Deuterium depleted water experiment- Day 32

Day 32 of my deuterium depleted water experiment. 

6 months to a year to live without chemo?.... apparently. Deuterium depletion protocol for my Mother

I haven't mentioned this much, but my Mother was diagnosed with oesophageal cancer not long after my diagnosis 5 years ago. There was no cancer, let alone any disease in my family before I was diagnosed with my malignant brain tumour. All the compelling evidence that we had compiled strongly supported the idea that for her, the cancer was directly caused by alendronate, a drug she was taking for her osteoperosis. We conducted extensive research into this at the time, and were shocked with what we found. After speaking to researchers who were looking into the association between alendronic acid use and incidence of oesophageal cancer and enquiring about the type of damage to the lining of the oesophagus things became even more clear. I actually wrote about this in a blog post from a couple of years ago...

https://mybraincancerstory.blogspot.com/2016/05/meeting-my-heroes-and-learning-about.html

After treatment (chemo and radiation).... and diet change... she appeared to recover without the need for surgery. The tumour seemed to disappear after the gruelling treatments, however about a month ago we discovered she had a tumour in the colon (which has since been removed with surgery) and disease that has spread to other areas including the lymph nodes, with nodules in the lungs. This is deeply unpleasant of course.

Following a long consultation with her oncologist, we were informed that the nodules in the lungs were most likely malignant and the degree of spread was such that any treatment from here on would only be palliative and that prognosis would be poor, even with treatment. We were given a prognosis of 6 months to a year, depending on whether on not she would decide to have chemotherapy and partly dependent upon results of a lung biopsy.

She decided not to have the biopsy as prognosis would be poor either way. We could understand that a biopsy could help to determine the lineage of this disease (if they are not just 'benign' nodules- some type of fibrosis possibly from radiation 5 years ago), but prognosis either way would still be far from favourable so we agreed it wasn't necessary for the path she felt was right for her. The other issue is quality of life. If you have a 'terminal' disease and treatment (for the few who actually respond to it) aims to give a few months more life while making you ill in the process, you have to ask what the point in that is.

We decided to opt for metabolic therapies instead and say no to chemotherapy in this instance. It was an informed decision based on all the information we had and my Mother feels 'happy' with this treatment plan. She felt so ill during treatment for her last cancer, and this cancer was most likely caused by treatment from the first so it just made a lot of sense to avoid it this time. We want to treat it by building her up rather than knocking her down with 'palliative' treatment that was likely to be ineffective even for this purpose.

Why not aim high and try and do what few even dare to consider? Treating cancer with kinder treatments to restore homeostatic mechanisms and support mitochondrial function.

My Mother is a smart woman and as such is skeptical of anything I say, which I love. We had long discussions about deuterium depletion and after outlaying my case for it with the underpinning mechanisms of these treatments she was open to trying it and became convinced that this was the right path for her to follow for her. We have nothing to lose trying this and in the worst case scenario her quality of life is likely to improve.

Without hesitation, we then immediately contacted Dr. Que Collins from the Centre for Deuterium Depletion and got to work with a protocol that would be suitable for her based on her personal situation and disease state. You can find out more about the centre and the relationship between deuterium and cancer see the link below:

http://www.ddcenters.com/conditions-cancer-2-2/

The deuterium depletion protocol that she has decided to follow looks like this:

Deuterium depletion water therapy (Preventa)

Nutrient dense, low deuterium ketogenic foods

Breathing therapy

Natural light therapy

Red and near infrared therapy

Body temperature cycling

Environmental mitigation

Metabolic supplementation

Deuterium Depleted Water used in clinical trials- Preventa

Red light therapy- JOOVV
https://joovv.com

This plan will evolve as we go on and her cancer markers will be assessed at regular intervals. I have decided to document her progress and how she feels throughout this 'journey'. This is all quite significant, because she has decided to NOT opt for the standard of care (biopsy, chemo, radiation), so any response is certainly meaningful and cannot be ignored.

We hope for the best. I love my Mother with all my heart and strongly feel this is the most logical step forward. I will keep you updated on her progress.

abcam Cancer and Metabolism Conference 2018- 1/3

I recently attended abcam’s Cancer and Metabolism conference in Cambridge and realise that I haven’t written about it yet. 

In a nutshell, the event covered major aspects of metabolic transformation in cancer and attempted to highlight potential therapeutic approaches to target cancer-specific metabolic pathways. The conference allowed me to build on my existing knowledge of metabolism and metabolic signalling in cancer and introduced me to more advanced concepts, novel methods, and emerging technologies to target these pathways.

I was also introduced to a collaborative European wide research project called TRANSMIT: Translating the role of Mitochondria in Tumorigenesis. 

The angle they are taking with TRANSMIT is viewing cancer as not only a genetic, but also a metabolic disease. 

TRANSMIT Project- https://www.transmit-project.eu

Personally I think it is a metabolic disease with metabolic solutions and the genetic mutations are as a result of mitochondrial dysfunction. With healthy mitochondria it is my belief that you simply do not get cancer. However… whether it is cause or effect, the focus on cancer metabolism is a huge step in the right direction for me and I am greatly encouraged by seeing this type of event take place and to be able to have these conversations. 

The research I came across at this conference was all work that could directly be translated to the patient (‘from bench to bedside’) so I found this more engaging than most conferences I have been to. 

More and more now scientists are not only investigating the conribution of oncogenes and tumour suppressor genes (an approach which, as the primary focus over the years has been woefully ineffective), but we are also focusing on the intricate metabolic plasticity that transformed cells undergo to survive the adverse, volatile tumour microenvironment conditions. 

The mitochondria is the star player here, and rightly so, because they act as key players in cancer metabolic restructuring due to their crucial role in powering all functions of the cell by producing complex molecules for function, growth and survival. When these normal processes become aberrant, causing dysfunction, as is the case with cancer, this biosynthetic powerhouse of the cell is forced to adapt through more anaerobic respiration, and so is forced to provide energy and metabolites to the cell in different ways. 

These cells are very clever and can learn how to survive by using different substrates to stay alive and will become more resiliant with time if provided with the fuel that it needs to thrive. It will then become more able to use alternative substrates for energy as it adapts and learns, and here we have parallels with Darwinian biology. In the absence of nutrients, cancer cells can even scavenge from cellular debris in a process called ‘macropinocytosis’, so this is worth considering with any metabolic therapy, most likely it seems when necrotic tissue is a hallmark of disease as it often is with glioblastoma. That’s my opinion anyway, seems to make sense. Cancer doesn’t want to die, as a result of these metabolic abnormalities we have an occurance of mutations in metabolic enzymes encoded by both nuclear and mitochondrial DNA. 

It is my belief therefore, that more solid tumours would be most responsive to any kind of metabolic approach, as they have clear margins, are less diffuse and invasive, and as such have likely not yet progressed to being able to use multiple substrates to become more resilient to targeted metabolic therapies. More aggressive malignancies will likely require a combination approach of dietary manipulation and drugs targetting key metabolic targets in line with what the tumour’s metabolic signature may dictate. 

Electron microscopy morphology of the mitochondrial network
in gliomas and their vascular microenvironment-
https://www.sciencedirect.com/science/article/pii/S0005272810007437

As I began listening to the talks, the main research challenges became eminently clear. 

Firstly, we need to continue to learn about the bioenergetic plasticity of cancer in general. We have established that mitochondrial function and respiration play fundamental roles in the development and progression of cancer. The main challenges here are noted below numerically and although of major importance as a primary substrate for most cancers, its not all about the glucose:

1. Many malignancies have been shown to be able to utilise not only glucose, but also glutamine for generating cellular energy and provide metabolic building blocks to proliferate.

2. As stated, many cancers generate most of their cellular energy via mitochondrial respiration and oxidative phosphorylation (OxPhos). Glutamine is the preferred substrate for OxPhos in tumour cells.

3. Cancer cells are remarkably adaptable at using different substrates for fuel. They can even use metabolic substrates donated by ‘stromal cells’ for cellular energy generation via OxPhos. Stromal cells are present in the tumour microenvironment and are not necessarily malignant themselves but can provide the tumour with substrates it needs to keep growing.

4. Bioenergetic plasticity of cancer is a major consideration if we want to attempt to predict, understand and monitor a metabolic approach to treating cancer more effectively.

See below a poster displaying an outline of the work various research groups are undertaking as part of the TRANSMIT project:

How might we achieve this:

1. By targeting metabolic enzymes and coenzymes

2. Learning more about metabolic features of cancer cells in general. This can help us with therapeutic efficacy testing and biomarker discovery. 

Primary aims that I could see from this research:

1. Help to overcome chemoresistance

2. Come up with metabolic intervention strategies. 

3. Better understand the role of the mitochondria in cancer initiation and progression. 

4. Understanding of metabolic signatures of tumours that may respond to the ketogenic diet or specific nutrient deprivation diets. 

Dietary and drug strategies covered:

1. An energy restricted ketogenic diet. (high fat, low carb, adequate protein)

Most cancer cells thrive on glucose as major energy source and partly posess dysfunctional mitochondria leading to a reduced ability to metabolise fat. This approach is being studied as an adjunct to the standard of care. It may reduce tumour growth and prolong survival. 

2. Amino acid deprivation diets.

- Glutamine (protein restriction, temporary inhibition of enzymes involed likely more suitable)

- Methionine, cysteine

3. Fasting and diets that mimic a fasted state.

4. Drugs and drug targets

- Glutaminase inhibitors as a major target for the majority of cancers. For brain cancer perhaps more important in neuroblastoma (considered a real glutamine hog) and tumours that use up glutamine as the primary or major fuel alongside glucose as major substrates.

- Tryptophan degrading enzymes (overcoming tumour immune resistance)

- Citrin blockers- citrin is upregulated in multiple cancers.

- Targeting other novel metabolic pathways (aspartate, folate, serine, sapienate)

- Dichloroacetate (DCA)- PDK inhibitor (Pyruvate dehydrogenase kinase)- mitochondrial enzyme activated in a variety of cancers. Pyrimidine biosynthesis and growth of SDH (Succinate dehydrogenase) deficient cells is also inhibited by this drug.

- Biguanides and Kinase Inhibitors (KI)- induce opposing effects on key metabolic pathways that fuel cancer (eg. inhibition of mTOR. MTOR regulates mRNA translation initiation). 

Areas of focus: TRANSMIT

1. Cancer bioenergetics of different tumours. 

I have MR Spectroscopy, for example, and we can identify different metabolic signatures pertaining to different types of brain tumour fairly accurately from this. There may be some problems looking at areas where there is brain damage however, showing false positive results as you may see high signalling activity. It can sometimes be difficult to differentiate between malignant activity and areas of brain damage. 

2. How metabolic factors influence how cancer cells adapt to survive and proliferate could identify mitochondrial metabolic biomarkers for characterising the transformation from benign to cancer cells. 

What TRANSMIT is working on more specifically:

-Metabolic reprogramming of cancer cells- ie coordination of glutaminolysis and glycolysis. 

- Work with cancer cell models, metabolic intervention strategies.

- Improve our understanding of cancer pathology. 

- Understanding the role of fumarate hydratase in tumorigenesis.

- The mitochondrial complex 1 driven regulation of the hypoxic response in cancer cells. 

- Identifying coenzymes in cancer cells. 

Deuterium experiment part 1- Preparation.

This is the first stage of my deuterium depletion experiment. 

Please see links below the videos on Youtube to understand the link between deuterium and cancer and how you may effectively deplete deuterium from the body. 

The tests I have used will provide me with a baseline for levels of deuterium in the body. The kit I have used measures breath as a marker of deuterium in tissues and saliva or urine for deuterium in biological fluids. The two measures when taken together are used to determine the body's ability to deplete deuterium. 

Breath analysis

Deuterium depleted water (DDW)

Considerations about starting drinking the water.

Testing levels of deuterium in the body.

Orexin/hypocretic receptor signalling and cancer.

Let's consider Orexin/hypocretin receptor signalling and how we may exploit this system for brain cancer management.

As we can see in the diagrams below, orexin neutrons regulate various activities such as wakefulness, feeding, reward and thermogenesis.

A ketogenic diet, normalisation of sleep/wake cycles, fasting, stimulation of thermogenic pathways and giving the brain fuels it thrives on could act as key strategies we can adopt to take advantage of the fact that orexin appears to have potential as a novel, highly-specific treatment for various localised and metastatic cancers. This is not quite as simple as it may sound as you can always have too much of a 'good' stressor or thing before it becomes 'bad'- eustress vs distress.

We know of course that fat is a very efficient source of energy for the brain and ketone bodies are neuroprotective, the body energy level influences orexin neuronal activity to coordinate arousal and energy homeostasis. Management of chronic stress is also key as inputs from the lymbic system are important to regulate activity of orexin neutrons to evoke emotional arousal or fear-related responses.

Also consider that the brain has an abundance of mitochondria and the matrix water in the presence of cancer either by cause or effect appears to be high deuterium. Normal cells are very good at adapting to changes in levels of deuterium (in terms of reduction) but abnormal cells are not.

From my research on the subject it seems clear and viable that you can achieve greater mental stability by a kind of filtration process to deplete deuterium by drinking deuterium depleted water, as has been shown in studies of depressive disorders. We also see several studies on how deuterium depleted water can shrink tumours by restoring fumarate hydratase activity. Fumarate hydratase acts as a tumour suppressor. Here is an example of how fumarate hydratase and deuterium depletion control oncogenesis, effectively helping to put the breaks on cancer proliferation: http://cancerres.aacrjournals.org/content/74/19_Supplement/1426.short

I have little doubt that Orexin signalling cascades will also be affected by this in a positive way for cancer patients. A lot of this is theory, but it is backed by some sound science. I still have a lot of questions but I think I may have a few interesting theories on this.

Here is a nice review of orexin's unprecedented potential as a highly-specific treatment for various localised and metastatic cancers: http://journals.sagepub.com/doi/full/10.1177/2050312117735774

Reaction to Tessa Jowell's death, thoughts on repurposed drugs and deuterium. Update on Sativex.

Links relating to subjects mentioned: Deuterium content of water increases depression susceptibility https://www.sciencedirect.com/science/article/pii/S0166432814004884 Ketogenic substrates, water and drugs promote deuterium depletion of mitochondrial metabolic matrix water, offering a means to prevent tumor cell growth.- https://www.sciencedirect.com/science/article/pii/S0306987715004399#f0005 AKT as Locus of Hydrogen Bond Network in Cancer.- https://www.ncbi.nlm.nih.gov/pubmed/28590011 Tumour Treating Fields- https://www.novocure.com/our-therapy/ Essential reading about water, especially if you're into all that reverse osmosis, alkaline stuff or drink tap water.- https://www.hindawi.com/journals/jchem/2013/472323/

L-Carnitine, ketolytic enzymes and therapeutic ketogenic diets for cancer management.

L-Carnitine plays an absolutely vital role in the metabolism of fatty acids.

Mo Farah is recently, somewhat controversially been pruported to have had an injection of L-Carnitine before the 2014 London Marathon for performance gains. It is worth noting that Mo Farah is an endurance athlete, so fat is the predominant fuel source. Fat oxidation rate is high so if you can sustain this for a longer period of time you can improve limits of exhaustion.

Carnitine shuttle (1)

This IV administration by Mo Farah is now being seen by the media in this country as 'cheating within the rules' with increased scrutiny recently of 'marginal gains' in athletic performance and sport in general after the cycling 'scandal' with Team Sky riders making the most of Therapeutic Use Exemptions (TUEs) that are known to improve performance for endurance athletes.

What helps athletes often has great potential for cancer patients- ie. infusion of nutrients, certain drugs, nutritional supplements, hyperbaric chambers, cold induced thermogenesis, infrared saunas, etc.

It is interesting....

Like Mo Farah I also take L-Carnitine because it ensures efficient transfer of long-chain fatty acids to mitochondria for subsequent β-oxidation. The brain has an abundance of mitochondria and if you subscribe to the mitochondrial defect theory of cancer as I do its kind of a no brainer (pun intended) that you would want to make the most of everything you can do to do try and restore mitochondrial function here. This can potentially be very beneficial for ensuring that ketone bodies produced during fasting, or fats on the ketogenic diet actually get used so that we can attempt to attain more healthy mitochondria.

This is what I take

There is exhaustive evidence showing how supplementation with L-Carnitine could benefit cancer patients, mostly for reducing general fatigue during chemotherapy (2) but also for normalising lipid metabolism for more general health (3). Anti-dementia effects have been proposed and suggested when co-administering L-Carnitine with medium chain triglycerides (MCTs) and other agents (5, 6). A higher rate of absorption would result in rapid perfusion of the liver, and a potent ketogenic response.

Perhaps an important consideration: 

If you are thinking of taking this as a brain cancer patient however, it may be worth some exploration to see if your tumour has increased activity of ketolytic enzymes to see if it can use fats to proliferate. You can ask about this from histological findings. 

Ketone body ketolytic enzymes to assess expression of include (4): 

Succinyl CoA: 3 Oxoacid CoA Transferase (OXCT1)

3-hydroxybutyrate dehydrogenase 1 and 2 (BDH1 and BDH2) 

Acetyl-CoA acetyltransferase 1 (ACAT1) 

This can be the case in more aggressive tumours rather than typically lower grade, more solid tumours. I suspect this may be because the tumour is more diffuse, and as such the cell membrane may lack integrity and become more permeable. This is a theory I have based on research looking at alterations of membrane integrity and cellular constituents in neuroblastoma and glioma cells (8). 

I could be completely wrong with that theory, but either way there is often an overexpression of Fatty Acid Synthase (FASN) in high grade gliomas (7), a key lipogenic enzyme in glioma stem cells (GSCs), as well as other important metabolic enzymes, meaning aggressive tumours will try to use whatever they can to grow and thrive and are excellent at adapting to use alternative fuels when you restrict main substrates. These tumours will use glucose, amino acids, fats and nucleic acids for energy, and while the demand will be different for each, as the tumour becomes more aggressive the amounts will change and it becomes more and more resistant to even the most aggressive treatments. 

1. https://www.researchgate.net/figure/Schematic-representation-of-the-glyoxylate-pathway-and-the-carnitine-shuttle-in_fig1_5424693

2. https://www.spandidos-publications.com/10.3892/mco.2018.1557

3. http://onlinelibrary.wiley.com/doi/10.2903/j.efsa.2018.5137/full

4. https://nutritionandmetabolism.biomedcentral.com/articles/10.1186/1743-7075-10-47

5. https://patents.google.com/patent/US20180036274A1/en

6. Odle, J., 1997. New insights into the utilization of medium-chain triglycerides by the neonate: observations from a piglet model. The Journal of nutrition, 127(6), pp.1061-1067.

7. https://www.ncbi.nlm.nih.gov/pubmed/24789255

8. https://www.sciencedirect.com/science/article/pii/0006899382911568

Telomere biology and cancer

When I was first diagnosed I asked my oncologist about my prognosis and was told... 'well the good news is that you are still quite young.' He then went on to tell me dates for both the best and worst case scenarios. 

With biological age being so important for survival I asked 'Well then what if I just try and keep my biological age as young as possible?'. He said, 'Interesting point, well you can certainly try.'....

Telomere biology- try to stay young by supplementing with a bioavailable form of magnesium, vital for over 300 enzyme reactions in the body. Most of us are deficient and supplementation can improve sleep, energy levels, reduce seizure activity for those of us with epilepsy and improve mood.

http://www.mdpi.com/1422-0067/19/1/157/htm

World Cancer Day

I am in my 5th year since being diagnosed with incurable brain cancer. I should be happy right? Well, sometimes yes, sometimes no. Its complicated. 

There have been many occasions that I didn't think I would make it this far. I feel incredibly fortunate, but even now I am still picking up all the pieces and coping with a 'new normal'. You learn to cope better with time, but its like grieving for a life lost. There is a new me that I don't recognise and have had to get to know, even if the essence of who I am stays the same, if you look closely behind the eyes can tell a different story.

Sometimes people may just think I should leave it behind me and 'get on with it', but I can't, as, like it or not, its with me every day and I am scarred by it. The invisible disabilities,- the uncertainty,- and 'living in the moment' is how I live. day by day. I have to... and I have little choice. 

Every day I experience some type of brain dysfunction that keeps me on my toes despite my best efforts to control it all. Mind over grey matter you could say... though it doesn't always go to plan. 

Today I am thinking of all those who have lost their battle as well as all those still fighting. I don't like all these war like terms to describe such indescribable and personal thoughts, feelings, and experiences, but its all we have sometimes as its incredibly difficult to sum it all up with the appropriate words. 

How can you? Its all relative and its so personal. 

Behind the smiles, laughs and appearances on social media and in public I remain somewhat empty inside, part of me is still missing. I get incredibly frustrated at times when I feel my seizure threshold is low and I can't have the social life I used to have or be as active as I used to be. I am a very introspective person and I can beat myself up at times whenever I am left alone with my thoughts. At the same time I am a problem solver and a perfectionist, desperately trying to find solutions to every problem. What if sometimes there are no solutions? We can still try our best to 'manage' I suppose. 

Part of me feels bad about thinking this as I feel I should be happy to just be able to not have grand mal seizures and be able to walk and talk. My speech will get slurred on occasion and I get some worrying sensations, but I haven't completely lost the speech in a while now. Sometimes people misread my body language because parts of my face go numb, but I try to hide this. Inside this pains me and it is a constant reminder that I have limits now. 

I try my hardest to have a positive outlook on life, but I experience an empty feeling that I've had ever since my first seizure and then all I have had to deal with since my diagnosis. Then there is my age, the time in life where you typically start to feel about romantic love, a career, a family, etc. My experiences undoubtely make me think long and hard about this and what to do. A cancer diagnosis affects so many aspects of someone's life, and often those around them. 

I have experienced profound loss, losing good friends and losing parts of my life that I previously took for granted. 

Whenever I hear of someone who has 'lost their battle', a part of me dies a little too as I feel the pain that is left behind with loved ones having to somehow pick up the pieces. I could never appropriately sum up in words how I really feel. 

Every day I have a unique pain and internal suffering, yet I have moments of delirious happiness where I look at the simplest things in life with the wonderment they deserve while everyone else seems to just pass by and not see the beauty. Everyone has their struggles, I understand that, but there is light. Life is a series of moments and there is light and shade. Every good story has this, and your life is a story. How do you want it to be? People, places and experiences that make me smile. These are the good moments that I cherish, and I have had that this weekend as I reflect and enjoy the beauty of nature. I am grateful for these moments and I have been able to control my symptoms very well over the past couple of weeks with just a few wobbles. I am also grateful that I have been able to share this indirectly with friends. 

There will always be moments of pain and I don't want to hide this any more. I know my symptom triggers, but again, these are scars and it has taken me a good few years to come to terms with this. For me personally it is my brain, which is kind of important, but I still have empathy for others with other types of cancer because there are unique aspects of it that are difficult to understand unless you have been there. 

Its all relative and everyone has their struggles, even people without cancer, but there is the other side of it to... 

The other side is that it really opens your eyes. 

Depending on how you choose to deal with it, a cancer diagnosis can open your eyes to what you are truly capable of and it can allow you to see the world in a different way. You realise that many of the clichès are true and you have an appreciation of the fact that 'life is short' and we must make the most of it. Sometimes, admittedly, it takes time to realise this, even after a cancer diagnosis.

I am incredibly thankful for what I have and to still be here and I'm working hard to stay happy but I'm still working on it 5 years on. I still believe my cancer is incurable and will be back in future, I don't know when, and I don't think this is being negative, as it is what it is. It is an incurable form of cancer and regrettably I had some palliative treatment for it, which for this type of cancer ironically increases risk of recurrence the longer you live. That might sound strange to some, but they don't expect you to live long enough to experience that. Sometimes living longer than your life expectancy puts you under a strange kind of pressure to be happy, and I'm working out what happiness really means to me. This is something everyone probably thinks about from time to time, but I've had a massive kick up the bum and its been a pretty wild ride.

I also feel I have a duty to try my best to make things better for myself and others in future. I promise I will try my very best to do all I can and while I do that I will make efforts to be a better person and to live the life that I want to live. 

LIFE IS FOR LIVING! 

This is the greatest message of all and one that I feel we all need to remember. 

I wish for a world where we can at least say that cancer is a chronic condition we can live WITH than one that we die OF. I think this is possible and it is why I am hopeful I will be successful in an important interview I have coming up on the 22nd of this month. 

I wish for a better future for all cancer patients and their families and I'll try my very best to make some kind of impact, however small. 

Thank you for all your love and support along the way, it genuinely means so much to me and keeps me sane! 

Blue light blocking glasses and cancer, epilepsy

These are the best blue light blocking glasses I have had and they don't look dorky. If you understand about the negative effects of artificial light at night you will understand how useful these can be to normalise natural melatonin secretion in the evenings. Endogenous melatonin produced by the pineal gland is one the most potent anti-cancer molecules known to man, as I have mentioned previously in this blog. The most noticeable benefit for me is improved seizure control after sunset. The effect of melatonin and sleep aids has been investigated for years as potential anti convulsive agents for good reason and the mechanisms of action go beyond improved sleep quality (although this is still HUGELY important for seizure control).

Blue light blocking glasses from BLUblox- https://www.blublox.com

Melatonin is a very powerful antioxidant with numerous physiological functions. The interplay between clock genes and light entering the retina is an intricate, delicate process that regulates normal cell division and associated regulatory processes. Clock genes can even influence the pharmacokinetics of chemotherapeutic agents so this is worth investigating and asking your oncologist if you are a patient reading this. You can then determine what time of day might be most effective for the type of chemotherapy you are taking. If you would like to learn more, the official name for this form of study is Chronopharmacology.

Known mechanisms of melatonin

The mechanisms underlying melatonin's ability to interfere with tumour metastases are numerous and involves several mechanisms involved with modulation of cell-cell and cell-matrix interaction (3).

General functions include:

a) Direct free radical scavenging, 

b) Ttimulation of antioxidative enzymes, 

c) Increasing the efficiency of mitochondrial oxidative phosphorylation and reducing electron leakage (thereby lowering free radical generation), and augmenting the efficiency of other antioxidants. 

Fig. 1- several mechanisms for the known effects of melatonin. (1)

'There may be other functions of melatonin, yet undiscovered, which enhance its ability to protect against molecular damage by oxygen and nitrogen-based toxic reactants. 

Numerous in vitro and in vivo studies have documented the ability of both physiological and pharmacological concentrations to melatonin to protect against free radical destruction.' (2) 

References:

1. Jung, B. and Ahmad, N., 2006. Melatonin in cancer management: progress and promise. Cancer Research, 66(20), pp.9789-9793.

2. Reiter, R.J., Tan, D.X., Mayo, J.C., Sainz, R.M., Leon, J. and Czarnocki, Z., 2003. Melatonin as an antioxidant: biochemical mechanisms and pathophysiological implications in humans. ACTA BIOCHIMICA POLONICA-ENGLISH EDITION-, 50(4), pp.1129-1146.

3. Su, S.C., Hsieh, M.J., Yang, W.E., Chung, W.H., Reiter, R.J. and Yang, S.F., 2017. Cancer metastasis: Mechanisms of inhibition by melatonin. Journal of pineal research, 62(1).