5 tips and tricks to slow your aging process
Before going further, you must understand the difference between age and aging. Age is the number of years you have lived, while aging is a process where the health function slowly declines. And over time, the body becomes more and more susceptible to chronic diseases. Most people see aging and dying as related outcomes. But in reality, everyone dies of two possible causes: they either die of accidental trauma or get sick and succumb to some form of chronic disease.
We have already started the causes of aging, but is there anything we can do about it?
Yes, you can follow some tips and tricks to significantly slow your aging process and stay healthier to stay less vulnerable to chronic diseases.
1:Increasing the Effectiveness of Sirtuins Pathways
These are longevity genes and can significantly impact our body in terms of endurance, heart health, cognitive function, and, more importantly, how well we age. Since they play a vital role in our body’s aging process, you can do things to boost sirtuins pathways.
We know that calorie restriction will slow aging in many species. Some researches have revealed that molecules that are responsible for restricting the aging process interact with sirtuins. These longevity genes create new mitochondria, stimulate apoptosis or program death cells, autophagy or recycling cells, and several other functions.
Sirtuins can only function in the presence of NAD+, which stands for Nicotinamide Adenine Dinucleotide. It’s a derivative of Nicotinic acid, also called Niacin or vitamin B6. It comes in two forms NAD+ and NADH, a coenzyme that helps turn nutrients into energy. It also helps in energy production in energy production in mitochondria.
Since NAD is necessary for the normal functioning of sirtuins, it has also been seen that NAD’s are also used by DNA repairing proteins called PARP’s, which are primarily found in aged people. Although it is necessary to activate sirtuins and PARPs, too much activation can exhaust NAD+ supplies can induce cell death if the damage is too severe.
Too much activation of the PARP can induce overexpression of the P53 protein, which is responsible for eliminating cancer cells. Still, the more it’s activated, the more it accelerates the aging process. As you age, the NAD+ levels go down, and the sirtuins become less functional. As a result, the body suffered slow mitochondrial function. In addition, it increased oxidative stress, which leads to chronic inflammation, cognitive dysfunction, and a significant increase in free radicals, which damages the DNA.
You can deal with declining NAD+ by supplementing with NAD precursors. Several NAD precursors are available in the market, depending on the level of absorption and effectiveness, such as NMN or nicotinamide mononucleotide and NR, which stands for nicotinamide riboside. There is still an open debate on the efficacy of both drugs, but some studies have shown that NMN has edged out NR in many aspects.
The recommended dosage of both the drug is approximately 250 to 300 mg per day. But some researchers have also suggested taking 1 gram a day.
Another possible way to accelerate the production of sirtuins is by taking Resveratrol. It boosts the activity of sirtuins by increasing mitochondrial function like calorie restriction. So supplementing Resveratrol can also be used to expand the lifespan of the body. You can also consider pterostilbene, which has similar properties to Resveratrol and occurs in the same type of plant as Resveratrol. Both of them are potent anti-inflammatories, antioxidants and show activity to fight off cancer cells. Pterostilbene, in some cases, has performed better than Resveratrol, and it stays seven times longer than Resveratrol.
We recommend you not to self-medicate and consult a licensed health professional before taking any medication.
2:Activating AMPK pathways
Activating AMPK pathways will keep your body tissue young and slow aging throughout the body as ATP molecules are broken down, and the energy is released in the mitochondria resulting in AMP production.
AMPK is an enzyme called that stands for AMP-activated protein kinase. Kinases transfer a phosphate group from a high-energy molecule to a specific substrate. AMPK increases AMP levels and decreases levels of ATP. Cells do not make or store fat when AMPK begins, instead they burn fat and transport glucose which results in low fat, low blood sugar, and increased insulin sensitivity.
Activated AMPK is also responsible for stimulating autophagy, mitochondria biogenesis, renewal of cellular components. They also stimulate the growth of SIRT1. SIRT1 is one of the sirtuins enzymes which helps in DNA repair. AMPK also contains the signaling of the nuclear actor – KappaB pathway. It is pro-inflammatory, resulting in chronic inflammation.
Some studies show that AMPK suppresses processes related to biological aging, however, AMPK declines sharply with age. AMPK activation can be suppressed by inflammation. With the increase in calorie intake, AMPK activation is also significantly reduced. The cells decrease their energy-releasing ATP-generating activities. Instead, they shift to energy-storing processes, generating new fat deposits and creating excess new glucose molecules.
When you boost AMPK activity, tissues look young and ageing slows down throughout the body. These activities also suppress chronic diseases associated with old age. These can be cardiovascular diseases, metabolic syndrome, liver diseases, etc.
However, you can boost your AMPK through calorie restriction to the extent that you might not sustain it or exercise which involves stimulating muscle contraction. Many studies recommend that exercise positively affects AMPK. Furthermore, they indicate that the higher the intensity, the more AMPK is activated.
HIIT, also known as high-intensity interval workout, is effective at activating AMPK. AMPK can also be activated by consuming dietary fiber, especially glucomannan, a particular type of soluble fiber or several nutrients like Alpha-lipoic Acid or ALA activate AMPK pathways in muscle tissue. Quercetin can increase AMPK in fat, muscle, and liver. Fish oil, curcumin, and EGCG from green tea can also activate AMPK. And finally, there’s metformin, which is a prescription drug that is used to treat type 2 diabetes. Significant numbers of researchers, including David Sinclair from Yale University, took metformin as part of their anti-aging regime.
Since it might be beneficial for anti-aging, it does have some tolerable side effects like stomach upset. Metformin is one of those molecules that can replicate the effects of calorie restriction. And since it’s a prescription drug, you can ask your doctor to get one.
From a physical point of view, we recommend you to exercise strenuously, and as from a medication point of view, it’s better to consult a health expert who has experience on the matter.
3:Removing Senescent Cells from the body
The cells in our body either stop dividing or start to dysfunctional as we start growing. They can hurt the surrounding cells as they are metabolically active; such cells are called senescent cells.
Cellular senescence is one of the most famous and exciting research on longevity. The cell cycle starts with a process called mitosis, which means replicated chromosomes separate into two different identical nuclei. Back in 1960s, two researchers – Lenord Hayflick and Paul Moorhead, discovered that about one cell stops dividing after 50 divisions, and they termed this tendency as the Hayflick Limit.
At the end of every chromosome, there is a cap called telomeres. The chromosome replicates each time a cell divides, and a tiny amount of material is lost every time from the end of telomeres. These erode continuously throughout the life of the cell until they reach the Hayflick limit. Then, they almost disappear, leaving the DNA information bare. And the vital information gets ruined as no telomeres are left to protect the DNA information.
This also makes the DNA vulnerable to damage. Other factors that can shorten telomeres can be stress, smoking, obesity, lack of exercise, and poor nutrition. Let’s take for an instance that the damage to the DNA is severe. In this case the cells stop functioning normally and might enter into the state of Apoptosis, which is the programmed death of cells. But in most cases, the cells goes through a senescent state in which the cells usually stop working instead of dying.
Since senescent cells cannot replicate like normal cells, they are still metabolically active. They typically invoke immune responses by releasing certain pro-inflammatory substances like cytokines, chemokines, and extracellular matrix proteases. These substances are called SASP (senescence-associated secretory phenotype). Although SASP are secreted in small amounts, the effects are enormous and can badly affect the surrounding tissue of the microenvironment. They can also interfere with the normal function of other processes like tissue regeneration and remodeling. This may cause chronic inflammation and cancerous tumors.
We accumulate more senescent cells as we grow older, and these cells have a significant contribution to the aging process. Researchers have been studying molecules called senolytics. These molecules selectively induce health in senescent cells and remove SASP. Senescent cells have a pro-survival gene that prevents them from Apoptosis. Two drugs which can be found in the market that can selectively kill senescent cells are: Dasatinib – used in the treatment of leukemia, and the other is Quercetin – a flavonoid antioxidant and plant pigmentation available in deep-colored plants. Both drugs can remove senescent cells but are effective in different tissues of the body.
Dasatinib helps to remove senescent fat cell progenitors, which are biological cells similar to stem cells. However, they are more prone to differentiate into a specific target cell. In addition, Quercetin helps to remove human endothelial cells. Also combining two drugs forms a synergy that is effective in removing some types of senescent cells. As little as 30% of senescent cells are sufficient to slow aging down.
Not all senescent cells are harmful; they play significant roles in cellular reprogramming and wound healing. So this situation is more like a balance. The role of senolytics is to clear enough senescent cells. This slows down the aging process without disturbing cellular reprogramming or wound healing.
To use Dasatinib, you need a prescription since it is used to treat leukemia, and it’s expensive. On the other hand, Quercetin can be found easily in the market. It can be supplemented with natural foods like red wine, green tea, kale, blueberries, dark chocolate, etc. It is also known as an anti-inflammatory and natural antihistamine, promoting healthy liver and skin.
Analytics is more related to cancer research. There are many studies being conducted to find out how senolytics can target cancer-preventing pathways. One of the experimental anti-cancer drugs is Navitoclax which induces Apoptosis in senescent cells and also works as a protective agent against memory loss in mice genetically engineered to cause Alzheimer’s.
The adverse effects of excess senescent cells can be way out of proportion, exhibiting harmful effects on the surrounding tissue microenvironment. Since most of the drugs are still in an experimental stage or harder to obtain, we can supplement Quercetin in the form of natural food. It is widely available and easily affordable.
4:Keeping mTOR and AMPK pathways in Balance
The term mTOR stands for mechanistic target of RapamycinRapamycin. It’s an enzyme encoded by the mTOR gene. It is also a kinase, which means these enzymes catalyze the transfer of phosphate group from high energy phosphate.
After an expedition In 1960 in Easter islands, local inhabitants named Rapanui have natural products from plants and soil that had possible therapeutic value. In 1972 a soil bacterium was discovered and had a potent antifungal activity. It was later called Rapamycin, Rapa to pay homage to the inhabitants of Rapa Nui and Mycin for antifungal activities.
Some tests also revealed that RapamycinRapamycin had potent immunosuppressive and anti-cancer activity. In 1994 an enzyme “target of rapamycin” was discovered in mammalian tissue. So now, this enzyme and the pathway that it activates is called mammalian target of RapamycinRapamycin, mTOR pathways.
Whenever there’s plenty of nutrition and calorie available in the body, we will be active, and our muscles will consume a lot of energy. The mitochondria increase the working capacity, and ATP production goes up. The cells divide more, and we tend to grow and repair. mTOR is the protein that senses this condition and turns up the heat. However, when the body goes into calorie restriction conditions, the mTOR pathways are inhibited.
mTOR pathway includes two distinct complexes, mTOR complex -1 and mTOR complex-2. It acts as a central hub for integrating signals from upstream pathways, providing growth factors like IFG-1 and IFG-2, insulin, and amino acids. It also plays a role in sensing cellular nutrients, oxygen, and energy levels. Thus, this pathway acts as a molecular switch to regulate cellular growth and proliferation in response to nutrients, but all of this growth and higher energy levels come at a price.
Though mTOR produces energy and performance, it also produces junk in the process. And in Autophagy, these junk products are broken down and recycled. But Autophagy can only kick in when the mTOR pathway is inhibited. So we can say that the mTOR pathways are great for growth and energy but bad for extending lifespan. For example, animals that proliferate like mice, insects, and worms have a short lifespan, but animals with prolonged growth like elephants and whales have a long life span. However, if you notice within species, more giant animals have a shorter lifespan than small ones; for example, big dogs have a shorter lifespan than small ones.
Too much mTOR pathway activation can contribute to many chronic diseases like cancer, obesity, type-2 diabetes, and neurodegeneration. Conversely, inhibiting the mTOR pathway improves insulin sensitivity and promotes Autophagy.
Another enzyme called APMK stimulates both Autophagy and inhibits mTOR. Since RapamycinRapamycin being a potent antifungal, immunosuppressive and anti-cancer drug, it also inhibits the mTOR pathway and prevents it from activating. Several studies have show rapamycin extends lifespan in mice by 60%. Another study shows that dogs who took RapamycinRapamycin also got cardiovascular benefits similar to mice.
Inhibiting the mTOR pathway cannot be all bad; activating to some extent can do good like heal wounds for growing muscle and more energy. As we age, we need those things, but as we grow older, sarcopenia sets in, where the body suffers a loss of muscle mass. So, We need to develop new muscle by including more amounts of protein in our diet.
Taking RapamycinRapamycin is not an answer. MTOR pathways must be activated sometimes, especially in aging adults. We need to cycle between the periods when the mTOR pathway is activated. We are growing tissue, healing and boosting energy production, and periods when the mTOR pathway is inhibited where Autophagy is activated and clearing out toxic cellular waste.
Since the primary activating factors kick in the presence of excess amino acid, so you can consider changing your protein intake. For example, if you try weight lift exercises, we suggest that exercise takes around six protein powder scoops. And on the day of a cardio workout, we recommend you take two scoops of protein powder. You can also try the Keto diet to get an adequate amount of protein for better results.
The other way to balance out this situation is by inhibiting of mTOR pathway and achieving Autophagy. That can be done by activating AMPK pathways. To start, they consume less amino acid and perform HIIT sessions. Sadly there is no way to measure when mTOR pathways or AMPK pathways are activated. We think you can assume when you are gaining muscle mass and feeling an increase in strength, then mTOR is started. But when you improve your cardiovascular fitness and mitochondrial health, AMPK is activated. The only way to determine is to check in 10 to 20 years how your body is holding up.
5:Performing HIIT Training
Performing HIIT training can give you several benefits like weight loss, triggering the EPOC effect, increasing VO2 max, regular blood sugar, normal BP, and increasing overall energy. It also increases testosterone, HGH, and nitric oxide levels to improve libido.
HIIT can also have powerful anti-aging properties. It can slow down aging. It can also expand your health and age lifespan. HIIT mainly focuses on your mitochondrial health. As we know, mitochondria are tiny structures residing in our body cells, and different cells can have an additional amount of mitochondria. Its function is to generate energy that we need to live and function, and they do this by burning sugar in the presence of oxygen in our bloodstream. Mitochondria oxidize that sugar to turn it into ATP. APT cells fuels our muscle, brains, and our organs. A typical adult needs 200 to 300 moles of ATP in a single day. Mitochondria is also responsible for apoptosis or the programmed death of the cells.
Two things determine our mitochondrial health; the first is how many mitochondria we have and how well each mitochondrion functions. Mitochondria are produced through the process of mitochondrial biogenesis. As we age, mitochondrial biogenesis starts declining, and the amount of mitochondria also decreases. And the ones we do have don’t function at peak efficiency and begin to malfunction. Mitochondrial dysfunction is the reason behind all chronic diseases. In addition, mitochondrial dysfunction leads to the ageing of every organ in our body, including the skin.
Human beings have two different ages. The first is the chronological age which means the number of years we have lived. And the second is the biological age that appears based on our looks, cognitive abilities, mobility, and activity level. Mitochondrial health can impact a person’s biological age dramatically.
Mitochondrial health can be improved in three different ways. The first way is to increase the mitochondria in the body, enhancing mitochondrial health and getting rid of those not functioning correctly. Mitochondria create more of themselves to adapt to physical stress. Since HIIT triggers mitochondrial biogenesis, it cranks up the production of mitochondria. The only downside to the workings of mitochondria is that they make more oxidative reactive species or free radicals.
HIIT training requires significantly high energy levels. These energy levels are needed so that mitochondria respond by regulating ATP production, which improves the function of mitochondria.
However, you can get rid of the dysfunctional mitochondria by putting your body through autophagy. Mitochondria that fail to meet ATP production are removed and replaced with new functional mitochondria.
You can also opt for aerobic exercises and take a VO2 test to check your performance and detect the actual increase in health and function of mitochondria. VO2 test measures the maximum amount of oxygen you can take while exercising at absolute peak performance. The more oxygen you consume, the better health condition you have. All oxygen consumption happens in mitochondria. Here, oxygen is used to burn off sugar and relapse ATP.
Improvements in the VO2 max test state that the body’s capacity of consuming oxygen is good. It also says that the functioning of mitochondria is at its peak. As per the study, older people who did HIIT sessions had impressive gains in mitochondria levels. In addition, skin biopsies conducted on them after three months of training programs revealed that their skin got a boost in collagen production and felt more hydrated.
We recommend that you perform at least 4 HIIT sessions a week, and you will feel the difference in just a few months.
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