Dr Guan's 30 year research about cGP and the science of ageing.
Medical researchers and scientists have for many years been researching ways in which to synthetically increase the IGF-1 hormone (insulin-like growth factor 1) .
The IGF-1 hormone is responsible for promoting the growth of new cells and capillaries. This is especially important as the body ages. The IGF-1 cannot be directly or artificially increased by supplementation.
Then our Chief Scientist, Dr Jian Guan made a world first discovery. She discovered that a molecule called cGP (cyclic Glycine-Proline) was responsible for controlling the IGF-1 hormone in our body. Thus by increasing the level of cGP in our body, the cGP will essentially command the IGF-I to build more blood vessels.
Dr Jian Guan, was then recognised as the world-wide authority on cGP. In 2017 she discovered that NZ blackcurrants contained high volumes of natural cGP which when taken would regulate optimum levels of IGF-1 in the body.
Dr Jian’s clinical scientific research studies validated the levels of cGP the human body needs. Trials were then undertaken to establish how our product cGPMAX™ could deliver enough natural cGP to the body to lift and maintain IGF-1 levels in the human body.
The culmination of the research has led The cGP Lab to develop our hero ingredient called cGPMAX™.
The cGP Lab has developed products that confidently and consistently deliver the recommended daily dose of natural cGP from New Zealand blackcurrants.
The cGP Lab are now utilising this knowledge to further research the testing and commercialisation of other sources of natural cGP and the effects of supplementation of cGPMAX™ on various health conditions, including metabolic syndromes.
The Impact of cGP on Neurological Conditions
Memory Loss Caused by Poor Circulation in Ageing Brains
A healthy brain constantly produces new blood vessels to replace the loss of capillaries (small blood vessels). The body’s ability to make new blood vessels diminishes with age . As a result, the capillary nets that deliver oxygen and nutrients to brain cells are getting fewer and fewer with age. Undernourished brain cells do not work and the build-up of toxins can kill the brain cells slowly causing brain degeneration.
The function of cGP is to encourage the cells in the brain to make new blood vessels [1, 4] and taking a daily dose of our cGPMAX™ supplement allows the body to produce more blood vessels, increasing blood circulation in the brain. A study shows that older healthy people with higher levels of cGP in their blood circulation show better memory and other cognitive function . Gradually increasing the level of cGP in the blood as the body ages is the key to keeping cognitive function normal whereas people with dementia show a gradual decreasing of cGP as they age .
Increasing cGP levels through supplementation or intervention, such as cGPMAX™ may help older people retain their memory and slow down the progress of memory decline and preventing dementia.
Brain Degeneration in Parkinson’s Disease
The body’s ability to make new blood vessels is also impaired in the brains of people suffering from Parkinson’s , partially due to their impaired IGF-1 function .
The function of IGF-1 becomes impaired due to high levels of the IGF binding protein (IGFBP)-2, as was present in the brains of people suffering from Parkinson’s . The IGFBP-2 acts as a locker to prevent IGF-1 from being functional. As a result , more IGFBP-2 impairs the IGF-1 function. Taking additional cGP via a cGP supplement can unlock the IGF-1 from the IGFBP-2, resulting in improved IGF-1 function, thus helping the brain to produce more blood vessels, thus improving brain function.
We conducted a small clinical trial to test whether increasing cGP through supplementing cGPMAX will lead to any improvement in PD patients [11, 12]. Four weeks supplementation of cGPMAX (previously known as Brain shield) increases the level of in the blood and brain with a positive result of reduced anxiety and degression [11, 12].
Poor vascular function and changes to the IGF-1 function in human brains is known to contribute to dementia in people with Alzheimer’s.
The IGF-1 function is determined by amount of protein and amount of IGF-1 that has been unlocked by cGP . Compared to the non- Alzheimer’s cases, the IGF-1 function is significantly impaired which contributes to brain degeneration typical of people suffering from Alzheimer’s . As found in the brains of Parkinson’s diseases, IGFBP-3 is increased in the brain of Alzheimer’s diseases, which locks in IGF-1 and further impairs IGF-1 function .
The amount of cGP that acts to unlock IGF-1 from IGFBP-3 is also increases. This self-made defence, however, is not sufficient to stop brain degeneration. The supplementation of cGPMAX™ into the brain may also help an Alzheimer’s brain to strength the IGF-1 function by unlocking more IGF-1 from IGFBPs.
Ischemic Attack, Commonly Known as a Stroke
A stoke occurs when the blood supply to a part of the brain is suddenly disrupted.
Within 3 days after a stroke event, the patient’s level of cGP is low compared to non-stroke participants . However, their cGP level gradually increases during the first 3 months following the stroke, while patients make a steady recovery . The study found that 3 months after a stoke, patients with higher levels of cGP at the time of their stroke made a better recovery . The body’s self-made recovery plateaus after 3 months. The patients may make a better, faster and longer-term recovery if the cGP level increases through an intervention at the time of stroke.
High blood pressure is the result of poor circulation and reduced vascular function. The most common cause of high blood pressure is aging and metabolic disorders.
People with metabolic disorders especially high blood pressure have a low level of cGP  and have higher chance of having a stroke, cognitive impairment and premature brain aging. Increasing levels of cGP through supplementation may normalise blood pressure and reduce organ fat, thereby improving blood vessel function and overall circulation.
In summary, IGF-1 function starts to decline at around 45 years of age. In response, the body’s demand for cGP increases to maintain normal IGF-1 function. The body’s self-made protection by producing more cGP may not be sufficient to maintain health. When body starts to lose the ability to make cGP, cGP levels will decline, as seen in people with hypertension, stroke or dementia [6-8].
To counteract this, increasing cGP in your body by supplementing with cGPMAX will help to maintain your health. Dr Jian’s research has shown that maintaining high levels of cGP helps to keep your mind and body healthier as you age.
Do you want to find out more about the 30 years of research that has gone into developing cGPMAX™ ?
A Selected List of cGPMAX™ Scientific Papers
2021 Singh-Mallah G, Ardalan M, Singh K, Kang D, McMahon C, Mallard C and Guan J. Administration
of cyclic glycine-proline during infancy improves adult spatial memory,
astrocyte plasticity, vascularization and GluR-1 expression in rats. Nutritional Neuroscience. August 20212021 Kang D, Waldvogel H, Fan D, Wang A, Faull R, Curtis M, Shorten P and Guan J. The autocrine regulation in human brain of Alzheimer’s diseases. Accepted with revision in Psychoneuroendocrinology2020 Fan D, Pitcher T, Dalrymple-Alford J, MacAskill M, Anderson T and Guan J. Plasma cGP/IGF-1 molar ratio is associated with cognitive status of Parkinson disease. Alzheimer’s Dement. 2020;1–10. 2019 Li FX, Liu K, Gray C, Harris P, Reynolds C, Vickers M and Guan J. Cyclic glycine-proline normalizes systolic blood pressure in high-fat diet-induced obese male rats. Nutrition, Metabolism & Cardiovascular Diseases. 30: 339-346 2019 Li FX, Liu K, Wang A, Harris P, Vickers M and Guan J. Cyclic Glycine-Proline Administration Normalizes High-Fat Diet-Induced Synaptic Expressions in Obese Rats. Neuropeptides 76, 101935, 10.1016/j.npep.2019.05.0062019 Fan D, Krishnamurthi R, Harris P, Barber PA, Guan J. Plasma cyclic glycine proline/IGF-1 ratio predicts clinical outcome and recovery in stroke patients. Annals of Clinical Translational Neurology 2019;0 2018 Fan D, Alamri Y, Liu K, MacAskill M, Harris P, Brimble M, et al. Supplementation
of Blackcurrant Anthocyanins Increased Cyclic Glycine-Proline in the
Cerebrospinal Fluid of Parkinson Patients: Potential Treatment to
Improve Insulin-Like Growth Factor-1 Function. Nutrients 2018;10:714. doi:10.3390/nu10060714. 2018 Alamri Y, The use of dietary supplements and perceived quality of life in patients with Parkinson's disease. J Clin Neuroscience 56: 137-1362018 GUAN J, SINGH-MALLAH G, LIU K, SHORTEN P, THOMPSON J, MITCHELL
E, TAYLOR R, HARRIS P, BRIMBLE M, THORSTENSEN E AND MURPHY R. The role for autocrine regulation of IGF-1 in pregnancy related obesity, a potential biomarker for weight changes. Journal of Biological Regulators and Homeostatic agents 32(3): 11-25 2017 SINGH-MALLAH G, MCMAHON CD, GUAN J and SINGH K Cyclic-glycine-proline promotes post-lactational involution in mammary glands of rats through inhibiting IGF 1 function. Journal of Cellular Physiology 232 (12) 3369-3383doi: 10.1002/jcp.25782 2016 SINGH-MALLAH G, SINGH K, MCMAHON CD, HARRIS P, BRIMBLE MA and GUAN J, Maternal-infantile
transfer following oral administration of cyclic-glycine-proline in
lactating rats and its effect on improving memory in the offspring Endocrinology 157(8):3130-9 2017 YANG P, WALDVOGEL H, Scott E, FAULL R, DRAGUNOW M, TURNER C, AND GUAN J. Endothelial degeneration of Parkinson disease is related to alpha-synuclein aggregation. Journal of Alzheimer’s Disease & Parkinsonism 7: 370. doi: 10.4172/2161-0460.1000370 2017 YANG P, WALDVOGEL H, FAULL R, DRAGUNOW M, TURNER C, AND GUAN J. Vascular remodelling is impaired in Parkinson’s diseases, Journal of Alzheimer’s Disease & Parkinsonism 7: 313. doi: 10.4172/2161-0460.1000313 2015 Yang P, Pavlovic D, Richard Faull, Mike Dragunow Beth Synek, Clinton Turner Henry Waldvogel and Guan J, String vessel formation is increased in the brain of Parkinson disease. J of Parkinson Diseases. 5 (2015) 821–83620152015 GUAN J, HARRIS P, BRIMBLE M, LEI Y, LU J, YANG Y AND J GUNN A, The
role for IGF-1 derived small neuropeptides as a therapeutic target for
neurological disorders. Expert Opinion on Therapeutic Targets. Invited review 2015 Feb 5:1-9 2015 PHILLIPS GMA, SHORTEN PR, WAKE GC AND GUAN J, Dynamical modelling of the effect of insulin-like growth factor -1 on human cell growth. Mathematical Bioscience Journal 2015 Jan; 259:43-54. 2014 GUAN J, GLUCKMAN PD, YANG PZ, KRISSANSEN G, SUN K, ZHOU Y, WEN
JY, SHORTEN P, WAKE G, MCMAHON CD, THOMAS MF, PHILIP G, CHEN W, S MOON, A
REN AND LIU DX, Cyclic glycine-proline regulates IGF-1 homeostasis by altering the binding of IGFBP-3 to IGF-1 Scientific Report, 4, 43882014 MATHAI S, GUNN AJ, BRIMBLE MA, HARRIS PW AND GUAN J. Neuroprotection with Glycin-2methyl-Proline-Glutamate (G-2mPE) after hypoxic-ischemic brain injury in adult rats. Journal of Experimental Stroke Translational Medicine 6: 1-1120132013 GUAN J, MATAI S, LIANG HP AND GUNN JA Insulin-like growth factor-1 and its derivatives: Potential pharmaceutical application for treating neurological conditions. Recent Patents on CNS drug discovery 2013 8(2) 142-168 2013 Guan J, Pavlovic D, Darkie N, Waldvigel H, Green C and Nicholson L. Vascular degeneration of Parkinson Disease. Brain Pathology 23(2) 154-164 (impact factor 4.7 doi: 10.1111/j.1750-3639.2012628)2012 MATHAI S, GUNN AJ, BACKHAUS A AND GUAN J Window of opportunity for neuroprotection with an antioxidant, Allene Oxide Synthase, after hypoxia-ischemia in adult male rats, Journal of Neuroscience and Therapeutics 18(11):887-94 2012 ZHANG R, KADAR T, SIRIMANNE E, MACGIBBON A AND GUAN J Age-related memory decline in rats is associated with vascular and microglial degeneration, Behavioural Brain Research 1;235(2):210-7 2010 GUAN J, ZHANG R, L DALE GANDAR AND VICKERS M. NNZ-2591, A novel diketopiperazine, prevented scopolamine-induced acute memory impairment in the adult rat. Behavioural Brain Research 210, 221-228. 2009 GUAN J AND GLUCKMAN P. Endogenous small neuropeptides
and their analogues: a novel strategy for the development of
pharmaceuticals for neurological conditions, invited review by British Journal of Pharmacology 157, 881-8912009 SHAPIRA S, MATHAI S, ZHANG R AND GUAN J Delayed
peripheral administration of the N-terminal tripeptide of IGF-1 (GPE)
reduces brain damage following microsphere induced embolic damage in
young adult and aged rats. Neuroscience Letter 454 (1) 53-572009 KRISHNAMURTHI, R V M., KIM A H., MATHAI S. RONG ZHANG AND GUAN J. Delayed treatment with a novel diketopiperazine improves motor function after 6-OHDA lesion in rats. British Journal of Pharmacology 156, 662-672.2008 JACOBSON L, ZHANG R, ELLIFFE D, CHEN C, MATHAI S, MCCARTHY D, WALDVOGE H AND GUAN J. Co-relation of cellular/vascular changes and spatial memory during aging in rats Experimental Gerontology 43, 928-9382007 GUAN J, MATHAI S, HARRIS P, BRIMBLE M, WEN JY ZHANG R and GLUCKMAN P Peripheral
administration of a novel diketopiperazine, NNZ 2591 prevents brain
injury and improves somatosensory-motor function following
hypoxia-ischemia in adult rats. Neuropharmacolocy 53: 749-762 2007 SVEDIN P, GUAN J*(co-responding author), MATHAI S, ZHANG R, WANG XY, HAGBERG H AND MALLARD C Delayed
peripheral administration of a GPE analogue induces astrogliosis and
angiogenesis and reduces inflammation and brain injury following
hypoxia-ischemia in the neonatal rat. Developmental neuroscience 29: 393-402 2005 BAKER A M, BATCHELOR D C, THOMAS G B, CLARK R G, RAFIEE M, LIN H AND GUAN J Central
penetration and the stability of N-terminal tripeptide of insulin-like
growth factor-I, glycine-proline-glutamate in adult rat. Neuropeptides 39(2) 81-872004 GUAN J, THOMAS G B, LIN H, MATAI S, BACHELOR D C, GEORGE S, FERNANDEZ J AND GLUCKMAN PD Neuroprotective
effects of the N-terminal tripeptide of insulin-like growth factor –1,
glycine-proline-glutamate (GPE) following intravenous infusion in
hypoxic-ischemic adult rats. Neuropharmacology Vol 47 (6): 892-9032004 KRISHNAMURTHI R, STOTT S, MAINGAY M, FAULL RLM, MCCARTHY D, GLUCKMAN PD AND GUAN J. N-terminal tripeptide of insulin-like growth factor –1 (GPE) improves functional deficits after 6-OHDA lesion in rats. NeuroReport 15(10); 1601-1604 2003 GUAN J, BENNET L PD GLUCKMAN AND GUNN AJ, Insulin-like growth factor-1 and the ischemic brain. Progress in Neurology 70 (6), 443-462 2000 GUAN J., KRISHNAMURTHI, R., WALDVOGEL, H.J., FAULL, R.L.M., CLARK, R. AND GLUCKMAN, P. N-terminal tripeptide of IGF-1 (GPE) prevents the loss of TH positive neurons after 6-OHDA induced nigral lesion in rats. Brain Research 859 (2) 286-292,1999, GUAN J, WALDVOGEL H, FAULL R, GLUCKMAN P AND WILLIAMS C The
effects of the N-terminal tripeptide of insulin-like growth factor-1,
glycine-proline-glutamate in different regions following
hypoxic-ischemic brain injury in adult rats. Neuroscience 89: 649-659