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Top Nutrients for Brain Health

Article at-a-glance:

  • Certain nutrients promote brain health, which is crucial for maintaining quality of life as you age
  • Acetyl-L-Carnitine is an amino acid that protects the brain from oxidative stress and supports healthy memory and mood
  • Alpha Lipoic acid is an antioxidant and sulfur compound that supports learning and memory
  • Huperzine A has shown beneficial effects in people with memory loss and Alzheimer’s disease
Anxiety Word Cloud

Your remarkable brain only makes up about 2% of your body weight yet it consumes 20% of your oxygen and calories.1 It not only gives rise to memories, thoughts, and emotions, it helps regulate every aspect of your body. Maintaining a healthy, fit brain is critical to the quality of life as we age.2

And indeed, as a population, we’re aging. Over the next two decades, those 65 and older will soar to 72 million—that’s 1 in 5 Americans. And it’s predicted that the majority of 65-year-olds alive now will live into their 90s.3  We know that chronic illness increases with age—whether heart disease, high blood pressure, insomnia, depression, osteoporosis, or even cancer. But perhaps the scariest decline of all to contemplate is losing your mind and having your brain fail. 

How can you protect your brain as you age? Diet and exercise are important. Certain nutrients have also been shown to promote brain health, including cognition, mood, and memory. These can go a long way towards keeping your brain (and you) humming along at top speed.

Along with a good multivitamin and mineral supplement—one that contains important B vitamins, magnesium, and trace minerals like Supreme Multivitamin—melatonin has been shown to normalize oxidative damage in brain tissue. Since melatonin levels fall with age, this molecule is important.Vitamin D deficiency is considered a silent epidemic, and levels of vitamin D have been correlated with mood.5

But in particular, three nutrients, which are all in MitoForte, have been shown to powerfully protect the brain and support healthy brain function. 

Acetyl-L-Carnitine

L-carnitine exists as two forms in the body. One is straight L-carnitine. The other is acetyl-L-carnitine (ALCAR). L-carnitine does not cross the blood-brain barrier (BBB) and enter the central nervous system. Instead, it remains in the periphery and feeds cells in the muscles, liver, and other tissues. The body can convert L-carnitine into ALCAR, which, in contrast to L-carnitine, can cross the BBB and enter your central nervous system (CNS) and nourish the brain. 

Both L-carnitine and ALCAR play a key role in energy metabolism by shuttling fatty acids into its energy-producing pathway. This is especially important in the brain since the brain requires a lot of energy. It’s also thought to be neuroprotective. 

In animal studies, ALCAR protected the brain’s mitochondria (our cell’s energy powerhouses) and reversed mitochondrial decay. In one study, feeding aged animals ALCAR not only restored mitochondrial function and lowered oxidative stress in the brain, but it also led to better cognition and more physical activity.6 And when ALCAR was added to the drinking water of aged mice for eight weeks, high levels of oxidative molecules were restored to the lower levels found in young mice. Older mice also began to behave a bit more like young mice, exploring the margins of their cage more often rather than staying in the center.7 In other mice studies, combining a sulfur compound called alpha-lipoic acid (ALA) and ALCAR reduced the number of damaged mitochondria in the neurons and improved brain function.8

In humans, research has shown that individuals suffering from major depressive disorder have lower concentrations of ALCAR than healthy, non-depressed individuals. In fact, the severity of depression has been correlated with levels of ALCAR.9 Human studies have also found that ALCAR may be a useful nutrient for promoting brain health by slowing the decline in brain function due to age. Studies on ALCAR alone or in combination with other nutrients found that it improved cognitive performance in adults with probable Alzheimer’s disease.10 The amount of ALCAR used in clinical trials typically ranged from 1000 to 3000 mg per day. 

Alpha Lipoic Acid

Alpha-Lipoic acid (ALA) is a sulfur compound that has powerful antioxidant activity. It’s required to burn sugars for energy and has been studied for its ability to help people with diabetes, multiple sclerosis, weight management, and cognitive decline. Research has shown that ALA may protect brain cells from conditions such as stroke, multiple sclerosis, and Alzheimer’s disease. It is also thought to promote learning and healthy memory. ALA plays a critical role in mitochondrial energy metabolism and helps increase other antioxidants such as ascorbate (vitamin C) and glutathione.11

In one randomized, controlled clinical trial, a blend of 600 mg of ALA plus Omega-3 fatty acids promoted health in people with Alzheimer’s disease. Thirty-nine individuals suffering from Alzheimer’s disease were studied, and it was found that those who took a blend of Omega 3 fatty acids and ALA helped slow decline in their ability to perform activities of daily living. Their cognitive decline was also slowed.12 

In another promising pilot study, 43 people with Alzheimer’s were given 600 mg of alpha-lipoic acid for up to 48 months. Disease progression in those with mild dementia slowed and the researchers concluded that “alpha-lipoic acid might be a successful neuroprotective therapy option for Alzheimer’s disease” and recommended follow-up research.13

Yet another study gave 600 mg of ALA daily to 120 Alzheimer’s disease patients divided into two groups, those with diabetes mellitus and those without. ALA is known to have positive effects on glucose metabolism and insulin resistance, which are altered in diabetes. After sixteen months, cognitive improvement was seen in 43% of patients with diabetes, and 23% of those without. The researchers conclude that ALA “could be effective in slowing cognitive decline in patients with Alzheimer’s disease and insulin resistance.”14 

Huperzine A

Huperzine A (HupA) is a compound derived from the Chinese herb Huperzia serrata. It is one of a group of molecules that inhibits an enzyme called acetylcholinesterase (AChE), and which is being studied in Alzheimer’s disease. This enzyme, which is found in muscles and nerves, is important for learning and memory.15

Huperzine A is also generally neuroprotective and appears to protect neurons from oxidative stress, regulate the secretion of nerve growth factors, enhance cognition, relieve memory deficits in older individuals and protect cells against changes associated with Alzheimer’s disease. Its protective effects are associated with its antioxidant ability and its ability to increase levels of the neurotransmitter acetylcholine in the brain.16 It appears to protect mitochondria in the brain as well.17

It is thought that increased oxidative stress and free radical damage may be involved in Alzheimer’s disease, and this may be why Huperzine A has been shown, in double-blind, placebo-controlled trials, to benefit cognitive function and quality of life in people with Alzheimer’s disease. The dose of Huperzine A used in clinical trials was 400 micrograms per day. In fact, in China, the compound has been approved to be used in Alzheimer’s disease. In the US, it is sold as a dietary supplement to support healthy brain function and is very popular.18 As a dietary supplement in the US, it has not been approved by the FDA to diagnose, treat, prevent or cure any disease. 

Huperzine A may reduce the death of neuronal cells and increase the levels of acetylcholine, a brain neurotransmitter.19 Acetylcholine is low in the cerebral cortex of patients with Alzheimer’s disease.20

In clinical trials, Huperzine A has proved effective. In fact, according to a review and meta-analysis of six studies and a total of 454 Alzheimer’s patients by the prestigious Cochrane Group, Huperzine A has beneficial effects on cognitive function, behavioral disturbances, and general function in Alzheimer’s disease, with no obvious serious adverse effects.21

What You Can Do

If you’d like to get all these nutrients in one convenient product, take MitoForte. It provides high doses of these nutrients to promote healthy memory, mood, and energy. This formula was created based on my research into mitochondrial dysfunction and molecular pathways of disease. 

The journal article I wrote on this topic resulted in my being recognized as one of the Top 10 Cited Authors in the world by Elsevier, the world’s largest health publishing company. 

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References

1Raichle ME, Gusnard DA. Appraising the brain’s energy budget. Proc Natl Acad Sci U S A. 2002;99(16):10237-10239. [Article]

2Wang Y, Pan Y, Li H. What is brain health and why is it important? BMJ. 2020 Oct 9;371:m3683. [Article]

3Jenkins, JA. It’s time to rethink aging and retirement, AARP’s Jenkins says. Barrons. May 2021. [Report]

4Cardinali DP. Melatonin: Clinical Perspectives in Neurodegeneration. Front Endocrinol (Lausanne). 2019 Jul 16;10:480. [Article]

5Penckofer S, Kouba J, Byrn M et al. Vitamin D and depression: where is all the sunshine?. Issues Ment Health Nurs. 2010;31(6):385-393. [Article]

6Ames BN, Liu J. Delaying the mitochondrial decay of aging with acetylcarnitine. Ann N Y Acad Sci. 2004 Nov;1033:108-16. [Article]

7Sharman EH, Vaziri ND, Ni Z et al. Reversal of biochemical and behavioral parameters of brain aging by melatonin and acetyl L-carnitine. Brain Res. 2002 Dec 13;957(2):223-30. [Article]

8Aliev G, Liu J, Shenk JC et al. Neuronal mitochondrial amelioration by feeding acetyl-L-carnitine and lipoic acid to aged rats. J. Cell. Mol. Med. 2009, 13, 320–333. [Article]

9Nasca C, Bigio B, Lee FS et al. Acetyl-l-carnitine deficiency in patients with major depressive disorder. Proc. Natl. Acad. Sci. USA 2018, 115, 8627–8632. [Article]

10Ferreira GC, McKenna MC. L-Carnitine and Acetyl-L-carnitine Roles and Neuroprotection in Developing Brain. Neurochem Res. 2017 Jun;42(6):1661-1675. doi: 10.1007/s11064-017-2288-7. [Article]

11Shay KP, Moreau RF, Smith EJ et al. Alpha-lipoic acid as a dietary supplement: molecular mechanisms and therapeutic potential. Biochim Biophys Acta. 2009 Oct;1790(10):1149-60. [Article]

12 Shinto L, Quinn J, Montine T et al. A randomized placebo-controlled pilot trial of omega-3 fatty acids and alpha lipoic acid in Alzheimer’s disease. J Alzheimers Dis. 2014;38(1):111-20. [Article]

13Hager K, Kenklies M, McAfoose J et al. Alpha-lipoic acid as a new treatment option for Alzheimer’s disease–a 48 months follow-up analysis. J Neural Transm Suppl. 2007;(72):189-93 [Article]

14Fava A, Pirritano D, Plastino M, et al. The Effect of Lipoic Acid Therapy on Cognitive Functioning in Patients with Alzheimer’s Disease. J Neurodegener Dis. 2013;2013:454253.  [Article]

15Maurer SV, Williams CL. The Cholinergic System Modulates Memory and Hippocampal Plasticity via Its Interactions with Non-Neuronal Cells. Frontiers in Immunology. 2017;8(1489). [Article]

16Zhang HY, Tang XC. Neuroprotective effects of huperzine A: new therapeutic targets for neurodegenerative disease. Trends Pharmacol Sci. 2006 Dec;27(12):619-25 [Article]

17Gao X, Tang XC . Huperzine A attenuates mitochondrial dysfunction in beta-amyloid-treated PC12 cells by reducing oxygen free radicals accumulation and improving mitochondrial energy metabolism. J Neurosci Res 2006; 83: 1048–57. [Article]

18Zangara A. The psychopharmacology of huperzine A: an alkaloid with cognitive enhancing and neuroprotective properties of interest in the treatment of Alzheimer’s disease. Pharmacol Biochem Behav. 2003 Jun;75(3):675-86. [Article]

19Zhu XD, Giacobini E. Second-generation cholinesterase inhibitors: effect of (L)-huperzine A on cortical biogenic amines. J Neurosci Res 1995;41:828– 35. [Article]

20Bowen DM, Allen SJ, Benton JS, et al. Biochemical assessment of serotonergic and cholinergic dysfunction and cerebral atrophy in Alzheimer’s disease. J Neurochem 1983;41: 266– 72. [Article]

21Li J, Wu HM, Zhou RL, Liu GJ, Dong BR. Huperzine A for Alzheimer’s disease. Cochrane Database Syst Rev. 2008 Apr 16;(2):CD005592 [Article]

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