Information Wellness Blog

The low-calorie keto diet has become popular as an effective means of weight loss and improved health, but can it reverse biological aging? According to one study, very low-calorie ketogenic diet could decelerate biological aging.

Ketone fuel may work by switching neurons away from sugar-fueled neurons to using more ketone fuel instead. This decreases free radical and reactive oxygen species production that contribute to premature aging.

Ketosis

Your body relies heavily on glucose, an energy source derived from carbohydrates found in food. When your glucose reserves run dry, however, your body uses fat as fuel instead and creates ketones to fuel cells in your body before exiting as urine as waste products.

Dieting with low-carbs and high-fats is proven to put the body into ketosis – which you can tell is happening because your breath, urine and blood smell fruity or like nail polish remover. Although a ketogenic diet is a safe and effective way to lose weight, not everyone finds it suitable. Before beginning on one, be sure to discuss it with your physician first.

Researchers have recently demonstrated how a ketogenic diet can reverse the effects of aging in brain cells. Ketones found in blood can provide more energy to brain cells than glucose can even when calories are equal, possibly because ketones increase P-53 protein production which acts to destroy senescent cells and therefore slowing down aging processes.

A ketogenic diet is a high-fat, low-carbohydrate meal plan used to treat various health conditions, such as epilepsy, inflammatory bowel disease and diabetes. Scientists are exploring whether such a diet could also slow biological aging – this refers to how rapidly cells age due to obesity, stress or poor diet – so researchers are observing whether such a plan affects DNA methylation rates which ultimately determine how quickly the body ages.

Researchers have also discovered that a high-fat, low-carbohydrate ketogenic diet can enhance the body’s ability to use glycolysis and gluconeogenesis during times of stress. They studied young and aged rats that underwent time-restricted feeding (TRF) with either a standard diet or ketogenic diet and found that KD improved metabolic switching from glycolysis to gluconeogenesis as well as physiological response to stress hormone epinephrine; TRF alone reversed markers of insulin-related metabolic deficits while KD + TRF had additive benefits on these variables.

Cellular Senescence

Cellular senescence is an irreversible process that occurs when cultured cells no longer replicate or die, but they continue to secrete harmful cytokines that damage surrounding tissues and cells, potentially leading to cancer, fibrosis, inflammation and age-related frailty. Since certain drugs can effectively clear out senescent cells this field has gained prominence within biomedical research; an increasing number of studies are looking at ways repurposing existing drugs or supplements for their senolytic or senomorphic properties.

Senescence can be caused by various stimuli. Some stimuli, like DNA damage, oxidative stress and oncogene activation can trigger it; while other factors, like telomere shortening and mitochondrial dysfunction may contribute internally. At any rate, its main characteristics include loss of proliferation/regeneration capacity, inhibition of apoptosis and secretion of pathogenic cytokines known as Senescence-Associated Secretory Phenotype (SASP).

Though initially beneficial, accumulating senescent cells can contribute to age-related organ or tissue dysfunction and impair healthy tissues’ response to stress or disease, even degrading cognitive function in the brain. Researchers are currently developing drugs called senolytics which target these harmful senescent cells specifically and destroy them, eliminating harmful cells altogether.

Studies conducted over recent years have demonstrated that clearing away these senescent cells can halt or delay age-related diseases in various tissues and organs. For instance, targeting p16Ink4a-expressing senescent cells with the senolytic agent AP20187 significantly extends mouse longevity [8], while human subjects suffering from metabolic syndromes such as diabetes or fibrosis experienced significant improvements to organ function after treatment with Neo-SASP [9].

As our understanding of cellular senescence has advanced, it has become evident that senolytic therapy could be applied in many clinical conditions. Additionally, there has been increasing interest in the use of senolytics combined with other therapeutic approaches to treat age-related diseases; however, much work remains to be done before these senotherapeutic agents can be safely and effectively utilized by patients. This includes further validating the causal links between senolytic interventions and their targeted phenotypes, improved identification of senescent cell subtypes, and conducting large-scale placebo-controlled trials to assess efficacy and safety in different patient populations and disease contexts.

Oxidative Stress

Oxidative stress refers to an imbalance between free radicals and antioxidants that can damage our bodies. Free radicals are oxygen-containing molecules with uneven numbers of electrons that make them highly reactive, attacking other cells with ease. On the other hand, antioxidants donate their electrons to neutralize free radicals, lessening their impact and protecting us from further damage.

Human bodies produce free radicals naturally as part of normal metabolic processes; however, environmental toxins, poor diets and excessive stress can increase free radical levels considerably, damaging cells and tissues and leading to chronic diseases such as heart disease or diabetes. Long-term exposure can contribute to chronic stress conditions like this one as well.

Oxidative stress not only accelerates skin aging but can also damage DNA and proteins in our cells, leading to cancer, dementia, heart disease and many other diseases. Oxidative stress has also been linked with neurodegeneration associated with Alzheimer’s Disease.

Diets consisting of fruits, vegetables and healthy fats may help alleviate oxidative stress. A detoxification program may also prove effective; one that removes or limits chemical-laden cleaning products can be particularly helpful.

Research suggests that certain supplements can also help mitigate oxidative stress. Glutathione, an essential molecule depleted by long-term oxidative stress, was the subject of a 2021 clinical trial which demonstrated its benefits on red blood cell damage, cognition strength and gait speed among older adults supplementing with glutathione supplementation. Resveratrol found in grapes and red wine has also been proven to lower oxidative stress while supporting immunity systems.

Other supplements that can help lower oxidative stress include omega-3 fatty acids from fish, flax seeds and chia seeds; curcumin from turmeric; N-acetylcysteine (NAC), which helps mitigate its toxicity; as well as mindfulness meditation as an aid to manage stress; these practices are also key in relieving oxidative stress toxicity which contributes to mental health problems like depression and anxiety – so it’s wise to seek medical assistance if these symptoms arise.

Insulin Resistance

Insulin resistance is a condition in which muscle, fat and liver cells become less responsive to insulin produced by your pancreas to help manage blood glucose levels. When this happens, too much sugar builds up in your blood and cannot enter cells for energy use; your body then starts producing additional amounts of insulin as it attempts to rectify this issue, potentially leading to type 2 diabetes over time if left untreated.

Insulin resistance can occur for anyone at any age; those at greater risk include those who have certain inherited genetic conditions like myotonic dystrophy, Donohue syndrome and Werner syndrome are particularly at risk. You could also become insulin resistant if your thyroid fails to produce enough thyroid hormone to keep metabolism operating smoothly (hypothyroidism). Certain medications, including steroids, antidiuretics and high blood pressure medications could also contribute to this problem; physical inactivity or being overweight increases this risk further.

Studies have demonstrated that ketogenic diets can improve insulin resistance by increasing activity of protein Akt, responsible for cell senescence. While most people with this condition show no symptoms, it can often be identified only during health examination or blood work procedures. Common indicators may include waistlines over 40 inches for men and 35 inches in women; an A1C level of 100 milligrams per deciliter or higher two hours after eating a test meal; or skin with dark velvety patches called “acanthosis nigricans.”

Researchers who recently published their findings in Nutrients found that following a very low-calorie ketogenic diet (VLCKD) can reverse epigenetic aging by six years, through weight loss on VLCKD combined with increased activity of protein Akt and elevated ketone bodies. They say their research can provide scientists with insight into strategies to extend human lives and healthspans.