This is a very long report of a totally fascinating day organised and led by Dr Rachel Nicoll under the auspices of the Biolab Medical Unit. It was designed for health professionals so much of the supporting science was way above my head, but the message was clear. Mitochondria are one of the main generators of energy within the body – which makes their health and well being crucial to the functioning of virtually every one of our systems.
These are the areas covered over the course of the day so if want you can spool on down to the bit that attracts you. It is, however, all really interesting and you should really read the first section anyhow, just so that you understand what mitochondria actually are and do.
- What are mitochondria and what do they do?
- Mitochondria and Metabolic Disease – Obesity, Insulin resistence and Type 2 Diabetes
- Mitchondria and degenerative brain disease such as Alzheimer’s Disease
- Mitochondria and cancer
- Mitochondria and cardiovascular disease
- Mitochondria and autism
- The Cell Danger Response (CDR)
- Biolab – where/how to get mitochondrial health tests
- Professo Eija Pirinen – therapeutic effect of Vitamin B3/niacin in obesity
- Dr Sarah Myhill – mitochondrial disorders relating to ME and CFS
- Dr Jenny Goodman – Case histories – Multiple Sclerosis and Alzheimer’s Disease
- Lucille Leader and Gillian Crowther – Mitochondria in Parkinson’s Disease
If you would like to watch the whole day’s worth of presentations you can do so here. The slide presentations are all to be found here. The links I have given below go to Rachel’s website where the same ground is covered but in a good deal more detail.
What are mitochondria and what do they do?
So, what are mitochondria? The scientific explanation is complex but, for our purposes, they are sub units within cells whose purpose in life is to produce energy through something called cellular respiration. There can be up to 10,000 of them in each cell, egg cells having hundreds of thousands, but red blood cells and skin cells none at all. It is thought that they might be bacterial in origin as they retain many bacterial properties.
They feed on fatty acids (their preferred food), glucose, ketone from liver fat or, if really starved of other fuel, proteins.
They produce a chemical called ATP (Adenine, D-ribose, triphosphate) which is released from the cells and drives body processes. (Just to boggle your mind with numbers, there are around 1 billion molecules of ATP in the average cell and each is recycled around 3 times per minute. Each mitochondrial ATP cycle can create about 600 ATP molecules per second if required.)
A further important task of the mitochondria is to regulate apoptosis – the process by which damaged cells are destroyed to allow the creation of new healthy cells. Efficient apoptosis is crucial in, for example, the development of cancer. If damaged cells are not destroyed they can turn into cancerous cells.
How close is the relationship between mitochondria and microbiome?
There is increasing evidence of a strong association and ‘crosstalk’ between the two
For the full scientific analysis of what mitochondria are and how they operate, check in to Rachel’s new website www.hert.org.uk – the first lecture in the Mitochondria Day.
What can damage mitochondria?
Lots of things but crucially:
- Pharmaceutical drugs, especially statins and antibiotics
- Environmental toxins – pesticides and herbicides, toxic metals, persistent organic pollutants (POPs), volatile organic compounds (VOCs), air pollution, fluoride, smoking, disinfectants and electromagnetic radiation
Improving mitochondrial health
As Rachel says, ‘clinical mitochondrial therapeutic research is still in its infancy…. but just because there is no clinical trial, it doesn’t mean that the remedy doesn’t work. It just means that there is no clinical trial… but in 10 years time there may be.’ Meanwhile, all of the following seem to have mitochondrial benefits:
- Diet: caloric restriction, fasting, ketogenic diets
- Exercise, especially endurance and high intensity interval training
- Therapeutic hypothermia
- Near infrared radiation
- Pulsed electromagnetic fields
- Hyperbaric oxygen
She sees an issue with strict vegetarian and especially vegan diets which can be short of crucial mitochondrial nutrients including creatine, choline, carnosine, carnitine, taurine, Beta carotene, Vitamins K2, B12 and D and iron, zinc and magnesium.
She also suggests that caffeine is a better boost to flagging energies than sugar and that our mitochondria will benefit from flexibility in the food we offer them. For example, cycle between ketogenic and low GL healthy carbs to keep them on the ball.
For full details check Microchondria Day lecture 2a at www.hert.org.uk.
Mitochondria and Metabolic Disease – Obesity, Insulin resistence and Type 2 Diabetes
Which comes first? The mitochondrial malfunction or the metabolic disease?
Certainly, mitochondrial dysfunction is routinely found in obesity and insulin resistence and the evidence suggests that it could be a two way stream. Similarly in Type 2 Diabetes where the conventional medical approach has proved spectacularly unsuccessful. (The global prevalence of T2D rose from 4.7% in 1980 to 8.5%in 2014; Diabetes UK forecasts that prevalence may rise to 5 million by 2025, a rise of 43% in 16 years; the NHS currently spends nearly 10% of its total budget treating T2D.)
Current treatment for T2D focuses on lowering fasting blood glucose and improving glucose tolerance but this ignores the cause of the problem: an excess supply of blood glucose resulting from our low fat, high carbohydrate diets.
Another route?
A recent study by Professor Roy Taylor at Newcastle University suggests another route. He took a group of T2Ds off all glucose lowering medication for 3-5 months and gave them instead a commercial liquid diet replacement delivering around 850 calories a day. After 12 months the average weight loss was 12 kg and 46% of the trial group were no longer diabetic.
If mitochondrial health requires a flexible diet as suggested above, then could dietary inflexibility (as in an American diet which includes over-consumption of excessive carbohydrates) result in mitochondria getting stuck in metabolising glucose rather than fat, and therefore operating less efficiently?
Mitchondria and degenerative brain disease such as Alzheimer’s
T2D is closely associated not only with Alzheimer’s disease (50% increased risk) but with vascular dementia, Parkinson’s disease and Huntington’s disease.
Brain cells are especially vulnerable to iron and copper dysregulation, excess calcium, misfolded proteins (proteins that have folded themslves into the wrong shape) an excitotoxicity (literally over excitement/stimluation). Brains do however also have a waste clearing mechanism and it has now been realised that, contrary to long held belief, we do go on making new brain cells throughout our lives.
Studies of the early stages of Alzheimer’s Disease (AD) show defects in mitochondrial functioning. Several studies also show that the degrees of disability in AD correlate with levels of bioenergetic impairment in the brain – and that in AD brains, mitochondria produce high levels of free radicals and of calcium while themselves degenerating.
Conventional medicine thinks that it is the accumulation of amyloid plaques in the brain that is the cause of Alzheimer’s disease and therefore prescribes drugs designed to remove or at least neutralise these plaques. However, not only do these drugs not work, they often seem to make the disease worse.
New approaches
Dr Dale Bredesden – amaloid plaques
An entirely new theory based on the work of Dr Dale Bredesen suggests that there are three distinct types of AD each of which will need a different therapeutic approach.
- Type 1: driven by systemic inflammation. Develops in the 60s.
Type 2: driven by insulin resistance, high homocysteine and imbalances in
oestradiol, progesterone, testosterone, insulin and vitamin D. Develops in the 70s. - Type 3: driven by dementogens: toxins, microbes etc that affect the brain
Even more interesting, he suggests that far from being damaging, the accumulation of amyloid plaques may in fact be an immune system response. The plaques may actually be binding the toxins that are impairing brain function. (Studies have shown that not only are plaques present in the brains of normal healthy individuals but that the brains of 90 year olds who had retained excellent memories up till their deaths were riddled with plaques.)
This is all quite complicated so I suggest that if you are interested (who could not be fascinated) you go to Rachel’s site and read the full presentation.
Dr Stephanie Seneff and cholesterol
Some of you may already have heard of Dr Seneff in connection with the pesticide glyphosphate and the rise in autism but Dr Seneff also has views on cholesterol and statins.
Studies have shown that although only 2% of the body’s mass, the brain should contain 25-30% of the body’s cholesterol, mostly in the form of myelin, comprised of saturated fat, cholesterol, omega 3 fats and a few omega 6 fats. So cholesterol plays a critical role in much of the brain’s activity. It can also protect the brain from invasive bacteria and viruses. Cholesterol has been found to be low in people who died from trauma and sepsis while people who live to be 85+ are likely to have high cholesterol levels in their blood. And more. Post mortem studies of those with Alzheimer’s disease have shown that they had severe deficiencies of fatty acids in their cerebral spinal fluid.
Dr Seneff therefore asks whether the low fat craze could be partly responsible for the increase in neurodegenerative disease and whether high cholesterol could actually be protective.
Indeed, she goes further and suggests that statins, by lowering the level of healthy cholesterol in the brain could increase susceptibility to Alzheimer’s.
Once again, I suggest that if you are interested you go to Rachel’s site and read the full presentation.
Mitochondria and cancer
As with Alzheimer’s disease, conventional medicine has been spectacularly unsuccessful in combating – or even understanding – cancer which has increased in incidence from 1 in 16 in 1940 to 1 in 3 by 2018. Over a trillion dollars has been spent in that time on gene targeted therapies for cancer even though the American Cancer Society has now admitted that genes contribute no more than 5% of our cancer risk. So where should they be looking? How about the immune system?
The immune system in cancer
The immune response is the most important defence against cancer growth. The innate immune system is continually surveying the body for cancer cells and, when it finds them, despatching cytotoxic lymphocytes and natural killer cells which can recognise tumour cells and control their growth.
Nobel Laureate Otto Warburg back in the 1920s and very recently Professor Thomas Seyfried see cancer as a metabolic disease. A 2016 meta-analysis looked at 200 odd studies published between 1934 and 2016 and concluded that the most important difference between normal cells and cancer cells is how they generate energy – nothing to do with their genetic inheritance.
Indeed, Seyfried has shown that transferring the nuclei from a tumour cell to a healthy cell does not affect the healthy cell which remains healthy, while transferring healthy mitochrondria from non cancer cells to breast cancer tumour cells enables recovery in the tumour cell. Nothing to do with genetic transfer.
Supporting the immune system while eating a diet which will support healthy mitochondria therefore seems to be a priority. There also seems to be some evidence that combining this regime with hyperbaric oxygen therapy which could help trigger apoptosis (death) in the cancerous cells could be helpful.
Again, I suggest that if you are interested you go to Rachel’s site and read the full presentation.
Mitochondria and cardiovascular disease
After many years of decline CVD mortality is now rising in 12 out of the 23 nations studied in 2017. Why?
The heart depends on mitochondria for 95% of its ATP (energy); it has one of the highest energy demands in the human body. Everyday, cardiac mitochondria have to synthesise 6kg of ATP to meet cardiac energy requirements. This makes the cardiovascular system uniquely vulnerable and it is likely that everyone with cardiovascular disease (CVD) will have some form of energy deficiency. Angina, hypertension, atherosclerosis, ischaemia, heart failure and diastolic dysfunction all have their roots in failure of mitochondrial energy production.
Statins
Statins work by blocking the liver enzyme that makes cholesterol; blocking this enzyme reduces the production of CoQ10 and vitamin K2, both necessary for heart health and the prevention of some cancers. One study of rat mitochondria exposed to statins found mitochondrial swelling, collapse of mitochondrial membrane potential, DNA fragmentation, up to 96% decreased ATP levels. Statins are not good for mitochondria.
Worse. They don’t work.
A 2015 systematic review of statin trials found that in primary prevention trials (stopping people dying of heart failure), death was delayed by just 3.2 days. Among those with life-limiting illness, patients who discontinued statins had improved quality of life and fewer cardiovascular events. Furthermore, a 2015 study showed that statins can actually cause atherosclerosis and heart failure ‘through the depletion of coenzyme Q10…and thereby ATP generation.’
Statins also double the rates of diabetes, a key risk for CVD. A 2019 study found that statin users had a 220% higher risk of developing new onset diabetes. Those taking statins for up to 2 years had a 333% higher risk. Other studies have broadly confirmed these findings.
In 2019, a group of UK doctors and scientists, led by Dr Aseem Malhotra and including the editor of the BMJ and the past President of the Royal College of Physicians, wrote to the British Parliamentary Science and Technology Committee to express their concern. The Chair, Sir Norman Lamb MP, called for a full investigation into statins.
Dr Stephen Sinatra – the importance of mitochondria in the heart
Dr Stephen Sinatra was one of the first cardiologists to appreciate the crucial importance of mitochondrial energy production in the heart to keep blood pulsing through the body. He points out that energy levels (ATP, ADP, AMP) decline more than 30% in heart failure and more than 40% in coronary artery disease and ischaemic heart disease.
His suggestion is supplementing with coenzyme Q10, L-carnitine, magnesium and D-ribose all of which will support mitochondrial health and then provide further support with a caloric restriction, a ketogenic or a low carb/high fat diet and exercise – all recommendations for general mitochondrial health.
See Rachel’s site here for the full lecture.
Mitochondria and Autistic Spectrum Disorders (ASD)
As with T2D and cancer, despite the best efforts of both the research and the medical community, the incidence of autistic spectrum disorders has sky rocketed over the last 50 years: 1 in 5000 in 1970, 1 in 59 in 2021.
Research over the last 10 years has shown that hundreds of genes may play a role, with the collective contribution of all genes in ASD being around 40%, but no single gene accounts for more than 1–2% of autism. So what else could be involved?
- The gut? 9-70% of those with ASD disorders also have gastrointestinal complications.
- Either/both too little or too much serotonin reaching the brain?
- Environmental toxins? High levels of both fluoride and aluminium have been found in ASD brains. Both can result in a significant suppression of cellular energy.
- The immune system?
Studies have shown inflammation and immune dysregulation in the brains of autistic patients.
Mothers with an autoimmune disease are significantly more likely to have an ASD child than mothers without.
It appears that pregnant women who had an infection, an inflammatory response or an activated immune system through vaccination, have a higher risk of having an autistic child as maternal cytokines can cross the placenta and enter the immature foetal brain. - Mitochondrial malfunction? Up to 80% of children with ASDs demonstrate evidence of mitochondrial dysfunction.
Mitochondrial therapies such as the ketogenic diet and exercise have both been found to improve cognition, sociability, stereotypic behaviours and socia-emotional functioning in ASD patients.
See Rachel’s site here for the full lecture.
Cell Danger Response (CDR)
Cell Danger Response is a concept developed by Professor Robert Naviaux at the University of Southern California, San Diego, and is not a medical phenomenon that is currently recognised by conventional medicine.
What is the Cell Danger Response?
- Mitochondria can sense when a threat (pathogen, toxin, etc) is impending and initiate a cell danger response (CDR).
- This involves the release of ATP into the circulation (known as purinergic signalling) which in turn triggers immune responses.
- Meanwhile, cellular ATP usage is reduced many cellular and mitochondrial processes are shut down so that more ATP will be available to deal with the extracellular danger.
- When the CDR is triggered, our cellular priorities are reset to optimise survival. We start to display sickness behaviour: withdrawal from social contact, decreased speech, fragmented sleep, inflammation, aches and pains, gut microbiome changes, hypersensitivity to touch, sound and light.
- Naviaux describes children with autism being in a state of primed hypersensitivity as they encounter ever increasing amounts of environmental toxins with an underdeveloped detoxification system.
- In theory, if the danger (pathogen or toxin) is eliminated or neutralised, the CDR should be turned off but Naviaux believes that sometimes this doesn’t happen even when the danger has been removed.
- The CDR becomes stuck in a repeating loop that blocks healing. He likens this to cellular post-traumatic stress disorder (PTSD).
- He suggests that with the CDR stuck in the ‘on’ position, chronic disease can result. It could be autism or it could be T2D, CVD, etc.
- Since it was the release of the ATP into the circulation (the purinergic signalling) then anti-purinergic therapy should reverse the situation: if it was being ‘stuck on’ CDR that had caused the ASD symptoms then anti-purinergic therapy should improve them.
Naviaux trialled this theory first in mice and then in autistic boys, giving them just one intravenous infusion of low dose suramin, a well-studied anti-purinergic agent.
Suramin improved all the core symptoms of ASDs with just 1 dose. Two children who were previously non-verbal spoke their first sentences. All of the children who received suramin experienced catch-up development, with one child advancing through 3 years of schoolwork in 3 weeks. The peak benefit from the single dose of suramin occurred after 3 weeks, then decreased.
New trials are already planned.
For more details see Rachel’s site here, but scroll down to teh second half of the paper.
Other talks
Testing mitochondrial health
Mark Adams from Biolab detailed the tests that Biolab can offer to assess mitochondrial health. Check in to their site for more details.
Therapeutic effect of Vitamin B 3/niacin in obesity
Professor Eija Pirinen described the success that her team had had in treating mitochondrial disease conditions and obesity with B vitamins, primarily vitamin B3.
Dr Sarah Myhill – mitochondrial disorders relating to ME and CFS
Dr Sarah Myhill has been a pioneer in the area of mitochondrial malfunction and it was her groundbreaking work with Dr John Maclaren Howard at Biolab that finally established that poorly functioning mitochondria provide the key to Chronic Fatigue Syndrome, ME and fibromyalgia.
Her work can all be found in her 2014 book Diagnosis and Treatment of Chronic Fatigue Syndrome (reviewed here and can be bought from her site here). In it she uses her favourite analogy of a car to explain this complex subject – and how all systems need to work if the car (for which read body) is to function efficiently.
• Engine – Mitochondria
• Fuel – Diet and gut function
• Oxygen – Lungs
• Accelerator pedal – Thyroid
• Gearbox – Adrenals
• Service and repair – Sleep
• Cleaning oil – Antioxidants
• Cooling system – Detoxification
• Driver – The brain
Dr Jenny Goodman – Case histories – Multiple Sclerosis and Alzheimer’s Disease
Dr Jenny Goodman described two case histories (one MS and one AD) in which improved mitochondrial function, thanks to a detoxifying and high nutrient diet, had beneficial effects – effects which were lost when either patient reverted to their earlier diet and lifestyle.
Lucille Leader and Gillian Crowther – Parkinson’s Disease
Lucille Leader and Gillian Crowther described their work which has enabled mitochondrial dysfunction to be recognised as a major driver of Parkinson’s Disease – especially in the area of dopamine deficiency. They detailed dietary and supplementary approaches to treatment and the use of Mucuna pruriens, a natural source of L-Dopa which also contains other vital mitochondrial nutrients.
MHRA recognises the existence of Topical Steroid Withdrawal
Thank you for this very helpful summary.