Alzheimer’s is not genetic. And it’s definitely not irreversible.
You see, there’s nothing wrong with the “genes” of virtually every person who develops this awful disease.
Yet patients around the country are being misled into believing there’s nothinG that can be done about this awful disease.
And it’s just not true.
A new study finds that maintaining a healthy lifestyle can cut your risk of developing Alzheimer’s — even if you have genes that raise your risk.
Published in the Journal of the American Medical Association, it found that people with high genetic risk and poor health habits were about three times more likely to develop dementiA than those with low genetic risk and good health habits.1
The researchers also found that regardless of how much genetic risk someone had, healthy lifestyle habits like a good diet, adequate exercise, limiting alcohol and not smoking made dementia less likely.
Two Types of Alzheimer’s Disease
The first type of Alzheimer’s is known as “early-onset Alzheimer’s,” and it occurs before the age of 65 and runs in families. But it accounts for only 5% to 10% of all cases. So only a very small percentage of Alzheimer’s cases can be described as tRuly genetic.2
The second type, which is called late-onset, is the most common form. It tends to strike people after the age of 65. And it’s this form of Alzheimer’s that accounts for the worldwide explosion in dementia cases in recent decades.
3 Natural Ways to Protect Your Brain
Here at the Sears Institute for Anti-Aging Medicine, I’ve developed pioneering therapies to prevent, treat and even reverse Alzheimer’s.
One of these is telomerase activation. As you know, telomeres are the tiny protective caps at the ends of each strand of your DNA. Each time a celL divides, a little bit of each telomere gets used up and shortens.
And research suggests that many of the changes involved in aging and Alzheimer’s are orchestrated by the shortening of telomeres. The enzyme called telomerase helps rebuild your telomeres, slowing and even reversing the aging process.
I’ve written to you about the telomere studies we’re conducting at my clinic. We offer a unique series of tests that show how the body has biologically aged over time — it’s called Age Quotient Analysis (AQ). On average, the patients in my clinic who’ve gone through this age-reversing protocol have lengthened their telomeres, and grown 14 years younger.
Not everyone can come to my clinIc. But there are simple ways you can activate telomerase:
- First, increase your folate intake. Boosting your levels of folate (vitamin B6) combats inflammation triggered by high levels of the amino acid homocysteine, one of the greatest threats to your telomeres.3,4 The best sources are calf’s liver, dairy, poultry, meat, eggs, seafood, spinach, broccoli, asparagus and Brussels sprouts. Or, you can supplement with 800 mcg of folic acid every day for your telomeres.
- Next, add L-arginine and L-citrulline. These complementary amino acids increase telomere length by creating nitric oxide in your body, which in turn activates telomerase.5 You can add these brain boosters to your diet with watermelon, peanuts, tuna, almonds, sunflower seeds, walnuts, chicken, salmon and lobster. Or, supplement with L-arginine and citrulline in a 5-to-1 ratio. I reCommend daily doses of 6,000 mg of L-arginine and 1,000 mg of citrulline.
- Finally, step up the selenium. One study showed selenium caused telomerase production in cells to skyrocket, while others found that selenium protects DNA breaks, stops telomere loss and improves telomere function.6,7 Your best sources are garlic, and Brazil nuts, each of which has about 100 mcg of selenium. A good multi-nutrient supplement will give you at least 200 mcg of selenium, enough for telomerase activation. The problem is, the government’s recommendation is only 55 mcg. So only my and a very few other multi-nutrient formulas will give you enough; a full 200 mcg of bioactive selenium.
To Your Good Health,
Al Sears, MD, CNS
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Raban JS, et al. “Associations of physical activity and β-amyloid
with longitudinal cognition and neurodegeneration in clinically
normal older adults.” JAMA
2019 Jul 16.
2. Damoiseaux JS, et al. “Gender modulates the APOE ε4 effect in healthy older adults: Convergent evidence from functional brain connectivity and spinal fluid tau levels.” J Neurosci. 2012;32(24):8254-8262.
3. Richards JB, et al. “Homocysteine levels and leukocyte telomere length.” Atherosclerosis. 2008;200(2):271-227.
4. Paul L, et al. “Telomere length in peripheral blood mononuclear cells is associated with folate status in men.” J Nutr. 2009;139(7):1273-1278.
5. Vasa M, et al. “NO activates telomerase and delays endothelial cell senescence.” Circ Res. 2000;87:540-542.
6. Liu Q, et al. “[Effects of sodium selenite on telomerase activity and telomere length.]” Sheng Wu Hua Xue Yu Sheng Wu Li Xue Bao (Shanghai). 2003;35(12):1117-1122.
7. Ferguson LR, et al. “Selenium and its role in the maintenance of genomic stability.” Mutat Res. 2012;733(1-2):100-110.