The Eye-Brain-Alzheimer’s-Dementia Connection

Natural Brain Support bookThis is the first of a series of articles discussing how to maintain healthy brain function based on my newest book Natural Brain Support: Preventing and Treating Alzheimer’s and Dementia Naturally.

There is a strong connection between eye and brain health, and in fact the optic nerve is brain tissue and the retina was created prenatally from brain cells. Many of the nutrients discussed below are needed for healthy vision but also are found in the brain as well.

An eye doctor can often identify health issues because of observed changes in the retina. An eye doctor can detect hypertension, diabetes, multiple sclerosis, and even Alzheimer’s disease before it gets to the point that the specialists can identify them.

Causative or Contributing Factors

brain diseaseHere is a partial list of the possible causative or contributing factors that can result in dementia and Alzheimer disease (AD).  Some are direct result of lifestyle habits and some are indirect results of those habits along with genetic and epigenetic factors.

  • Compromised blood-brain barrier. It is fascinating that many of the essential nutrients needed in the retina to support retinal and optic nerve function are those allowed by the body to cross the blood-brain barrier into the brain. The blood-brain barrier (BBB) prevents unwanted material such as debris, toxins, bacteria, and viruses from reaching the brain from the body, and is essential for maintaining brain health. BBB brain homeostasis, regulation of influx and/or transport of efflux is essential for protecting the brain. A breakdown in BBB can result in neuroinflammation, neurodegeneration, as well as cerebral small vessel disease.1
  • Exposure to environmental factors. Gene expression can change through one’s lifetime due negative factors like poor childhood nurturing,  stress, and exposure to toxins (this is known as the study of epigenetics).2 Toxins take the form of contaminants like lead and smoke, some recreational drugs, and even some medications. Chronic stress, and chronic lack of sleep are other environmental factors. Environmental factors appear to have a wide-ranging role in risk to neurodegenerative disease and gene malformation.
  • High blood sugar levels. Many researchers feel that chronic blood sugar elevations are involved in depression and neurodegenerative disorders such as Alzheimer’s disease.3 4 5
  • Chronic hypertension may contribute to cognitive decline by causing cerebral small vessel pathology and increasing neurofibrillary tangles and amyloid plaques.6
  • Chronic inflammation. Over time chronic inflammation can cause the immune system to go into overdrive, resulting in it attacking its own healthy cells, even brain cells, disabling their ability to clear away waste such as amyloid plaque.7 Increases in chronic inflammation result in increases in oxidative molecules, chemokines, cytokines, and immune cells, which in turn result in insulin resistance in the brain, causing a cascade of events that end up affecting healthy neurons.
  • High cholesterol. Vascular dementia is characterized by plaque blocking blood (that carries oxygen and nutrients) to the brain.  It is so common that it is suggested that high cholesterol may be a cause. Research linking high cholesterol to Alzheimer’s are mixed, but a number of studies report that high total cholesterol levels significantly increase AD risk.8 9
  • Poor diet and lack of exercise. In contrast to the healthful effects of diets that are rich in omega-3 fatty acids and antioxidants, epidemiological studies indicate that diets with high contents of trans and saturated fats adversely affect cognition.10
  • Excessive alcohol/drug consumption. Alcoholism reduces vitamin B1 and B3, which in turn can contribute to dementia. It can cause changes to gene expression with permanent adverse side-effects. Excessive alcohol consumption modifies messaging patterns in the midbrain areas such as the nucleus accumbens. 11 12
  • Compromised mitochondrial function.  Impacted by many environmental factors are mitochondria, which are the energy ‘batteries’ within each cell. Mitochondrial dysfunction appears to be a critical factor in the beginnings of AD. 13 14 Slow/low metabolism develops as a function of aging in the brain15 and is evident in affected brain regions,16 17 where mitochondrial structure is altered.18 19

Essential Nutrients for Healthy Brain Function

These important nutrients for healthy vision are also essential and readily available nutrients for a healthy brain.

  • Glutathione is the antioxidant found in greatest quantity in the brain and has been found to be deficient in the brains of many of the patients with brain illnesses. Glutathione levels are of interest to AD researchers because glutathione levels are depleted in AD patients, 20 21 22 as well as in brains of Parkinson’s patients. Glutathione is not absorbed well in capsule of pill form, so as a supplement we recommend sublingual or intraoral spray forms.
  • Curcumin induces neurogenesis, protects against oxidation of fats, and reduces neuron deterioration due to free radicals in neurodegenerative conditions.23 24 25 Curcuminoids enhance amyloid-beta uptake by macrophages of Alzheimer’s disease patients. 26
  • Gingko biloba has been linked to a healthy brain with a partial list of benefits including: neuroprotective results with beneficial effects of memory, and cognitive function and reduced cell death.27 Research does support that gingko may increase neurogenesis which is the production of new brain neurons, raise BDNF (brain-derived nerve factor) levels supporting neurogenesis, enhance cognitive function and help in reducing amyloid beta plaque for those with Alzheimer’s.28 29

In addition, we have developed several brain support supplement packages.  These packages contain the above nutrients as well as other brain-friendly nutrients not discussed above in detail: medicinal mushrooms, omega-3s, antioxidants, amino acids, and herbs.

Brain & Memory Support Package 1 contains:

    • MycoBotanicals Brain 60 vegcaps, with nerve and brain support medicinal mushrooms,
    • Oceans 3™ – Better Brain 90 gels, with a range of antioxidants including essential fatty acids and astaxanthin.
    • Advanced Eye and Vision Support Formula. Our whole food, organic, GMO free eye and brain formula with lutein, zeaxanthin, bilberry, organic tomato, broccoli, spinach and more.
    • Brain Cell Support – 60 caps,  contains cognizin citicoline, which has been found by researchers at Harvard to be helping in improving memory and cognitive function. Combined with acetyl L-carnitine (better than L-carnitine for neural support), DMAE, phosphatidylserine, and a number of brain cell supportive plants such as ginkgo biloba and gotu kola, Brain Cell Support helps to increase neurotransmitters production, including acetylcholine and aids in elevating mood.

For a comprehensive review of what one can do to both help prevent and treat dementia and Alzheimer’s Disease, see Natural Brain Care: Preventing and Treating Alzheimer’s Naturally. This 400 page book provides a detailed look at how to help prevent and treat Alzheimer’s and dementia naturally.

Next: Learn more about Alzheimer’s disease

  1. Li Y, Li M, Zuo L, Shi Q, Qin W, et al. (2018). Compromised Blood-Brain Barrier Integrity is Associated with Total Magnetic Resonance Imaging Burden of Cerebral Small Vessel Disease. Front Neurol. Apr 6;9:221. ↩
  2. Bird A. (2007). Perceptions of epigenetics. Nature. May 24; 447(7143):396-8. ↩
  3.  Andreoulakis E, Hyphantis T, Kandylis D, Lacovides A. (2012). Depression in diabetes mellitus: a comprehensive review. Hippokratia. Jul;16(3):205-14. ↩
  4. Huang C, Chung C, Leu H, Lin LY, Chiu CC, et al. (2014). Diabetes mellitus and the risk of Alzheimer’s disease: a nationwide population-based study. PloS One. Jan 29;9(1):e87095. ↩
  5. Chew BH, Sherina MS, Hassan NH. (2015). Association of diabetes-related distress, depression, medication adherence, and health-related quality of life with glycated hemoglobin, blood pressure, and lipids in adult patients with type 2 diabetes: a cross-sectional study. Ther Clin Risk Manag. 2015;11:669-81. ↩
  6. Den Heijer T, Launer LJ, Prins ND, van Dijk EJ, Vermeer SE, et al. (2005). Association between blood pressure, white matter lesions, and atrophy of the medial temporal lobe. Neurology. Jan 25; 64(2):263-7. ↩
  7. NIH. What Happens to the Brain in Alzheimer’s Disease. Retrieved from https://www.nia.nih.gov/health/what-happens-brain-alzheimers-disease. ↩
  8. Kivipelto M, Ngandu T, Fratiglioni L, Viitanen M, Kåreholt I, et al. (2005). Obesity and vascular risk factors at midlife and the risk of dementia and Alzheimer disease. Arch Neurol. Oct; 62(10):1556-60. ↩
  9. Whitmer RA, Sidney S, Selby J, Johnston SC, Yaffe K. (2005). Midlife cardiovascular risk factors and risk of dementia in late life. Neurology. Jan 25; 64(2):277-81. ↩
  10. Greenwood CE, Winocur G. (2005). High-fat diets, insulin resistance and declining cognitive function. Neurobiol Aging. Dec; 26 Suppl 1():42-5. ↩
  11. Csoka AB, Szyf M. (2009). Epigenetic side-effects of common pharmaceuticals: a potential new field in medicine and pharmacology. Med Hypotheses. Nov; 73(5):770-80. ↩
  12. Renthal W, Nestler EJ. (2008). Epigenetic mechanisms in drug addiction. Trends Mol Med. Aug; 14(8):341-50. ↩
  13. Swerdlow RH, Burns JM, Khan SM. (2014). The Alzheimer’s disease mitochondrial cascade hypothesis: progress and perspectives. Biochim Biophys Acta. Aug; 1842(8):1219-31. ↩
  14. Picone P, Nuzzo D, Caruana L, Scafidi V, Di Carlo M. (2014). Mitochondrial dysfunction: different routes to Alzheimer’s disease therapy. Oxid Med Cell Longev. 2014():780179. ↩
  15. Scarpulla RC. (2008). Transcriptional paradigms in mammalian mitochondrial biogenesis and function. Physiol Rev. Apr; 88(2):611-38. ↩
  16. Mosconi L, Brys M, Switalski R, Mistur R, Glodzik L, et al. (2007). Maternal family history of Alzheimer’s disease predisposes to reduced brain glucose metabolism. Proc Natl Acad Sci U S A. Nov 27; 104(48):19067-72. ↩
  17. Murray J, Tsui WH, Li Y, McHugh P, Williams S, et al. (2014). FDG and Amyloid PET in Cognitively Normal Individuals at Risk for Late-Onset Alzheimer’s Disease. Adv J Mol Imaging. Apr; 4(2):15-26. ↩
  18. Hirai K, Aliev G, Nunomura A, Fujioka H, Russell RL, et al. (2001). Mitochondrial abnormalities in Alzheimer’s disease. J Neurosci. May 1; 21(9):3017-23. ↩
  19. Moreira PI, Siedlak SL, Wang X, Santos MS, Oliveira CR, et al. (2007). Increased autophagic degradation of mitochondria in Alzheimer disease. Autophagy. Nov-Dec; 3(6):614-5. ↩
  20. Mazzetti AP, Fiorile MC, Primavera A, Lo Bello M. (2015). Glutathione transferases and neurodegenerative diseases. Neurochem Int. Mar;82:10-8. ↩
  21. Shukla D, Mandal PK, Ersland L, Gruner ER, Tripathi M, et al. (2018). Multi-Center Study on Human Brain Glutathione Conformation using Magnetic Resonance Spectroscopy. J Alzheimers Dis. 2018;66(2):517-532. ↩
  22. Saharan S, Mandal PK. (2014). The emerging role of glutathione in Alzheimer’s disease. J Alzheimers Dis. 2014;40(3):519-29. ↩
  23.   Tiwari SK, Agarwal S, Seth B, Yadav A, Nair S, et al. (2014). Curcumin-loaded nanoparticles potently induce adult neurogenesis and reverse cognitive deficits in Alzheimer’s disease model via canonical Wnt/B-catenin pathway. ACS Nano. Jan 28;8(1):76-103. ↩
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  26. Zhang L, Fiala M, Cashman J, Sayre J, Espinosa A, et al. (2006). Curcuminoids enhance amyloid-beta uptake by macrophages of Alzheimer’s disease patients. J Alzheimers Dis. Sep; 10(1):1-7. ↩
  27. Ibid. Zhang. (2006). ↩
  28. Yang G, Wang Y, Sun J, Zhang K, Liu J. (2016). Ginkgo Biloba for Mild Cognitive Impairment and Alzheimer’s Disease: A Systematic Review and Meta-Analysis of Randomized Controlled Trials. Curr Top Med Chem. 2016;16(5):520-8. ↩
  29. Wightman EL. (2017). Potential benefits of phytochemicals against Alzheimer’s disease. Proc Nutr Soc. May;76(2):106-112. ↩