Air Pollution - Ultra-Fine Nanoparticles Major Threat for Brain & Lung and Aging

Air pollution is a pervasive and often ignored factor in the aging process. Airborne ultra-fine (nanoparticles) pollution particles are microscopic and pose special dangers to health. Researchers agree that ultra-fine air pollution particles are a major threat in negative health consequences in humans. (1)  While being very detrimental to the lungs, long-term exposure to ultra-fine particles also damages the cardiovascular system, contributes to atherosclerosis plaque formation and may lead to degenerative brain diseases - including Alzheimer's disease. These very small particles are able to travel deep into lung tissue and into the blood stream. As a result, there are significant increases in systemic oxidative stress, inflammation with increased DNA damage and mutagenicity. (2-6) Telomere length, which is an indicator of biological aging, becomes shorter in people living in air pollution areas. Shorter telomeres is associated with accelerated aging.(7-8)

Neuroinflammation. Especially alarming is the effect of ultra-fine particles on the brain. Airborne nano-sized particulate matter migrates through the lungs into the bloodstream and eventually into the brain. Longtime exposure to ultra-fine air pollutants leads to chronic brain inflammation which leads to neurodegenerative diseases. Epidemiological research has linked ultra-fine air particulate matter as a significant environmental  factor involved in Alzheimer's Disease and Parkinson's Disease.(2) 

Ultra-fine pollutant particles are produced by high heat sources including automobiles, trucks, airplane exhaust and factories and play a significant role in health and longevity. Urban areas, transit routes (highways and roads) and airports are major sources of pollutants but the suburbs are not immune. Such pollutants are so small that most people are unaware that they are inhaling toxic pollutants. Airborne fine particulate matter is a major component of air pollution.

Sources of ultra-fine particle pollutants:

(1) City / Urban Areas Particulate Matter. Urban areas create a confluence of major activity which generate ultra-fine air pollution. In studies involving six China urban areas, ultra-fine particulate matter (PM), including polycyclic aromatic hydrocarbon (PAH), were analyzed. The particulate matter was determined as having cytotoxicty to the bronchial cells of the lungs.(9) Substantial sources of outdoor PAHs in particulate pollution include cars and trucks.

(2) Highways / roadways. high volumes of traffic on highways are significant sources of ultra-fine particulate matter and PAH which is then distributed to surrounding areas and runoff into water ways. People living close to major roadways have increased health risks due increased air pollution exposure. Road paving and asphalt manufacturing are also major sources.

(3) Indoor sources. Burning of biofuels including coal and wood create dangerous levels of emissions. Also emissions from cigarette smoke.

(4) Diesel exhaust - classified as a group 1 carcinogen. Shown to cause lung and possibly bladder cancer.Contains nitric oxide and fine particulate matter.

(5) Airports / Aircraft turbine engines - these aircraft engines produce significant levels of hazardous ultra-fine air pollutants (including benzene and formaldehyde) at both in flight and ground levels. In fact, air quality impacts areas extend far from the airports. The LA times reports that communities as far as 10 miles from LAX airport  are exposed to unsafe levels of air pollutants from aircraft engine exhaust.(10)

 Natural Support:

SULFORAPHANE -  Sulforaphane is a potent activator of phase 2 detoxification in the body. In a study in high air pollution areas in China, sulforaphane beverages were shown to signifcantly increase metabolism and excretion of hazardous air pollutants benzene and acrolein in participants.(11)  Further studies indicate that through activation of Nrf2, sulforaphane enhances protection against airborne toxin carcinogens and carcinogenesis. (12) Sulforaphane also protects against oxidant effects of diesel emission by invoking an over expression of antioxidant enzymes.(13)

 N-ACETYL-CYSTEINE - Offers  protection against air pollution induced inflammation. Includes specific mitigation against formaldehyde induced lung damage. Formaldehyde is a major emission toxin from airplane exhaust.(14)


XGEVITY  (Glucoraphanin / Sulforaphane and N-Acetyl-Cysteine)

AIR VITALITY (Glucoraphanin / Sulforaphane and N-Acetyl-Cysteine)



(1) Chen R, et al. Beyond PM2.5: The role of ultrafine particles on adverse health effects of air pollution.  Biochim Biophys Acta. 2016 Dec

(2)  Heusinkveld HJ, et al. Neurodegenerative and neurological disorders by small inhaled particles. Neurotoxicology. 2016 Sep

(3)  Valavanidis A, et al. Airborne particulate matter and human health: toxicological assessment and importance of size and composition of particles for oxidative damage and carcinogenic mechanisms. Environ Sci Health C Environ Carcinog Ecotoxicol Rev. 2008 Oct-DecBottom of Form

(4) Pope CA, et al. Exposure to Fine Particulate Air Pollution Is Associated with Endothelial Injury and Systemic Inflammation. Circ Res. 2016 Oct 25

(5) Bai Y, et al. Fine particulate matter air pollution and atherosclerosis: Mechanistic insights. Biochim Biophys Acta. 2016 Dec

(6) Risom L, et al. Oxidative stress-induced DNA damage by particulate air pollution. Mutat Res. 2005 Dec 30

(7) Martens Ds, et al. Air Pollution Stress and the Aging Phenotype: The Telomere Connection.  Curr Environ Health Rep. 2016 Sep

(8) Ward-Caviness CK, et al. Long-term exposure to air pollution is associated with biological aging. Oncotarget 2016 Oct 25

(9) Yang L, et al. Pro-inflammatory response and oxidative stress induced by specific components in ambient particulate matter in human bronchial epithelial cells. Environ Toxicol. 2016 Aug

(10) Ridgeway L. New concerns raised about air pollution at LAX. May 30, 2014

(11) Egnar PA, et al. Rapid and sustainable detoxication of airborne pollutants by broccoli sprout beverage: results of a randomized clinical trial in China.

(12) Kensler TW, et al. Keap1-nrf2 signaling: a target for cancer prevention by sulforaphane. Top Curr Chem. 2013.

(13) Wan J, et al. Antioxidant enzyme induction: a new protective approach against the adverse effects of diesel exhaust particles. Inhal Toxicol 2007.

(14) Wang M, et al. N-acetylcysteine: A promising drug against formaldehyde-induced damage in lung epithelial cells.  Med Hypotheses. 2014 Nov

Herbal Extracts - Neurogenesis & Recovery of Cognition Impairments

Aging of the brain involves the loss of neurons (hippocapmus shrinkage), loss of synapse integrity between neurons, build-up of toxic amyloid proteins, neuron tangles, defects in blood flow  and chronic inflammation. Under normal age progression, these events do not happen over night and may take years before impairments in cognition become noticed.

Ultimate anti-aging strategies for the brain and memory should target the progressive decline of the brain and promote reversal and recovery of some cognition impairments.

Emerging research in the study of herbal ingredients show their tremendous potential use in mitigating the decline in brain function with age.

  • NEUROGENESIS - is the formation of new neurons, specifically in the hippocampus area in the brain.The hippocampus is essential in providing the capacity for memory and learning. Dementia and Alzheimer's disease are associated with brain shrinkage which is correlated to the loss of neurons in the hippocampus. The formation of new neurons may reverse brain shrinkage.

                    Herbs and Extracts

    •  Andrographolide - As an extract from Andrographis Paniculata. Lab research has shown stimulation of neurogenesis in the hippocampus by andorgrapholide. Specifically " increased cell proliferation and the density of immature neurons in the dentate gyrus." (1) The dentate gyrus is an area of the hippocampus involved in memory formation.
    • Centella asiatica - Acts as a potent memory enhancer, via  increasing hippocampus neurogenesis and support for brain tissue regeneration. (2)
    • Baicalin (3)
    • Panax Ginseng (4)
    • Curcumin (5)
    • Epimedium (Icariin)  (6)
    • Apigenin (7)
    • BRAIN TISSUE REGENERATION. While in the same theme as neurogenesis, brain tissue regeneration refers to the enhancement and regeneration of critical neuron structures - axons and dendrites. Dendrites transmit signals from the synapse to the body of the neuron. Axons transmit signals away from the body of the neuron and are covered with a myelin sheath which increase speed of the impulse providing rapid impulse transmission. Aging degenerates the structural integrity of dendrites and axon/myelin complex.

                         Herbs and Extracts

    •  Centella asiatica - Improves structural integrity of axons / myelination and proliferation of dendritic branching and length. Such improvements have been shown to enhance learning and improve memory. (8) Centella asiatica also has been shown to improve learning and memory in normal lab mice.
    • Luteolin - Baicalin - promote neuronal survival and neuron differentiation through the outgrowth of neurites  (axons and dendrites) from the neuron.(9.10)
    • Rosemary (Carnosic Acid) - Strongly promotes neurite outgrowth as a function of powerful Nrf2 activity. Suppressed Nrf2 activation suppresses neuron differentiation.(11)

      • RECOVERY OF COGNITIVE IMPAIRMENT - the  to reversal of certain functional impairments which may improve cognitive function. Many research animal models for cognitive impairment are characteristically similar to Alzheimer's disease (AD). Impairment usually involves cerebral vascular disease, synaptic dysfunction. and more.
                Herbs and Extracts
      • Andrographolide - Impairment of synaptic function between neurons plays a significant role in the loss of cognitive function. This is seen in the progression of AD. In research animals with AD-like cognitive disease, the treatment of andrographolide over a 3 month span imporved synaptic function and protected important synaptic proteins.
      • Furthermore, andrographolide has been shown to reduce inflammation in the brain and levels of pathological tau protein and beta amyloid in animal models.(12)
      • Andrographolide reduces inflammation and dysfunction of the cerebral endothelial cells, which may affect vascular flow to the brain.(13)
      • Centella asiactica - in senescence-accelerated lab mice, which had accelerated aging of the brain, administration of centella asiatica significantly improved synaptic plasticity and reduced beta amyloid build-up. Such treated mice showed significant benefits in memory and learning. (14)
      • NEUROPROTECTION - AMYLOID & NON-AMYLOID (α-synuclein) TOXICITY | CHRONIC INFLAMMATION - The aging brain is under continual assault and must be protected to prevent cognitive decline and loss of neurons. Key areas of protection include the build-up of amyoid plaques which are toxic to neurons and synapses. Moreover, chronic inflammation in the brain accelerates destruction of the brain and is believed to be the facilitator of degenerative brain diseases.
        • Centella asiatica (15)
        • Epimedium (Icariin)(16,17)
        • Apigenin and luteolin (18,19)
        • Baicalin (20)
        • Schisandra (21)
        • Rosemary (Carnosic Acid)(22)
      • REVERSES INSULIN RESISTANCE IN BRAIN NEURONS - Aging brains become increasingly incapable of using glucose as an energy source. Without this energy neurons age faster and die. Reversing the insulin resistance maintains healthy neurons. Brain insulin resistance is associated with Alzheimer's Disease.
      • Further reduction in glucose availability is caused by methylglyoxal - a powerful intermediate in the formation of Advanced Glycation End Products (AGEs).
      • Curcumin - Improves insulin sensitivity in neurons. (23)
      • Sulforaphane - Reverses reduction of glucose uptake by neurons caused by methylglyoxal (a precusor of advanced glycation end products). Sulforaphane also normalizes brain-derived neurotrophic factor (BDNF) signaling, which is critical for maintaining brain function. BDNF pathways are disrupted in Alzheimer's Disease. (24)










      (1)   Varela-Nallar L, et al. Andrographolide Stimulates Neurogenesis in the Adult Hippocampus. Neural Plast, 2015.

      (2)  Sirichoat A, et al. Effects of Asiatic Acid on Spatial Working Memory and Cell Proliferation in the Adult Rat Hippocampus. Nutrients. 2015 Oct 5

      (3) Zhang K, et al. Baicalin promotes hippocampal neurogenesis via SGK1- and FKBP5-mediated glucocorticoid receptor phosphorylation in a neuroendocrine mouse model of anxiety/depression. Sci Rep. 2016 Aug 9

      (4) Jiang B, et al.  Antidepressant-like effects of ginsenoside Rg1 are due to activation of the BDNF signalling pathway and neurogenesis in the hippocampus. Br J Pharmacol. 2012 Jul;

       (5) Pluta R, et al. Neurogenesis and neuroprotection in postischemic brain neurodegeneration with Alzheimer phenotype: is there a role for curcumin? Folia Neuropathol. 2015

      (6) Li F, et al. Icariin decreases both APP and Aβ levels and increases neurogenesis in the brain of Tg2576 mice. Neuroscience. 2015 Sep 24

      (7) Taupin P. Apigenin and related compounds stimulate adult neurogenesis. Mars, Inc., the Salk Institute for Biological Studies: WO2008147483. Expert Opin Ther Pat. 2009 Apr


      (8) Yogeswarin L, et al. Recent Updates in Neuroprotective and Neuroregenerative Potential of Centella asiatica. Malays J Med Sci 2016 Jan.

      (9) Chen PY, et al. Up-Regulation of miR-34a Expression in Response to the Luteolin-Induced Neurite Outgrowth of PC12 Cells. J Agric Food Chem. 2015 Apr

      (10) Li M, et al. Neuronal differentiation of C17.2 neural stem cells induced by a natural flavonoid, baicalin. Chembiochem. 2011 Feb 11;

      (11) Kosaka K, et al. Role of Nrf2 and p62/ZIP in the neurite outgrowth by carnosic acid in PC12h cells. J Biochem. 2010 Jan;



      (12) Rivera DS, et al. Andrographolide recovers cognitive impairment in a natural model of Alzheimer's disease (Octodon degus). Neurobiol Aging. 2016 Jul 5

      (13) Chang CC, et al. Andrographolide, a Novel NF-κB Inhibitor, Inhibits Vascular Smooth Muscle Cell Proliferation and Cerebral Endothelial Cell Inflammation. Acta Cardiol Sin. 2014 Jul;

      (14) Xing L, et al. Beneficial effects of asiaticoside on cognitive deficits in senescence-accelerated mice. Fitoterapia. 2013 Jun.


      (15) Gray NE, et al. Centella asiatica Attenuates Amyloid-β-Induced Oxidative Stress and Mitochondrial Dysfunction. J Alzheimers Dis. 2015

      (16) Zhang L, et al. Icariin reduces α-synuclein over-expression by promoting α-synuclein degradation. Age (Dondr.) 2015 Aug

      (17) Chen YJ, et al. Neuroprotective Effects of Icariin on Brain Metabolism, Mitochondrial Functions, and Cognition in Triple-Transgenic Alzheimer's Disease Mice. CNS Neurosci Ther, 2016 Jan

      (18) Dirscherl K, et al. Luteolin triggers global changes in the microglial transcriptome leading to a unique anti-inflammatory and neuroprotective phenotype. J Neuroinflammation 2010 Jan

      (19) Rezai-Zedeh K, et al. Apigenin and luteolin modulate microglial activation via inhibition of STAT1-induced CD40 expression. J Neuroinflammation. 2008 Sep

      (20) Chen C, et al. Baicalin attenuates alzheimer-like pathological changes and memory deficits induced by amyloid β1-42 protein.  Metab Brain Dis. 2015 Apr

      (21) Song F, et al. Schizandrin A Inhibits Microglia-Mediated Neuroninflammation through Inhibiting TRAF6-NF-κB and Jak2-Stat3 Signaling Pathways. PLoS One. 2016 Feb 26;

      (22) Habtemariam S. The Therapeutic Potential of Rosemary (Rosmarinus officinalis) Diterpenes for Alzheimer's Disease. Evid Based Complement Alternat Med, 2016


      (23) Feng HL, et al. Curcumin ameliorates insulin signalling pathway in brain of Alzheimer's disease transgenic mice. Int J Immunopathol. 2016 Jul 27

      (24) Angeloni C, et al. Neuroprotective effect of sulforaphane against methylglyoxal cytotoxicity. Chem Res Toxicol, 2015 Jun 15

      Sulforaphane - Inhibiting Glycation New Target for Alzheimer's Disease

      Alzheimer's Disease (AD) and other neurodegenerative diseases, involve a complex etiology in both the initiation and progression of the disease. In AD known disease factors involve amyloid plaques, neurotangles (fibrils), inflammation and oxidative stress. Further research into this disease indicates that glycation of the amyloid, neurotangles and neurons may dramatically escalate destruction of the brain and accelerate disease progression. Mitigating glycation in the brain provides another target in the prevention of neurodegenerative diseases.

      SULFORAPHANE targets the effects of oxidative stress and inflammation, both dominating factors in degenerative brain disease, including reduction of damage attributed to  the damaging glycation. Glycation of proteins, which occurs by the irreversible attachment of sugar to causes an accumulation of damaged brain proteins and is believed to be an important causative factor in AD.(1)

      • Methylglyoxal (MG) - the role in Alzheimer's Disease. Glycated proteins lead to the formation of toxic Advanced Glycation Endproducts (AGEs) and are a significant source of inflammation. AGEs are found in high amounts in  the brains of Alzheimer's patients in conjunction with amyloid plaques and neurotangles.Methylglyoxal (MD) is a potent precursor of AGEs and is directly responsible for increased oxidative stress and deterioration of brain function.
      • Sulforaphane increases cellular protection and enhances Methylglyoxal breakdown. Sulforaphane protects the brain by multiple paths.
          1. Increases critical levels of intracellular glutathione -offering significant protection to the neurons including reduction of neuron death.
          2. Increases breakdown of MG by elevating enzyme glyoxalase activity. 
          3. Increases Brain Derived Neurotrophic Factor (BDNF). BDFN, which is neuro protective, and is reduced in AD patients. Lower BDNF levels are considered a biomarker for Alzheimer's.
          4. Maintains critical glucose uptake for neuron energy. Methylglyoxal blocks important glucose uptake by the neurons which is  totally reversed by sulforaphane. When neurons are deprived of glucose (their main energy source) they can not survive.
        •  Sulforaphane also is an inhibitory of neuroinflammation. Using human micro-glia like cells, sulforaphane has been shown to inhibit the proinflammatory cascade triggered by beta-amyloid peptides, thereby significantly reducing damaging inflammation occurring in the AD brain.(2)


        XGEVITY (Glucoraphanin precursor to Sulforaphane)



        (1) Angeloni C, et al. Antiglycative activity of sulforaphane: a new avenue to counteract neurodegeneration? Neural Regen Res. 2015 Nov.

        (2) An YW, et al. Sulforaphane exerts its anti-inflammatory effect against amyloid-β peptide via STAT-1 dephosphorylation and activation of Nrf2/HO-1 cascade in human THP-1 macrophages. Neurobiol Aging 2016 Feb;