There are four main longevity pathways identified in organisms including humans: 1. AMP-activated protein kinase (AMPK) pathway 2. mTOR Pathway 3. Sirtuin Pathway 4. Nuclear factor-kappa B (NF-kB) pathway. In this blog we would like first like to address the AMPK pathway. AMPK is an important aspect of the new field of bioenergetics.
Although the above picture looks to be modern art it is actually a picture of molecular structure of AMPK which is an enzyme. An enzyme is a protein that performs chemical reactions. AMPK’s full name is 5’-AMP-activated protein Kinase. A kinase is an enzyme that transfers a phosphate ion to another protein, a reaction known as phosphorylation that acts as a biomolecular “on/off switch”, turning the activity of that protein either on or off. We should think of enzymes as traffic lights. They can slow, speed up, or stop metabolic processes. A metabolic pathway is a series of chemical reactions in a cell that build and breakdown molecules for cellular processes. Anabolic pathways synthesize molecules and require energy. Catabolic pathways break down molecules and produce energy. AMPK is more of a catabolic pathway. The following illustration shows this well:
AMPK IS CONSIDERED A CATABOLIC PATHWAY
Typically, most diseases in the body result when there are malfunctions related to a pathway. This is the reason that in order to truly address Anti-Aging one must address these four pillars of the pathways of aging. Malfunction of these pathways are what is called the upstream causes of aging. The AMPK pathway is one of the major players that can have a dramatic effect in slowing down aging. What affects the AMPK pathway will have many effects downstream from it.
WHAT EXACTLY IS AMPK?
The above diagram represents the cycle of how the body produces ATP from the assistance of AMPK. The metabolic protein AMPK has been described as a kind of magic bullet for health. Studies in animal models have shown that compounds that activate the protein have health-promoting effects to reverse diabetes, improve cardiovascular health, treat mitochondrial disease and even extend life span. AMP-activated protein kinase, or AMPK, is known as a master regulator of metabolism. It is a fuel sensing enzyme found in all mammalian cells. The science of bioenergetics is producing paradigm-shifting discoveries, including the role of AMPK in regulating the ways our bodies use and transform energy. Cells activate AMPK when they are running low on energy, and AMPK is activated in tissues throughout the body following exercise or during calorie restriction. In response, AMPK alters the activity of many other genes and proteins, helping keep cells alive and functioning even when they're running low on fuel. AMPK is the “switch” that is the link between metabolic disease, inflammation, and longevity. This “switch” tells our cells when to store and generate energy-containing molecules such as fat, and when to “hunker down” and use existing energy stores. For our survival, AMPK needs to maintain cellular homeostasis that requires efficient regulation of energy metabolism during rest and especially when under greater stress. AMPK controls energy metabolism in cells and helps to maintain an energetic balance by mobilizing the body’s fuel sources. AMPK gets activated by increased concentrations of AMP and ADP due to ATP depletion. AMP or adenosine monophosphate is a nucleotide that gets interconverted into ADP or ATP. This process helps to produce energy. AMPK uses AMP for maintaining homeostasis during high energy expenditure such as exercise. ADP or adenosine diphosphate is an organic compound found in cells that helps energy currents. ATP or adenosine triphosphate is an organic chemical that provides energy for all cellular processes, such as muscle contractions, nerve impulses, and chemical syntheses. It’s often called the energy currency of the cells. AMPK detects the number of ATP in cells and then regulates it when it gets too high or too low.
In different tissues throughout the body and at different time points in development, AMPK likely has varying effects.
Remember that ATP is intimately related to the mitochondria. AMPK is a kinase enzyme that transfers a phosphate ion to another protein. This is a reaction known as phosphorylation that acts as a biomolecular “on/off switch”, turning the of that protein either on or off. Many steps of phosphorylation occur between different proteins communicating to one another in a “cell-signaling cascade”. These signals take an input (such as a hormone, drug or exercise) and can induce any number of outcomes including cell growth, cell death, energy breakdown, energy storage or turning on specific genes for expression. Ultimately, cell signaling is required for all of the physiological processes that we perform as organisms and is key to how we adapt in training to become stronger, faster and fitter.
WHAT PROBLEMS ARISE WHEN AMPK PATHWAY IS NOT FUNCTIONING PROPERLY
The following illustration shows the various avenues of damage caused by the malfunction of the AMPK pathway. These malfunctions involve three of the cardinal areas where problems arise. Metabolic dysfunction is probably the biggest while loss of proteostasis (protein homeostasis) and the loss of genetic instability are not far behind:
We can see that AMPK problems lead to multiple problems and as we get older they seem to be compounded. Also important are the effects AMPK may have on the other pathways of aging. Like many things in life as we age the pathway becomes less active you will notice that AMPK effects all the other major pathways of aging.
We can see essentially most of the major pathways the are directly affected by the AMPK pathway. These include NFkB, Sirt1, and mTOR. In more practical terms the next illustration shows the “deadly effects” of an AMPK deficit. These are all aspects of an unhealthy individual who is rapidly aging and is showing the aspects of “inflammaging”.
We can see very well the far-ranging effects that a deficiency of AMPK will have upon the body. In some way shape or form all of these problems lead to increasing inflammation in the body. This inflammation which is associated with aging is now called “Inflammaging”. It seems that if we can get a handle on AMPK and prevent it deficits, we might just get a better handle on aging. There are a number of methods that we can improve how our body deals with the AMPK pathway. The next section discusses this in greater detail. Remember AMPK deficiency is not just genetic in nature.
One other significant finding in the AMPK pathway is the effect AMPK has upon the health of our gut bacteria. Many medical problems arise when our gut bacteria is not in a healthy state. Accumulating studies have demonstrated that AMPK activation enhances paracellular junctions, nutrient transporters, autophagy and apoptosis, and suppresses inflammation and carcinogenesis in the intestine, indicating an essential role of AMPK in intestinal health. Gut health and the mitochondria are intimately related. The flowing diagram show how AMPK and gut health affect metabolism, inflammation, and oxidative stress. We are aware that a number of diabetes medicines target AMPK and ultimately have their effects on the gut bacteria. Metformin is one such medicine. Although it is mainly used for diabetic control Metformin is used by many non-diabetics for its anti-aging, anti-cancer, and potential performance enhancing properties due to its effects on the AMPK pathway.
We can extrapolate this further on athletic performance. There seems to be a crosstalk between the gut microbiota and mitochondria during Exercise. This can be seen in the following illustration. Ultimately we need to remember that we are only as healthy as our mitochondria.
What we see is that endurance performance is increased by the relationship between the gut, AMPK, and mitochondria functions. We can see that it is very important to maintain our gut bacteria in the best of condition. This is why probiotics are very important in maintaining the AMPK pathway. Remember that a healthy gut is a healthy and typically a happy patient.
WHAT ARE BEST WAYS TO CONTROL AMPK PATHWAY
There are a number of methods to control and stimulate the AMPK pathway. Some involve medications and supplements. Diet seems to play a large role in managing the AMPK pathway. That is rather evident in the above diagram.
Exercise, we now know, is one of the most powerful AMPK-activating strategies. Activated AMPK promotes all the processes we look for to maintain a youthful profile: rapid, efficient release of energy, with little energy storage as fat or new sugar molecules. Thus, activated AMPK keeps us lean and active, with a steady renewal of cellular components. AMPK activity fades with age. Just as importantly, when excessive calories are available, the result is accelerated tissue aging. You can boost AMPK activity through exercise and/or calorie restriction, but should also make use of natural supplements that support AMPK activity. Boosting AMPK activity will keep your tissues young and slow aging throughout your body. It is now clear that, when caloric intake remains much higher than needed to sustain energy expenditure AMPK activation is markedly decreased. With reduced AMPK activity, cells decrease their energy-releasing ATP-generating activities, and instead shift to energy-storing processes that generate new fat deposits and glucose molecules leading to premature aging and diseases.
The above picture shows Barberries which are the red berries from the Berberis vulgaris plant. These compounds contain the compound called Berberine. Berberine acts similar to the common diabetes medicine called metformin. Berberine seems to be a potent activator of the AMPK pathway. It has minimal side effects. Also as stated earlier, it is crucial to maintain the health of one’s gut bacteria. What else seems to affect AMPK pathway in a positive way? What other supplements also are beneficial when dealing with the AMPK pathway. These supplements include Resveratrol, Alpha Lipoic Acid, Gynostemma (a form of Ginseng), Curcumin and Quercetin. They all seem to act as potent stimulators of the AMPK pathway. The good news is that our clinic now has the ability to deliver Quercetin and Curcumin via an intravenous route. The bottom line is that we can now take AMPK stimulation to the next level.
I am a huge fan of NAD+ supplementation. My family and I take an NAD supplement on a daily basis. In addition to that, we will occasionally take an Intravenous dose of NAD+. It is indisputable that as we age we absolutely need more NAD+ or we basically face an increasing assault by the ravages of aging. Can NAD+ be like a Trojan Horse and on the outside look promising but at the same time cause danger from the inside? Well if you go to an ill prepared clinic the answer is yes! Like most things in life there is no free lunch. Indeed, we are well aware that NAD+ and its precursors will have significant effects on a number of pathways in the body. The following diagram shows what happens with low NAD levels:
One of the Anti-Aging Pathways that NAD affects is the Sirtuin gene pathway. There are seven different components to the Sirtuin genes. The Sirtuins are a family of proteins that play a huge role in aging by regulating cellular health, especially the health of the mitochondria. They're responsible for critical biological functions like DNA expression and other aspects of aging. However, sirtuins can only function in the presence of NAD+, nicotinamide adenine dinucleotide, a coenzyme found in all living cells. NAD is an essential building block during energy production. The energy in this case is ATP. We lose up to 50% of our NAD levels between the ages of 40 and 60 as can be seen in the following illustration:
We must also remember that NAD+ is not just used for energy production but also is utilized by enzymes (PARP) that repair DNA damage. These enzymes are also huge consumers of NAD. The Sirtuin genes seems to have significance over the health of our mitochondria. Ultimately, the decline in mitochondrial function causes us to age. A prominent theory of aging holds that decaying of mitochondria is a key driver of aging. To slow down aging one needs to increase NAD+ and its precursors. This is absolutely the case and is practiced by many well-informed people and clinics. Unfortunately, most people and clinics for that matter seem to stop here. The premise is that NAD+ will slow aging and everyone goes on their merry way. What we need to realize that NAD+ alone may in some ways act as a Trojan horse. On the outside it seems to be a gift to our health which in many ways it is. But there are also some aspects of NAD+ therapy that might not be conducive to our health UNLESS WE ADDRESS THESE PROBLEMS AT THE TIME OF THE NAD TREATMENT.
I have previously mentioned one detrimental aspect of NAD+ treatment is its effect on Senescent cells. Remember a Senescent cell is a cell that should have died but continues to survive causing a variety of problems. I wrote an extensive blog on this subject some time ago. Please go to my website and check the blog I wrote entitled “NAD and Senescent Cells on a Collision Course”.
Unfortunately, most clinics are not aware of the potential problems NAD+ may cause with Senescent cells. It can actually make these cells thrive. So low and behold you actually may not make a patient healthier if he is given NAD+ without addressing Senescent cells. You may be going in the opposite direction and possibly cause a decline in their overall health. We have addressed the Senescent cell problem with Senolytic agents for some time now. The Senolytic agents that will directly attack the Senescent cells and aid in their elimination. We have done this for years and will continue to do so.
METHYLATION OR LACK OF IT: A MAJOR HIDDEN DANGER OF NAD THERAPY
Senescent cells can cause havoc by their inflammatory secretions but they are only one problem that can be increased by NAD+ therapy. The other major concern unleashed by NAD+ therapy concerns a process called methylation.
Methylation is the transfer of a methyl group (one carbon and three hydrogens) from one molecule to another in the body and is a fundamental element of our biochemistry. Methylation is accomplished by enzymes. Methylation can modify heavy metals, regulate gene expression, RNA processing and protein function. It is recognized as a key process underlying Epigenetics. Epigenetics involves essentially turning on and off switches of different genes.
The above diagram illustrates the intersection between methylation and control of our genes. As noted above, methylation generally acts as a suppressor for many of the gene regulatory elements such as insulators, promoters, enhancers and repressors. These regulatory elements play a significant role in maintaining the integrity of chromosomes and homeostasis of organisms. Epigenetics ensures that only a single allele (different forms of the same gene) should be expressed for that specific gene. This process is known as imprinting. In the case of failed imprinting, it can result in a spectrum of diseases. In simplistic terms, epigenetics involves putting a methyl group on a DNA strand. Methyl groups are organic molecules. What we are really dealing with is called DNA methylation. DNA methylation occurs when a methyl group is added to a DNA strand. DNA methylation is a tool to typically lock genes into their off position. Aberrant DNA methylation, which is a nearly universal finding in cancer results in disturbed gene expression. DNA methylation is modified by environmental factors such as diet that may modify cancer risk and tumor behavior. Abnormal DNA methylation has been observed in several cancers. These alterations in DNA methylation may play a critical role in cancer development and progression. Dietary nutrient intake and bioactive food components are essential environmental factors that may influence DNA methylation. In recent years, researchers have learned a great deal about DNA methylation, including how it occurs and where it occurs, and they have also discovered that methylation is an important component in numerous cellular processes. So, we can see that DNA methylation is crucial to our well-being and healthspan.
HOW DO DNA METHYLATION AND NAD THERAPY INTERSECT WITH EACH OTHER?
We are able to see the importance methyl groups play in our health and well-being. Below we see a diagram of the metabolism of NAD+. The problem develops when we start to
metabolize the byproducts of NAD+. Although NAD+ is used by the body to create ATP, NAD+ is also metabolized to a methylated nicotinamide molecule called MeNAM. The process of metabolizing NAD+ stresses the body’s “methyl pool,” the molecules that donate methyl groups. The methyl pool is crucial to maintain one’s health. A methyl group needs to be added to NAD+ to create MeNAM, which uses up methyl groups that are needed for other biochemical reactions. If adequate amounts of methyl groups are not available than methylation is diminished allowing genes to either be kept on or off sometimes resulting in significant problems. Also, when NAD+ treatments are given, as the NAD+ is metabolized it is converted into a compound called Methionine which is ultimately converted into a compound called Homocysteine. Homocysteine is a byproduct of methionine metabolism. It is a powerful pro-oxidant and free-radical generator known to be a leading cause of heart disease and other problems as the following illustration shows.
A clinical study of niacinamide supplementation showed not only an increase in MeNAM, but also an increase in homocysteine levels, which is an independent risk factor for heart disease. There appears to be a relationship between high levels of homocysteine and artery damage. That can lead to atherosclerosis (hardening of the arteries) and blood clots. We must also realize many individuals in the United States – some estimates are as high as 60% have a genetic defect in a critical enzyme involved in methylation – MTHFR. This makes methylation even more difficult. Here is a good illustration of the damage homocysteine causes to the vessels:
The MTHFR gene provides instructions for making an enzyme called methylenetetrahydrofolate reductase. This enzyme plays a role in processing amino acids, the building blocks of proteins. Methylenetetrahydrofolate reductase is important for a chemical reaction involving the vitamin folate (also called vitamin B9). Specifically, this enzyme converts a form of folate called 5,10-methylenetetrahydrofolate to a different form of folate called 5-methyltetrahydrofolate. This is the primary form of folate found in blood, and is necessary for the multistep process that converts the amino acid homocysteine to another amino acid, methionine. The body uses methionine to make proteins and other important compounds.
When dealing with homocysteine, if one gets adequate amounts of vitamin B6, either from foods or supplements, a portion of the body’s homocysteine is converted into cystathionine, an antioxidant and free-radical deactivator. About half of our homocysteine is detoxified by this process. The other half is detoxified by the addition of a methyl group. With the addition of methyl groups, homocysteine is converted to methionine by the transfer of the methyl group from a methyl donating compound such as Trimethylglycine (TMG). We have been using TMG for some time now in our clinics. In brief, TMG detoxifies homocysteine, recycles methionine and supplies B15. Thus, we are able to see that NAD+ treatment will worsen the ongoing shortage of methyl groups in the body. Unless methyl donating compounds are utilized with NAD+ treatment we will exacerbate the methyl group shortage which could adversely affect the patients’ health and well-being on a few different levels.
When we are giving a patient intravenous NAD+ we have found that Trimethylglycine (TMG) dramatically enables to patient to receive intravenous doses of NAD at a much faster rate. Typically, if the rate is too fast, patients will develop a variety of symptoms including flushing, chest tightness etc. Although these symptoms sound serious they are benign and cause the patient no problems other than some anxiety. One of the big reasons for eliminating these symptoms is the fact that Trimethylglycine is a potent and rich methyl donor. The propriety trick is to know when and how much TMG to use. By utilizing TMG as methyl donor, we are eliminating unpleasant symptoms and at the same time improving the patient’s health on many levels. So again, make sure the if you receive any type of NAD treatment that Senescent cells and the methyl group problem be addressed. Your health and well-being depend upon it.
The three above supplements are extremely important for optimal health but unfortunately, we have problems with their absorption. We may diligently take them orally on a daily basis which certainly helps but many times that may not be sufficient. However, if we are able to supplement our daily oral doses with Intravenous applications then we are talking about something special. We have been searching for Intravenous or injectable forms of these compounds for some time now and have finally found reliable sources. When something is delivered via an Intravenous route (IV) there is instant and significant absorption. Many times, the same can be said for an intra-muscular (IM) route as far as absorption is concerned. We are happy to report that these three compounds will now be an integral portion of our repertoire. The centers that have access to all these compounds are few and far between. The main problem with most of these compounds is their bio-availability. We can take them by mouth but how much of them will we absorb is a different story. This is the situation with many supplements and for that matter medications. The science of how compounds are absorbed is called pharmacokinetics. Pharmacokinetics involves the absorption, distribution, metabolism, and excretion of a compound.
Co Q10: A CRUCIAL FACTOR FOR THE BODY
Coenzyme Q10 is a member of the ubiquinone family of compounds. All animals, including humans can to some degree synthesize ubiquinones, hence, Coenzyme Q10 is not considered a vitamin. The name ubiquinone refers to the ubiquitous presence of these compounds in living organisms and their chemical structure, which contains a functional group known as a benzoquinone. Coenzyme Q10 is soluble in lipids (fats) and is found in virtually all cell membranes including the mitochondrial membrane. Remember that the cell membrane represents the eyes and ears of the cell. It interacts with the environment. Co Q10 is present in every cell of your body. However, the highest concentrations are found in organs with the greatest energy demands, such as the heart, kidneys, lungs and liver. Co Q10 is a fat-soluble, vitamin-like compound that seems to have many health benefits. As we can see from the following diagram it is vital for the production of energy in the body while at the same time serving as an anti-oxidant. It does this crucial work by its effects on the electron transport chain. The ability of Coenzyme Q 10 to accept and donate electrons is a critical feature to its function.
These properties make it helpful in the preservation of cells and the prevention and treatment of some chronic diseases. It's critical to add Co Q10 supplements as you age. After the age of 30, your natural levels of Co Q10 begin to diminish. By the age of 50, this depletion of Co Q10 continues to accelerate. By age 70, your natural Co Q10 levels may be 50% lower than they were when you were a young adult. It is widely known that statins severely deplete your body's natural levels of CoQ10, which can be very dangerous. A Columbia University study found that within 30 days, your levels of Co Q10 can be decreased by half. However, statin drugs aren't the only culprit. In fact, there is a long list of pharmaceuticals that rob your body of Co Q10. Nearly 50% of American adults take at least one prescription daily, it's more important than ever to supplement with Co Q10 so you can be sure your body has the necessary levels needed for proper cellular energy function and a strong cardiovascular system. Co Q10’s health benefits
are far reaching. We now have an injectable form of Co Q10 that will dramatically increase the amount of Co Q10 the body will absorb. This will pay the patient many health dividends including better health, more energy and less sickness. Remember that mitochondrial dysfunction is the basis of many diseases. Co Q10 fights mitochondrial problems making the mitochondria healthier enabling them to ward off diseases.
Quercetin-type Flavonols, the most abundant of the flavonoid molecules, are widely distributed in plants. Remember that a flavonoid is a group of plant chemicals found in fruits and vegetables.
They give fruits and plants their color and smell. Flavonoids are powerful antioxidant agents that help regulate cellular activity. They are found in a variety of foods including apples, berries, Brassica vegetables, capers, grapes, onions, shallots, tea, and tomatoes, as well as many seeds, nuts, flowers, barks, and leaves. Quercetin is also found in medicinal botanicals, including Ginkgo biloba, Hypericum perforatum, and Sambucus canadensis. In red onions, higher concentrations of quercetin occur in the outermost rings and in the part closest to the root, the latter being the part of the plant with the highest concentration. Quercetin in the pharmaceutical field is limited due to its poor solubility, low bioavailability, poor permeability and instability. Quercetin possesses diverse pharmacologic effects including anti-inflammatory, antioxidant, anti-cancer, anti-anaphylaxis effects and Anti-aging.
These aspects are evident in the following diagram:
The above diagram shows the main mechanism of Quercetin’s actions namely reducing oxidative stress. Oxidative stress is what I call an upstream cause of aging. If we control oxidative stress than we can eliminate or significantly alter the course of many degenerative diseases while at the same time slow down the clock of aging. As we can see, Quercetin is attacking some of the upstream pathways of aging. Although Quercetin is very powerful, the problem is delivering it to the places where it is needed. To improve the bioavailability of Quercetin, numerous approaches have been undertaken. These involve the use of promising drug delivery systems such as inclusion complexes, liposomes, nanoparticles also called micelles, which appear to provide higher solubility and bioavailability. If we can enhance bioavailability of Quercetin in the future, then it is likely to bring this product to the forefront of therapeutic agents for treatment of human disease. The fact that we can now deliver it via an intravenous route makes these other drug delivery systems not be as important. Certainly, they can be convenient, but at present they cannot compete with the intravenous route as far as absorption and efficacy are concerned. This is a monumental step.
In addition to the beneficial aspects already mentioned for Quercetin there is one other huge benefit. This benefit concerns the aspect that Quercetin has on Senescent cells. A Senescent cell is essentially a cell that should have died but continues to live. It has lost its ability to reproduce. It secretes a number of undesirable growth factors which encourage a variety of degenerative conditions and other health problems. Quercetin will act as a Senolytic agent. A Senolytic agent helps to clear out the Senescent cells. If we eliminate Senescent cells than we eliminate their growth factors which can cause havoc. In our office when we are utilizing NAD+ we make it standard practice to give the patient some Quercetin to help keep the Senescent cells at bay rather than encourage their health. We do need some Senescent cells but only in small numbers. Quercetin is a good protector from Senescent Cells.
CURCUMIN ALSO CALLED TUMERIC
Turmeric is a spice that has long been recognized for its medicinal properties. It has received interest from both the medical/scientific world as it is the major source of the curcumin. Turmeric is a spice derived from the rhizomes of the tropical plant Curcuma longa Linn, which is a member of the ginger family (Zingiberaceae). The bright yellow-orange color of turmeric comes mainly from fat-soluble pigments known as curcuminoids. Curcumin, the principal curcuminoid found in turmeric, is generally considered its most active constituent. It aids in the management of oxidative and inflammatory conditions, metabolic syndrome, arthritis, anxiety, and hyperlipidemia. It may also help in the management of exercise-induced inflammation and muscle soreness, thus enhancing recovery and performance in active people and athletes. In addition, a relatively low dose of the complex can provide health benefits for people that do not have diagnosed health conditions. Most of these benefits can be attributed to its antioxidant and anti-inflammatory effects. Ingesting curcumin by itself does not lead to the associated health benefits due to its poor bioavailability which appears to be primarily due to poor absorption, rapid metabolism, and rapid elimination. There are several components that can increase bioavailability. For example, Piperine is the major active component of black pepper and, when combined in a complex with curcumin, has been shown to increase bioavailability by 2000%. Personally, I have found the best form of oral form of Curcumin come from a product called Ultra Cur. The uniqueness of Ultra Cur comes from the whey protein scaffold on which Ultra Cur is delivered into the body. This scaffold dramatically increases the bioavailability. But we still must realize that an intravenous form will far surpass the bio absorption of any oral forms.
The diagram below shows the far-reaching medical benefits from Curcumin:
When discussing Curcumin from scientific point we need to address what pathways of aging it seems to address.
The following diagram shows some of these pathways:
In some of the pathways above we are able to see some significant pathways related to aging. One important pathway mentioned above is the NFkB pathway. This pathway is a master regulator of inflammation in the body. If it is stimulated it causes inflammation to get a foothold possibly resulting in many degenerative diseases and conditions. The Th-1 response results from our immune system. This portion of our immune system can result in autoimmune conditions. We need to remember many diseases may have their roots in an auto immune condition. The blocking of the COX-2 pathway is the mechanism of how many anti-inflammatories work. Increasing the amount of BDNF has many profound implications. BDNF plays a critical role in preventing cerebral atrophy and cognitive decline. We also know that BDNF has profound effects on muscle tissue. It helps muscles repair themselves, preserve their integrity, and prevent the typical decline we see with advanced age. We see Curcumin increases antioxidative enzymes which will help eliminate free radicals and the damage they cause. Lastly, there are many studies underway looking at the inhibition of cancer growth.
The next diagram shows some other aspects of Curcumin:
What is of great significance in this diagram is the fact that Curcumin acts as a transcription agent. A transcription agent will typically turn on genes that have become silenced due to a variety of reasons. In this case Curcumin will activate the P-53 gene. This gene is called the Tumor Suppressor Gene. This gene is on patrol to analyze cells as far as DNA damage is concerned. The diagram below explains the P-53 gene in simple terms. If the P-53 is not working properly than it allows cells with accumulated DNA damage to persist and possibly go on to cause degenerative diseases and cancers. When it is working properly than it eliminates the bad cells and repairs those cells worth repairing. We can see the far-reaching effects that Curcumin has upon our health and well-being.
Thus, we can see the multiple benefits that we can offer from the use of Intravenous Quercetin and Curcumin and injectable Co Q10. They would seem to be especially helpful as an adjunct to NAD+ and other treatments. I still believe in taking oral forms of these compounds but there is no doubt that we occasionaly need to supplement them with Intravenous or Injectable forms. Your life, health, and well being many depend upon it.