Every day, researchers are making new and exciting discoveries in the field of longevity and ageing.
While ageing will always be a normal part of life, there is a growing body of evidence to suggest that we can reverse some of the damage and greatly slow the ageing process.
So, what exactly is ageing?
In simple terms, ageing is a decline in the function of every cell in the body that eventually leads to death. Obesity, premature wrinkles, reduced mobility and cognitive dysfunction are symptoms of decline, and while death is unavoidable, the rate decline is optional.
The rate of age-related symptoms, signs and decline depends on a factors such as diet, lifestyle, stress and genes. This is because these factors impact the composition of the gut microbiome which determine whether the body is in a pro-inflammatory or anti-inflammatory state.
The combination of poor diet (processed food, alcohol) and lifestyle (inactivity, chronic stress, smoking, UV radiation) induce dysbiosis (altered microbiota), oxidative stress and chronic inflammation – all of which are known to greatly accelerate the ageing process.
The Hallmarks of Ageing
Research has identified a number of processes that contribute to ageing, as well as several markers that are considered to be the consequences, or hallmarks of ageing.
These include the rate of telomere shortening, cellular senescence, mitochondrial senescence and loss of the extra-cellular matrix.
The rate of telomere shortening
Telomeres are protective caps that are found at each end of our DNA and their role is to protect these ends from damage and regulate the transcription of genetic information as the cell divides. Telomeres shorten with age and when their length reaches a critical point, the DNA becomes damaged and the cell can no longer divide. The rate at which telomeres shorten varies between individuals and is dependent on both genetic and epigenetic (outside the gene) factors. (1) Epigenetic factors include availability of nutrients and the quality of the cellular environment – both of which can influence gene expression and alter the rate at which telomeres shorten. This means we can influence how quickly we age depending on the choices we make.
Cellular senescence is the cessation of cell division which renders the cell inactive. Senescent cells are often referred to as “zombie” cells because they are viable but no longer perform a function and actually cause damage to the tissue. Cellular senescence is the end result of telomere shortening, cumulative oxidative stress and chronic inflammation. Senescent cells remain in the tissue and slowly accumulate damaged components that further contribute to oxidative stress and chronic inflammation – therefore perpetuating a vicious cycle. (2)
The accumulation of senescent immune cells, also termed immunosenescence, is recognised as a key marker of ageing. This is because as the number of senescent immune cells increase, immune function declines and the capacity to remove damaged cellular components is reduced. Further accelerating the ageing process.
Mitochondria are organelles that are found within almost every cell in the body. Their role is to convert glucose, fats and amino acids into ATP, a cellular form of energy which is essential for DNA repair as well as cellular homeostasis and regeneration. Optimal mitochondrial function relies on a number of vitamins and antioxidants such as B-group vitamins, L-carnitine, alpha-lipoic acid, CoQ10 and glutathione. When these nutrients are in short supply, or if the demand on the mitochondria exceeds the supply (such as during prolonged stress, a nutrient deficient diet and certain medications), mitochondrial function starts to decline. This results in oxidative stress, mitochondrial dysfunction and a gradual progression to mitochondrial senescence. (3)
Deterioration of the Extracellular Matrix (ECM).
The ECM is a highly organised collection of collagen and fibres present within in every tissue in the body. ECM surrounds and cushions the cells, providing a conduit for cells to receive supplies, communicate with other cells and coordinate their functions. When the ECM becomes damaged and disorganised, cellular and tissue function declines. (5). This breakdown of ECM is most evident in wrinkling of the skin, but similarly occurs unnoticed within every organ and tissue in the body until symptoms develop. Dr Paul Clayton, a scientist and expert in the emerging field of Pharmaconutrition, identifies ECM deterioration as the most critical component of the ageing process as the loss of communication and transport between cells is the precursor of cellular and telomere decline. Research shows that ECM deterioration is driven by oxidative stress and chronic inflammation.
The connection between chronic inflammation and ageing has been termed inflammageing. (6). It is a multifactorial process that produces “molecular garbage” and chronic inflammatory signalling throughout the body. Many of these signals stem for a dysfunctional microbiome.
Research shows that chronic inflammation contributes to the ageing process by accelerating the shortening of telomeres, interfering with the translation of genetic information, reducing nutrient absorption and availability, and producing oxidative stress that destroys the ECM and results in mitochondrial and cellular senescence. These processes eventually produce a cellular and extra-cellular environment that is no longer conducive with life.
Research also shows that poor gut health is one the greatest contributors to chronic inflammation. This is because 80% of our immune function lies within the gastrointestinal tract and the gut microbiota directly communication and regulates these immune cells. This means that by supporting gut health it is possible to slow, delay or even reverse some of the signs and symptoms of ageing.
In order to slow the ageing process, the body needs to undergo a shift from a pro-inflammatory state to an anti-inflammatory state. Fortunately, this shift can be achieved through a change in diet, adequate supplementation and implementing certain lifestyle modifications.
Fig 1: Front. Immunol., 10 January 2018 | https://doi.org/10.3389/fimmu.2017.01960
The standard dietary advice is to consume an anti-inflammatory diet that is high in fresh fruit and vegetables with lots of healthy fats, fish, eggs, wholegrains, legumes and nuts. And of course, avoid pro-inflammatory pseudo-foods such as sugar, vegetable oils, trans fats, alcohol and all products that are processed and contain additives.
But it’s not that simple. If it were, then we wouldn’t have an obesity problem because almost everyone has tried this type of diet – and more than 80% have failed to achieve any long-lasting results.
The greatest problem in long-term success is overcoming habits that have been sustained for decades. This is because ultimately, we are not only addicted to food but also the habits and expectations we have created around food. In order to change these habits, we need to address neural circuits in the brain. This can be achieved through supplementing with brain-specific nutrients and incorporating dietary choices and techniques that reduce inflammation and send the right signals from the gut (and adipose tissue) to the brain. This involves managing every process that is responsible for maintaining an anti-inflammatory state – and this is where most diet plans fall short.
Certain dietary techniques have been shown to reduce inflammation and reduce or reverse various markers associated with ageing. These techniques include intermittent fasting, calorie restriction, ketosis and the circadian rhythm pattern of eating. They are very popular and there are many plans available, however, if practised incorrectly, these techniques can lead to dysbiosis, leaky gut and inflammation – and eventually sugar cravings, fatigue and metabolic changes that negate all the benefits.
In addition, when it comes to diet – there is no one size fits all. People with allergies and autoimmune conditions are unlikely to achieve an anti-inflammatory state if they eat certain foods such as grains and legumes. Some may need a low carbohydrate to reduce inflammation, while others may need a moderate carbohydrate intake to avoid thyroid or adrenal problems. Some do well with a higher fat intake while others gain weight.
BiomeMD® addresses individual needs through a health questionnaire that can determine the modifications that must be made into to optimise results.
When it comes to nutrients, there have been some promising discoveries in the field of longevity but as yet, no specific protocol has been established. It appears that the safest, most effective and most cost-effective approach is to ensure a therapeutic intake of nutrients that support essential processes such as microbial composition, immune function, mitochondrial function, detoxification and brain health. This is because optimal function of these processes helps to maintain an anti-inflammatory state throughout the body and brain – ultimately helping us make better choices in the long-term. BiomeMD® formulations include bioavailable, targeted nutrients at therapeutic doses to ensure these processes are fully supported. For more information on BiomeMD® nutrient formulations go to BiomeMD® Formulas page.
It’s important to regularly incorporate lifestyle modifications that have been shown to reduce inflammation in the body. These include:
Aiming for 7-8 hours sleep each night
Including some form of age-appropriate exercise each day
Eating, working and using technology within daylight hours
Getting out in the sun for 20 minutes each day
Managing stress through a combination of rest, meditation, spending time in nature and having positive family and social connections.
These are research-based, but also common-sense strategies that can help slow the ageing process and improve the experience of life at any age. BiomeMD® discusses these lifestyle modifications further and includes healthy recipes and two quick workouts that aim to assist the underlying processes involved in health, longevity and weight management.
1.Telomere shortening rate predicts species life span Kurt Whittemore, Elsa Vera, Eva Martínez-Nevado, Carola Sanpera, Maria A.Blasco Proceedings of the National Academy of Sciences Jul 2019, 116 (30) 15122-15127; DOI:10.1073/pnas.1902452116
2. Khosla, S., Farr, J.N., Tchkonia, T. et al. The role of cellular senescence in ageing and endocrine disease. Nat Rev Endocrinol16, 263–275 (2020). https://doi.org/10.1038/s41574-020-0335-y
3. Vasileiou PVS, Evangelou K, Vlasis K, et al. Mitochondrial Homeostasis and Cellular Senescence. Cells. 2019;8(7):686. Published 2019 Jul 6. doi:10.3390/cells8070686
4. Grabowska W, Sikora E, Bielak-Zmijewska A. Sirtuins, a promising target in slowing down the ageing process. Biogerontology. 2017;18(4):447-476. doi:10.1007/s10522-017-9685-9
5. Robert, L., Robert, A. M., & Fülöp, T. (2008). Rapid increase in human life expectancy: will it soon be limited by the aging of elastin?. Biogerontology, 9(2), 119-133
6. Front. Immunol., 10 January 2018 | https://doi.org/10.3389/fimmu.2017.01960