Decoding Biohacking for Improved Health
Understanding the Concept of Longevity
The quest for immortality has always intrigued mankind. While advancements in medical care have significantly increased lifespan, they often come with the burden of chronic diseases associated with aging, such as cardiovascular diseases, cancer, type 2 diabetes mellitus (T2DM), hypertension, and dementias like Alzheimer’s and Parkinson’s disease.
The ultimate goal, however, is to achieve a long healthspan with negligible senescence, which implies an absence of biological aging, such as reducing functional decline in organs and whole-body fitness, delaying loss of reproductive capabilities, and delaying death risk with age progression. Essentially, the aim is to extend youth, not aging. In achieving that, we may begin to push the boundaries on increasing healthy lifespan.
Cellular Aging and Its Implications
Cellular aging is determined by the cellular rate of damage versus rate of repair. The accumulation of aging-associated damage manifests as cells no longer functioning correctly as part of a collective that make up tissues of an organ, like cancer cells.
In healthy individuals, damage accumulation is managed through apoptosis, which is controlled cell death, and refined cellular housekeeping including autophagy and mitophagy; the process of eating up, breaking down, and recycling damaged inner-cell (intracellular) components (organelles). The nutrient glucose and the hormone insulin govern cellular quality control. Intracellular housekeeping enables the culling of inefficient and toxic cells from the herd. Over time a cell’s ability to trigger apoptosis becomes impaired, enabling gradual dysfunction to sneak by under the radar. Over time, the accumulation of these dysfunctional cells within an organ promotes the development of disease.
Role of Mitochondria in Cellular Health
Mitochondria are intracellular organelles; these organelles are remnant symbiotic protobacteria, originating from proteobacterium that came to live within an archaeal-derived host cell which was most closely related to Asgard archaea, a recently identified group of ancient single-celled organisms. In simple terms, a foreign single-celled ancient bacteria came to live inside the cells that eventually evolved into us.
Mitochondria have their own genome; polycistronic circular DNA, whilst their inner matrix membranes are rich in a phospholipid cardiolipin. Mitochondria produce the majority of our life-sustaining energy whilst also acting as a source of destruction for most of our cells. This occurs due to their use of oxygen to break down nutrients, in order to capture energy and store it in the energy carrier molecule ATP. Their need and use of oxygen is both life-giving and corrosive; complete oxidation of glucose produces more oxidative damage than oxidising fatty acids, and in the process produces excess superoxide, a form of oxygen with an added electron which is termed a free radical.
The Impact of Diet on Cellular Health
As mentioned above, we can produce energy from fat or from glucose (a sugar) through our cooperative mitochondria. The amount of glucose exposure is critical in achieving this balance between our mitochondria helping or harming us. Insulin is produced in response to carbohydrate intake, increasing absorption (and use) of glucose by our cells and mitochondria and reducing fat-burning.
Calorie restriction in yeast, nematode worms, and mice to primates increases lifespan with healthspan by inducing ketosis. It causes insulin to become low enough to allow ketogenesis (a product from beta-oxidation, the burning of fat) to occur. Upregulated fat-burning results in the production of molecules called ketone bodies, mainly by the liver (endogenous synthesis).
One of these ketone bodies is beta-hydroxybutyrate (BHB), derived from fatty acids that come either from our fat cells or from a meal. The ketone BHB is a fuel and signalling molecule, causing mitochondria and nuclei to adapt to metabolic changes. Fasting-mimicking diets such as time-restricted feeding, and very low carbohydrate/healthy fat diets (also known as ketogenic diets) also induce ketosis without the conscious effort of calorie restriction.
Insulin: The Aging Hormone
Insulin is the aging hormone, and a dietary pattern that regularly triggers too much insulin secretion prevents our ability to produce ketones, including BHB. Insulin suppresses ketogenesis (ketone production), depriving us of BHB’s anti-aging properties. The endogenous production of BHB, a powerful antioxidant that directly neutralises free radicals and ROS, has been shown to improve and prevent chronic diseases associated with aging conditions. So, we can control much of our aging by our dietary choices. Ketones such as BHB are produced when we are not overstimulating insulin secretion and requirement through our dietary choices.
Conclusion: The Power of Biohacking
We are often advised to eat to keep up our energy and health. However, perhaps a little less results in a little more with regards to healthspan and lifespan, and instead of calorie restriction, we can bio-hack through either eating as much as we want once a day, or eating non-insulin-stimulating foods. Doing both will further enhance their effects. The results are the same as fasting and calorie restriction, less insulin, and more ketones, in turn translating into healthier cells, a healthy you, and a chance to realise your maximal lifespan potential.
Bottom Line
The concept of biohacking to better health is a fascinating one, offering a new perspective on how we can potentially control our aging process through our dietary choices. It underscores the power of understanding our body's cellular mechanisms and how they respond to different nutrients. What are your thoughts on this intriguing approach to longevity? Do you think it holds promise for a healthier, longer life? Share this article with your friends and let's get the conversation started. Don't forget to sign up for the Daily Briefing, delivered every day at 6pm.
