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Preventing Brain Plaque is a Key Anti-Aging/Longevity Strategy

James Meschino DC, MS, ROHP
Beta-amyloid plaque is a protein that forms between brain cells from fragments of a protein normally found on the surface of brain cells. The accumulation of beta-amyloid plaque is known to damage brain cells in various ways, and its presence is a hallmark feature of Alzheimer’s disease. Researchers have been looking for ways to inhibit the accumulation of beta-amyloid plaque in the human brain, as a means to prevent age-related memory loss and Alzheimer’s disease. Thus far there are no drugs that can do it.

However, certain dietary and lifestyle factors as well ascertain supplements, appear to strongly influence brain plaque development. There is good evidence from human studies that a high fat diet increases risk for Alzheimer’s disease, and there is absolute proof that a high fat diet increases the development of Alzheimer’s-type brain damage in rodent studies. In these animal studies the Alzheimer’s type brain damage produced from a high fat diet involves stimulating the production of beta-amyloid plaque. Thus, reducing your intake of foods high in saturated fat, transfats and deep fried foods appear to be important dietary strategies to help prevent the accumulation of age-related brain plaque.

The Right Supplements Are Also Important
There is also evidence to show that certain supplements can inhibit the synthesis of beta-amyloid plaque in the brain. The strongest evidence is for the omega-3 fat DHA, as well as melatonin. DHA is an omega-3 fat found in fish and fish oil supplements. The pineal gland in the brain makes melatonin, but by age 40 there is a significant decline in melatonin production. The decline in melatonin may make us more prone to Alzheimer’s disease as we age. This is one of the reasons some health experts encourage melatonin supplementation after the age 40. It helps you get a good night’s sleep and it may also help protect the brain from plaque development. More recently Vitamin D has been shown to help break down beta-amyloid plaque. As such, taking these supplements daily may reduce brain plaque development and risk of Alzheimer’s disease.

Exercise Shows Remarkable Promise
A 2012 study in the Journal of Biological Chemistry (M. Maesako/2012) showed that regular exercise prompted the break down and elimination of beta-amyloid plaque, formed in the brains of mice after feeding them a high fat diet. This suggests that some of the brain plaque damage we have may be reversible before it gets to an advanced stage. Although more research is necessary to confirm the same thing happens in humans, previous human studies have shown that providing exercise to patients with memory loss problems improves their cognitive function.

Patients often ask me how to incorporate DHA, melatonin and vitamin D supplementation into their overall supplementation regime. Here is what I recommend:

  1. DHA – Take an Essential Fatty Acid supplement each day containing 400 mg each of fish, flaxseed and borage seed oil. Take 2-3 capsules per day
  2. Melatonin – After age 40 take a supplement one hour before bedtime containing: 500 mcg Melatonin, 10 mg 5HTP, 25 mg GABA, Bacopa 15 mg Monnieri (this combination helps protects the brain from free radicals, improves sleep quality and duration, naturally)
  3. Vitamin D – Take a high potency multiple vitamin and mineral supplement each day that includes: 1000 IU vitamin D, 1000 mg Vitamin C, 400 IU vitamin E, B-50 complex, 200 mg magnesium (all of these nutrients important for long-term brain health)

References:

  1. Masato Maesako, KengoUemura, Masakazu Kubota, Akira Kuzuya, Kazuki Sasaki, Ayae Kinoshita, et al.  “Exercise is more effective than diet control in preventing high fat diet-induced [beta]-amyloid deposition and memory deficit in amyloid precursor protein transgenic mice.”  The Journal of Biological Chemistry, 287, 23024-23033, June 29, 2012
  2. Lautenschlager N et al. Effect of Physical Activity on Cognitive Function in Older Adults at Risk for Alzheimer Disease. JAMA. 2008;300(9):1027-1037.
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