Tuesday, 16 February 2016

Terminology associated with Glissandra's products!

Mitochondria, Glutathione, ATP production, Redox Cycling are terms often used in Glissandra's products!




Mitochondria, located within the cells are responsible for generating energy to the body and is important for optimal bodily function and cell health. 


Glutathione, is the body's "master" built in antioxidant system.


ATP production, is the cell's ability to store and supply the body with energy resources. 


Redox Cycling is the ability for the body to recycle glutathione.









Glissandra™ Skincare Inc. 305-5811 Cooney Road Richmond, BC Canada, V6X3M1

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Skin protection with Glissandra. Protect against damaging rays.

Glissandra's proprietary ingredient Glissandrin helps to ward off the effects of UV and infrared damaging rays also known as solar-irradiation which induces oxidative injury to skin tissues and skin cells.

Glissandra makes UV protection simple and effective with their skincare and supplement product line.

Rain or Shine, Glissandra products are there to minimize the damaging effects of the sun.


Glissandra™ Skincare Inc. 305-5811 Cooney Road Richmond, BC Canada, V6X3M1

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Glissandrin versus Schisandrin by Glissandra Inc.


What is the differance between Glissandrin and
 Schisandrin?


Schisandrin is the chemistry located within the Schissandra Berry which is harvested from the North East part of China and used in Glissandra's products. Schissandrin's are known to contain anit-aging properties and have been utilized in TCM (traditional Chinese Medicine) for centuries. Considered a herb, the schissandra berry has been extensively studied, researched and documented in scientific journals.

Glissandrin, is Glissandra's propreitary ingredient consisting of a suite of Schisandrins such as vitamins A, B, C and -B. A labour of love, Glissandrin has been formulated to deal with the root cause of aging (mitochondria) and change cellular reactions to anti-oxidants (free radicals).


Glissandra's products deal with the root cause of aging rather than masking the effects.




Glissandra™ Skincare Inc. 305-5811 Cooney Road Richmond, BC Canada, V6X3M1

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Tuesday, 2 February 2016

UNCOUPLING FACTOR/PROTEINS


WHAT ARE UNCOUPLING PROTEINS?

Uncoupling proteins are transporters, present in the mitochondrial inner membranes that utilize the spread of protons (positive electoral atoms) to reduce the amount of oxidant damage generated through ATP production (transport of energy for metabolism).  Energy production is used to generate heat instead of producing energy for metabolism of cells.[i] The hypothesis that uncoupling proteins of the mitochondrial membrane can reduce body adiposity (fat) and that lower metabolic weight gain.[ii]




Note: There are 5 different types of uncoupling proteins each with their own functions and chemistry.[iii]  The subject of uncoupling proteins is scientifically advanced. The above statement is a shortened version of the extensive science behind the process. To research uncoupling proteins please refer to scientific journals as your source. 


[i] http://www.ncbi.nlm.nih.gov/pubmed/11484071
[ii] http://ww.ncbi.nlm.nih.gov/pubmed/11484071
[iii] http://www.guidetopharmacology.org/GRAC/FamilyDisplayForward?familyId=207
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Alzheimers, Huntington's, ALS and Parkinson's Neurodegenerative Diseases


Can brain degeneration be combatted?


Neurodegenerative Diseases


Brain Degenerative Diseases such as Huntington’s, Parkinson’s, Amyotrophic Lateral Sclerosis (ALS) and all forms of dementia including Alzheimer’s are all classified as diseases affected by brain. Degenerative brain diseases have an enormous impact on our aging society. Alzheimer's disease progressively robs its victims of their memory. Parkinson's disease leads to impairments in movement. Frontotemporal (occurring the front area of the brain) dementia causes bewildering changes in a person's thoughts and behaviour. Huntington's disease painstakingly deprives a person of their ability to walk, talk, think and reason, often as early as in their mid-30s and 40s. In all of these degenerative brain diseases, the time from the onset of symptoms until death can be as many as ten or twenty years, with many sufferers' lives characterised by a total loss of independence in their final years.[i]




Over production of ROS (oxidative stress) is a central feature of all neurodegenerative disorders.[ii] There is strong evidence that mitochondrial dysfunction and oxidative stress plays a  role in neurodegenerative disease pathogenesis, including  four of the more well-known diseases Alzheimer's, Parkinson's, Huntington's, and Amyotrophic lateral sclerosis (ALS).[iii]

Alzheimer's Disease

Alzheimer's disease is characterised by loss of neurons (specialized nerve cells) and synapses (nerve cell signaling) in the cerebral cortex (outer layer of frontal part of the brain playing a role in consciousness) and certain subcortical regions (functional, connective and developmental areas of the brain). This loss results in gross atrophy (shrinkage) of affected areas of the brain.

Parkinson's Disease

Parkinson's disease is the second most common neurodegenerative disorder. Parkinson's disease is a degenerative disorder of the central nervous system. It results from the death of dopamine-generating (neuro-transmitter that send signals to other nerve cells).


Huntington's Disease


Huntington’s Disease causes astrogliosis (decrease of brain and spinal cord cells) and loss of neurons (specialized nerve cells).  Areas of the brain are affected according to their structure and the types of neurons they contain, reducing in size as they cumulatively  lose cells.


Amyotrophic Lateral Sclerosis (ALS) also commonly known as Lou Gehrig’s Disease


Amyotrophic lateral sclerosis (ALS or Lou Gehrig’s Disease) is a disease in which motor neurons are selectively targeted for degeneration affecting movement and speech.


Aging and Neurodegeneration


The greatest risk factor for neurodegenerative diseases is aging. Mitochondrial DNA mutations as well as oxidative stress both contribute to aging.  Many of these diseases are late-onset, meaning there is some factors that change as a person ages for each disease. One constant factor is that in each disease, neurons (specialized nerve cells) gradually lose function as the disease progresses with age.[iv]  Cell health is imperative to mitigate the damaging effects associated with degenerative disease.






[i] http://www.neuroscience.cam.ac.uk/research/cameos/DegeneratingBrain.php
[ii] https://en.wikipedia.org/wiki/Neurodegeneration
[iii] https://www.ncbi.nlm.nih.gov/pubmed/17051205
[iv] https://www.ncbi.nlm.nih.gov/pubmed/17051205
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Tuesday, 26 January 2016

Schisandrin B can help with damaging effects of UV exposure.

Exposure to UV (ultraviolet) radiation can have an impact on health. Sunlight is the major cause of UV exposure.  Although sunlight has some benefits to the body such as the absorption of vitamin D and aiding in the treatment of specific medical procedures, care must be taken to avoid unnecessary exposure.

Free radicals (such as short wave UV radiation from the sun) alter the structure of the body’s cells eventually leading to cell death. Risks associated with overexposure to UV light are erythema (redness and inflammation) premature aging, eye damage, skin cancer/s and weakening of the immune system.


“Excessive exposure to ultraviolet radiation is associated with different types of skin cancer, sunburn, accelerated skin aging, as well as cataracts and other eye diseases. The severity of the effect depends on the wavelength intensity and duration of exposure”[1] 

Schisandrin B can be a protective barrier to UV exposure. Schisandrin B, a key component of Glissandrin™, can protect against solar irradiation-induced oxidative injury in skin tissue and skin cells, according to recent research findings from the laboratory of Dr. Robert Ko at the Hong Kong University of Science and Technology.[2]

As the largest organ in the human body, the skin serves as an effective barrier for protecting against various external threats. This includes exposure to harmful solar irradiation – particularly UV and infrared rays-which research has shown to be a major cause of skin aging. Although human skin tissue possesses non-enzymatic and enzymatic antioxidant defense systems (built in anti-oxidant eradication processes) to cope with the increased oxidative stress caused by solar light radiation, long-term exposure or overexposure to solar light can overwhelm the antioxidant system.[3] When the antioxidant system is taxed, cell death occurs which leads to aging.


What if there was a way to enhance the skin’s natural antioxidant defenses to prevent photo-aging entirely? Schisandrin B (Sch B) is able to do just that, ushering in a new era in UV protective skincare. Schisandrin B is derived from the Schisandra fruit, an herb commonly used in Traditional Chinese Medicine (TCM). This naturally occurring herbal ingredient has been found to produce tissue non-specific protection against oxidative injury by enhancing cellular and mitochondrial glutathione antioxidant status in the heart, liver, kidney, and brain.[4]



The countries with the highest rates of skin cancers may surprise you. 


The top three countries with the highest rates of skin cancer and ranked per death/100,000 people are New Zealand, Australia and Slovenia. Often, these individuals also are diagnosed with melanoma which is the most virulent form of skin cancer. Kiwi's (New Zealander's) and Aussie's (Australians) are sun loving nations with residents being approximately 13 more times likely to develop skin carcinomas.

The KEY in preventing skin damage is to take precautions such as limiting over excessive sun exposure, covering up when required and the constant application of UV protection products.  Another way to protect the skin from UV damage is to provide a protective barrier using Shisandrin B based products.


More information on Schisandrin B can be found at these independent websites:
• National Institutes of Health (http://www.nih.gov/)
• PubMed (http://www.ncbi.nlm.nih.gov/pubmed/)
• Natural Medicines https://naturalmedicines.therapeuticresearch.com (formerly National Standards)



[1] https://www.ccohs.ca/oshanswers/phys_agents/ultravioletradiation.html
[2] http://www.glissandra.com/clientinc/uploadProtectiveSkincare.pdf
[3] http://www.glissandra.com/clientinc/uploadProtectiveSkincare.pdf
[4] www.glissandra.com/clientinc/uploadProtectiveSkincare.pdf
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Friday, 15 August 2014

More from Prof. Robert Ko on the BFT debate with Dr. John

Professor Robert Ko
AUGUST 2, 2014

Dr. John, please find below my answers to your questions.

Respectfully, Robert

1. What is the clinical evidence that Glissandra effects anti-aging benefits on skin? How are they documented?

已經證明，以防止在體內和在體外通過太陽能光照射引起的氧化損害。

lol - okay even us scientists need to have a sense of humour!

Seriously though, Glissandra has been shown to protect against oxidative damage induced by solar light irradiation both in vivo and in vitro.

  • That would qualify as antioxidant. Yet (based on what you have said) first it raises ROS (reactive oxygen species). Would you then say it is an a pro-oxidant first (ROS contributor) but then upon adaptation to repeated ROS stress (the signal) it becomes antioxidant (ROS quencher) with time?
  • Yes. Glissandra serves as a pro-oxidant which generates signaling ROS that can activate Nrf2-mediated expression of antioxidant genes. The dependency on cellular enzyme (CYP) to metabolically generate ROS is self-limiting such that pathological events will not occur.
Two clinical trials using Visual anti-aging assessments were conducted. The duration of the studies were 8 weeks. Data collected were tabulated and analyzed.

 North American Trial

Visual anti-aging assessments from 35 subjects of diverse ethnicities, with ages ranging from mid 20’s to late 60’s, from both genders.

South East Asia Trial

Visual anti-aging assessments from 28 subjects of Asian ethnicity with 17 subjects with age <45, 8 subjects with age 45-55, 3 subjects with age 55-65, from both genders.

  • Visual trials with or without controls? Single arm studies without histology are extremely weak on the evidence scale. There are literally tens of thousands of such studies in the world of aesthetics, all generally saying the same thing. Are we to believe them all? It would help immensely to have some validation with split face, controls, serial histology, tape stripping for gene expressions or cytokines, etc.
  • The development of Glissandra as skincare product is based on the over 20 years of research on its Schisandra berry-derived active component, which has been shown to be able to enhance the mitochondrial structural and functional integrity in various tissues, particularly under conditions of oxidative stress. Topical application of the active component at certain critical concentrations was found to produce similar biological effects on animal skin tissue and cultured human fibroblasts. With the strong belief that the enhancement of Skin Qi - cellular energy status can increase the vitality of skin cells, we suggest the development of Glissandra as skincare product. The pre-market testing conducted on human subjects, though having low scientific merit as implicated, is instrumental to collect users feedback prior to the product launch. Surprisingly, Glissandra produces many unexpected beneficial outcomes in human subjects. As far as the basic research is concerned, the "Proof-of-Principle" testing outcomes support the postulated application of the active component in skincare product. 
Both studies documented dramatic effects on various signs of skin aging from end users.


  • Define dramatic. I consider plastic surgery to be dramatic? Compare to that.
  • Professor Robert Ko AUGUST 15, 2014

  • Many obvious improvements on skin before and after use which may not be as dramatic as those of "successful" plastic surgery. However, we believe that Glissandra offers a natural way to enhance the vitality of skin cells rather than doing spot fixing as in the case of plastic surgery.
2. How is the active delivered? What vehicle? In what doses? Continuous vs discontinuous? How deeply does it penetrate?

The active is delivered by passive diffusion. The active is lipophilic, and is readily absorbed by skin.


  • Have you measured it? What you describe defies known stratum corneum absortion dynamics. The stratum corneum (SC) is a radically different biomembrane compared to other membranes in the body in function and composition. The SC is less permeable for lipophilic compared to the water-soluble compounds. Diffusion alone is rarely enough. Most botanically-derived substances e,g, antioxidants, vitamins) have great difficulty getting past the stratum corneum. Retinoids are an exception. But the stratum corneum would seem to be a weak place to carry out hormesis, due to its rapid turnover (memory effects) and the transformation of cells from metabolically active to organelle stripped as they mature from basement membrane to surface. Some measure of penetration seems to me to be crucial to support the hypothesis.
  • Professor Robert Ko AUGUST 15, 2014
  • Given the low molecular weight and high lipophilicity of the active component of Glissandra, its bioavailability to skin tissue/cells should not be an issue. Whether or not  hormetic response can be triggered in Stratum Corneum would also be dependent on the concentration of the hormetic agent. As long as mitochondria are present in the cells, Glissandra can produce the effect.  After all, "dramatic" effect were observed in human users. 
3. How is Glissandrin transported into cells to affect mitochondrial functions? By which known mechanism?

Glissandrin is readily transported via diffusion into the cytoplasm and then mitochondria . The active compound is metabolized by cytochrome P-450 enzymes (in both cytosolic and mitochondrial compartments), with resultant generation of signaling ROS which in turn activate the MAPK/Nrf2 pathway. The consequent increased expression of antioxidant genes can enhance the mitochondrial antioxidant capacity and thus the mitochondrial ATP generation.


  • That is a concept that may works in cell cultures, but not in vivo. Nearly everything that happens in skin depends on active trans[port or some sort of receptor-triggered event cascade. Since the outer layers of the stratum corneum is metabolically speaking remarkably hypoactive, you need to explain how this would all work NOT in a culture of keratinocytes or fibroblasts, but in intact live human skin.
  • PROFESSOR ROBERT KO AUGUST 15, 2014

  • Sorry. I don't see why the active component of Glissandra cannot elicit  cellular responses in skin cells, either cultured or intact (in vivo), via the CYP-catalyzed ROS-mediated MAPK/Nrf2 signaling pathway.
4. What cell populations in skin is it affecting?

As the active compound of Glissandra is bioavailable to all tissues in the body, it is reasonable to assume that Glissandrin is bioavailable to all types of skin cells.

  • You speak of “all tissues of the body” as though Glissandra is being ingested and transported via the circulation. That paradigm doesn’t hold for topically applied substances. First you have to show its site of deepest penetration/action (epidermis, dermis, subdermis), and if epidermal only, what layer (stratum corneum vs deeper epidermis). Very few substances get past the stratum corneum in physiologically active quantities. That is the function of skin – to keep things out. We have to assume that topical Glissandra is not arriving via the circulation.
  • You need to demonstrate what cells it is acting on and how it gets there.
  • PROFESSOR ROBERT KO AUGUST 15, 2014

  • Topical application of Glissandra produces beneficial effect on skin tissues but not other tissues in the body. Oral administration of the active component of Glissandra was found to enhance the mitochondrial structural and functional integrity in various tissues.
5. If there is ROS signaling – what is the signal cascade? What other well known biochemicals are affected?

The signaling cascade involves the redox-sensitive MAPK/Nrf2 pathway. The activation of Nrf2 increases the expression of antioxidant genes such as enzymes in the glutathione antioxidant systems and superoxide dismutase, etc.

  • PROFESSOR ROBERT KO AUGUST 15, 2014

  • Chronic UV exposure at a desirable (safe) dose can produce a similar hormetic antioxidant response. Whether or not the extent of UV exposure can be effectively controlled within a safe limit is questionable, not to mention a sunburn which is a manifestion of overdose. As mention earlier, the prooxidant effect of the active component of Glissandra is self-limiting (ie. safe).
6. As with other mitochondrial stressors is there a shift toward anaerobic glycolysis?

Glissandra differs from other metabolic stressors in that it won't increase the cellular energy demand and thus a shift toward anaerobic glycolysis.

  • Let’s focus on the ROS production and disposal, and its consequences. If Glissandra increases ROS production, what is the ROS disposal mechanism, and why is it good to keep applying an ROS stimulus (as a hormetic signal) after the hormesis has taken place? Why continue to use daily an ROS generating topical? Why would that not risk micro-inflammation, which would then become chronic, with other (undesirable) adaptations? Why not a sensitizing dose and then a booster say every 2-3 weeks?

  • Thanks for indulging our curiosity.
  • PROFESSOR ROBERT KO AUGUST 15, 2014

  • A good question indeed. The signaling ROS is reduced by GSH (Glutathione), with resultant change in cellular GSH redox status, which in turn trigger the redox-sensitive signaling pathway and elicit antioxidant response. GSH will be regenerated from its oxidized form through glutathione redox cycling. Recurrent application of Glissandra is essential to keep this cycle working and set the cellular antioxidant machinery on a "ready" mode. 

  • I look forward to continuing to share our science with you and your readers.
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