incredibly common.
He goes on to assert you have the pathophysiology of the disease for about 20 years before the diagnosis is made. By age 85, says Bredesen, nearly half of all people are affected by Alzheimer’s. Bredesen’s breakthrough program is known as ReCODE and later in this article I’ll share more about how it can effectively help you reverse Alzheimer’s. For now, as you may know, the apolipoprotein (ApoE) gene has long been embraced as one of the most important genetic risk factors for Alzheimer’s disease.
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Everyone inherits a form of APOE from their parents — either type E2, E3 or E4. Bredesen affirms the common belief that genetic predisposition plays a role, noting an estimated 75 million Americans have the single allele for the problematic ApoE4 (E4) gene, which gives them a 30 percent lifetime risk of developing the disease. Approximately 7 million have two copies of that gene, putting them at a 50 percent lifetime risk. About ApoE, Medical News Today says:4
“Normally, ApoE’s role is to provide instructions for creating the protein of the same name. In combination with fats, ApoE creates lipoproteins, which help transport and regulate levels of cholesterol throughout your bloodstream. However, the E4 version of the gene seems to be particularly damaging to the brain, with several studies showing that this genetic variant increases the risk of toxic beta-amyloid and tau buildup.”
Scientists Identify How E4 Raises Alzheimer’s Disease Risk
Given the genetic links to this disease, in a 2018 study published in the journal Nature Medicine,5 researchers from the Gladstone Institutes in San Francisco, California, sought to find out why the E4 variant was more harmful than the other variants, such as E3, and if anything could be done to correct the faulty gene.
In particular, the researchers investigated whether E4 was causing E3 to lose function or if the presence of more E4 led to the toxic effects. Dr. Yadong Huang, professor of neurology and pathology at the University of California, San Francisco, said in a news release:6
“It’s fundamentally important to address this question because it changes how you treat the problem. If the damage is caused due to the loss of a protein’s function, you would want to increase protein levels to supplement those functions. But if the accumulation of a protein leads to a toxic function, you want to lower production of the protein to block its detrimental effect.”
Another one of the issues Huang and his colleagues hoped to address in their research was the disconnect between the promising results shown through experiments involving lab mice and the subsequent lack of efficacy when the same methods have been applied to human trials. Huang said:7
“Drug development for Alzheimer’s disease has been largely a disappointment over the past 10 years. Many drugs work beautifully in a mouse model, but so far they’ve all failed in clinical trials. One concern within the field has been how poorly these mouse models really mimic human disease.”
Researchers ‘Fix’ E4 Gene Variant, Paving the Way for Potential Alzheimer’s Treatment
Applying stem cell technology to skin cells of Alzheimer’s sufferers possessing two copies of the E4 gene, Huang and his team created neurons. Also using skin cells, they created brain cells from healthy people who had two copies of the E3 gene. When compared to E3, the scientists noticed E4 had a pathogenic structure, which impeded its ability to properly function in the neurons, resulting in disease-causing problems.
The researchers noted the E4 gene variant was associated with increased tau phosphorylation and beta-amyloid production only in human, but not mouse, neurons. “Increased amyloid beta production is not seen in mouse neurons and could potentially explain some of the discrepancies between mice and humans regarding drug efficacy. This will be very important information for future drug development,” said Chengzhong Wang, Ph.D., who was one of the study authors and a former research scientist at Gladstone.
Further, when neurons that did not produce E3 or E4 were compared to neurons with added E4, only the latter group displayed Alzheimer’s-like changes, confirming that the presence of more E4 led to the toxic effects. One final step of the research involved treating E4-expressing neurons with a small-molecule structure corrector, which the scientists found useful to correct the defects and encourage E4 to behave more like the innocuous E3 variant.
Notably, this process eliminated Alzheimer’s pathology, restored normal cell function and helped brain cells to live longer.8 With further testing, it’s possible the structure corrector could prove to be a promising therapeutic approach to treating Alzheimer’s disease. While you are waiting for these types of scientific advances to transform the handling of active cases, let’s turn our attention to some of the lifestyle factors that may fuel your risk of Alzheimer’s.
If you are middle-age or younger, you still have some opportunity to make positive changes now that can help reduce your likelihood of having to deal with Alzheimer’s later. In fact, even if you’re already in your golden years, making the following changes will still be beneficial for your brain health.
High Sugar Diet and Diabetes Have Been Linked to Alzheimer’s
While insulin is usually associated with its role in keeping your blood-sugar levels in a healthy range, it also plays a role in brain signaling. In one animal study, when researchers disrupted the proper signaling of insulin in the brain, they were able to induce many of the characteristic brain changes seen with Alzheimer’s disease, including confusion, disorientation and the inability to learn and remember.9
It’s becoming increasingly clear that the same pathological process that leads to insulin and leptin resistance, as well as Type 2 diabetes, may also hold true for your brain. As you overindulge on grains and sugar, your brain becomes overwhelmed by the consistently high levels of insulin. Eventually your insulin and leptin signaling become profoundly disrupted, leading to impairments in your cognitive abilities and memory.
A study published in the American Diabetes Association’s journal Diabetes Care found that Type 2 diabetes is associated with a 60 percent increased risk of dementia.10 Research featured in The New England Journal of Medicine noted a mild elevation of blood sugar, such as a level of 105 or 110, is also associated with an elevated risk for dementia.11
A 2012 study published in the Journal of Alzheimer’s Disease12 revealed high-carb diets increase your risk of dementia by a whopping 89 percent, whereas high-fat diets lower it by 44 percent. The researchers stated, “A dietary pattern with relatively high caloric intake from carbohydrates and low caloric intake from fat and proteins may increase the risk of mild cognitive impairment or dementia in elderly persons.”
This connection between high-sugar diets and Alzheimer’s was again highlighted in a longitudinal study published in the journal Diabetologia13 in early 2018. Based on a series of assessments completed during the 10-year follow-up period, researchers noted the higher an individual’s blood sugar, the faster their rate of cognitive decline. The connection between high blood sugar and Alzheimer’s is why the disease has sometimes been dubbed “Type 3 diabetes.”
Lack of Sleep Damages Your Brain and Promotes Alzheimer’s
Studies linking poor sleep and beta-amyloid buildup as risk factors for Alzheimer’s disease continue to emerge. Earlier studies, involving lab mice, such as a 2013 body of research published in the journal Science,14 discovered your brain’s cells are reduced by up to 60 percent while you sleep, making it easier to flush away this cellular waste.
New research funded by the National Institutes of Health (NIH),15,16,17 used positron emission tomography (PET) to show that acute sleep deprivation impacts beta-amyloid buildup in human brain regions that have been implicated in Alzheimer’s disease. The study, involving 20 human participants, suggests your brain accumulates beta-amyloid deposits after just a single night of sleep deprivation. Said the study authors:
“We show that one night of sleep deprivation, relative to baseline, resulted in a significant increase in beta-amyloid burden in the right hippocampus and thalamus. These increases were associated with mood worsening following sleep deprivation but were not related to the genetic risk (ApoE genotype) for Alzheimer’s disease.”
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By pumping cerebral spinal fluid through your brain’s tissues, your body’s glymphatic system flushes waste from your brain back into your circulatory system and to your liver for elimination. Unfortunately, as highlighted in the NIH study, if you do not get enough sleep, the damaging plaques will build up.
Over time, they attack and degrade certain regions of your brain. As such, a brain affected by Alzheimer’s has lost most of its ability to remove the beta-amyloid waste products, mainly because it is caught in a vicious cycle: more amyloid, less deep sleep; less deep sleep, more amyloid.
Persistent patterns of poor sleep may actually be an early indicator of amyloid buildup, which could be causing very subtle brain changes well before disease develops. The latest sleep guidelines suggest most adults need about seven to nine hours of sleep a night, and children and teens need even more.
Prolonged Sitting Linked to Memory Problems in Middle-Age and Older Adults
A 2018 study published in PLOS One18 links too much sitting with memory problems in middle-age and older adults. Using high-resolution magnetic resonance imaging (MRI) on a group of 35 middle-age and older adults, researchers from UCLA noticed brain thinning in the medial temporal lobe, a brain region involved in the formation of new memories. The group was also evaluated for their levels of physical activity and daily time spent sitting.
Brain thinning can be a sign of cognitive decline and dementia in adults of middle-age and older. In addition to undergoing MRIs, participants were assessed according to their physical activity level and average number of hours per day they spent sitting during the previous week. Most participants said they sat an average of three to seven hours a day. Given this data, researchers concluded “that sitting for extended periods of time was closely associated with thinning in the medial temporal lobe.”19
I wonder if the study participants may have somewhat underreported their hours of sitting. After all, it is well-known that American adults spend an average of nine to 10 hours sitting each day. This level of inactivity cannot possibly be offset by even a daily 30- or 60-minute workout. To learn more about the negative effects of too much sitting, check out my article Sitting Too Much Ages You by 8 Years.
More Alzheimer’s Protection: Lutein, Zeaxanthin and Vitamin D
While there are many others I could mention, you may want to add the following nutrients and herbs to your diet to protect your brain against Alzheimer’s disease:
• Lutein and Zeaxanthin: In two separate yearlong, double-blind, placebo-controlled trials,20,21 researchers administering 10 milligrams (mg) of lutein plus 2 mg of zeaxanthin daily, or a placebo, noted significant improvements in macular pigment optical density (MPOD) and cognitive function in those receiving the supplements.
• Rosemary and Spearmint: A 2013 study22 conducted at the Saint Louis University School of Medicine with lab mice suggests the antioxidant extracts from these herbs improve learning and memory and reduce oxidative stress. “We found that these proprietary compounds reduce deficits caused by mild cognitive impairment, which can be a precursor to Alzheimer’s disease,” said Susan Farr, Ph.D., research professor geriatrics at Saint Louis University School of Medicine.
• Vitamin D: Not only does sufficient vitamin D help your immune system combat inflammation associated with Alzheimer’s, research shows seniors with a severe vitamin D deficiency may raise their risk for dementia by 125 percent.23 Furthermore, a vitamin D deficiency is associated with a substantially increased risk of all-cause dementia and Alzheimer’s disease.
The optimal vitamin D level for general health and disease prevention ranges between 60 to 80 nanograms per milliliter. If you are not able to receive regular sun exposure, you will want to take an oral vitamin D3 supplement along with vitamin K2 and magnesium.
Additional Lifestyle Strategies to Build a Healthier Brain
While you may think your brain is “programmed” to shrink and fail as a result of aging, the truth is you can build a disease-resilient brain through your daily choices, starting today. Lifestyle strategies that promote neurogenesis and regrowth of your brain cells include the following:
- Consider intermittent fasting, especially if you are insulin resistant, and adopt a ketogenic diet, the benefits of which I will discuss further below
- Get regular exercise, because physical activity produces biochemical changes that strengthen and renew your body and your brain — particularly the areas associated with learning and memory
- Increase your intake of brain-boosting foods, including healthy fat because fat is a great energy source for your brain (and so much better than sugar)
- Optimize your omega-3 fat intake and balance your omega-3 to omega-6 ratio; krill oil is an excellent choice because it also contains astaxanthin, which appears to be particularly beneficial for brain health
- Reduce your overall calorie consumption and particularly your carbohydrate consumption, including dramatically reducing (or eliminating) grains and sugar
ReCODE: A Powerful Strategy to Reverse Cognitive Decline
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While the prevalence of Alzheimer’s is rapidly increasing, the good news is you have some measure of control over this devastating disease. Overall, it’s estimated that genetics account for less than 5 percent of Alzheimer’s cases,24 and even if you have the aforementioned gene, it does not mean your fate is set in stone.
The statistics presented earlier by Bredesen may feel overwhelming, but he has identified more than four dozen variables that can have a significant influence on Alzheimer’s. It’s no surprise to me that mitochondrial dysfunction is at the heart of it all.
This makes logical sense when you recognize your mitochondria are instrumental in producing the energy currency in your body, and without energy, nothing works properly. Your mitochondria are also where a majority of free radicals are generated, so when your lifestyle choices produce higher amounts of free radicals, dysfunction in your mitochondria follows. The accumulation of mutations in mitochondrial DNA is also a primary driver of age-related decline.
While ReCODE looks at all of the contributing factors, restoring mitochondrial function is a cornerstone of successful Alzheimer’s treatment. One of the most powerful ways to optimize mitochondrial function is pulsed or cyclical ketosis, which is the main focus of my book, “Fat for Fuel.” Not surprisingly, Bredesen’s ReCODE protocol makes use of nutritional ketosis, and he’s becoming more familiar with cyclical ketosis as well.
In addition to ketosis, Bredesen recommends a mostly plant-based diet. The specific diet recommended is called KetoFlex 12/3, which involves a daily fasting period of 12 hours. For ApoE4-positive patients, 14 to 16 hours of fasting is advised. For more information on how ReCODE works, I recommend you read Bredesen’s book.
Sources and References
- 1 U.S. Centers for Disease Control and Prevention September 12, 2017
- 2 National Institute on Aging August 17, 2018
- 3 Neurology March 5, 2014
- 4, 6, 8 Medical News Today April 11, 2018
- 5 Nature Medicine April 9, 2018 [e-Pub ahead of print]
- 7 Gladstone Institutes April 9, 2018
- 9 Panminerva Medica September 2012; 54(3): 171-178
- 10 Diabetes Care February 2016; 39(2): 300-307
- 11 The New England Journal of Medicine August 8, 2013; 369: 540-548
- 12 Journal of Alzheimer’s Disease January 1, 2012; 32(2): 329-339
- 13 Diabetologia April 2018; 61(4): 839-848
- 14 Science October 18, 2013; 342(6156): 373-377
- 15 Proceedings of the National Academy of Sciences of the United States of America April 9, 2018 [e-Pub ahead of print]
- 16 Sleep Review April 15, 2018
- 17 MedicineNet.com April 9, 2018
- 18 PLOS One April 12, 2018 [e-Pub ahead of print]
- 19 LIVESCIENCE April 13, 2018
- 20 Nutrients November 14, 2017; 9(11): 1246
- 21 Frontiers in Aging Neuroscience August 3, 2017; 9: 254
- 22 ScienceDaily November 15, 2013
- 23 Neurology August 6, 2014 [e-Pub ahead of print]
- 24 Alzheimer’s Association, The Search for Alzheimer’s Causes and Risk Factors
