Alchemic Health

26/07/2021

Longevity: Life Extension Properties of Green Tea's Epigallocatechin-3-gallate (EGCG)

A unique compound from green tea called Epigallocatechin-3-gallate (EGCG) is gaining a lot of attention due to its positive impact on health and life extension. It is a plant-based compound called catechin and catechins are part of a group called polyphenols, of which EGCG being the most abundant and potent catechin in green tea(1). Based off its chemical structure, EGCG is classified as a potent antioxidant that may protect against cellular damage caused by free radicals. Additionally, research demonstrates that EGCG may be beneficial in reducing inflammation and offers protection against cardiovascular disease, cancer, diabetes, osteoporosis and neurodegenerative diseases(2).

Studies have shown that elderly Japanese people who drank more than 3 cups of green tea per day, were associated with lowered rates of death from stroke, heart disease and respiratory diseases (3)(4). Another study conducted over 6 years with 14,000 elderly Japanese people showed that drinking green tea was associated with lower mortality from all causes(5).

EGCG not only protects against disease, but it also addresses a number of mechanisms related to aging, making it a great tool for longevity. In cell-based studies, green tea polyphenols protected telomeres from shortening which suggests its potential for increasing longevity(6). Telomeres shorten with every cell division as we age, so by protecting telomeres we could see a possible increase in the Hayflick limit of the cell (increasing how many times a cell can divide before it becomes a senescent cell) which could lead to a longer lifespan. In animal studies, EGCG extends lifespan by reducing liver and kidney damage, lowering cellular senescence and improves age related oxidative stress and inflammation. It does this through the inhibition of NF-kB signaling by activating the longevity factors Fox03a and SIRT1(7)(8 ). It also triggers mitochondrial biogenesis which restores mitochondrial function, this then leads to increased energy (ATP production) and lowered cellular dysfunction which helps slow down the aging process. This increase in lifespan due to EGCG depends on known energy sensors such as AMPK/AAK-2, SIRT1/SIR-2.1 and FOXO/DAF-16. It has shown to be more effective in younger adults and declines with age(9). So, to gain the most benefits out of EGCG, it is advised to start taking it earlier in life rather than later as it is more effective in slowing down the aging process when we are young. Long term consumption of EGCG has shown to be safe and effective at addressing aging via its influence on several aspects of aging and senescence which increase health span and lifespan(10).

In addition to EGCG’s longevity benefits, it also improves cognitive health as we age. It helps reduce neurodegenerative diseases through increasing neuritogensis(11). This is the process of forming new neurites (that develop in axons and dendrites) which extend from the brain cell body. The process happens during the brain’s development and the term neurite is used to refer to the early stages of growth before the axon and dendrites are differentiated. EGCG is also neuroprotective, meaning it protects the neurological system. It is able to do this via decreasing reactive oxygen species, protecting cells against mitochondrial dysfunction and lowers glutamate excitotoxicity. It preserves mitochondrial energetics and limits neuronal damage and inflammation in the brain(12).

Overall EGCG is a great longevity compound to add to anyone’s supplemental stack or formula. It helps ward off age related diseases and may increase lifespan through numerous longevity pathways within the body. The best dose for therapeutic effects is around 200mg EGCG per day with meals. EGCG along with other longevity compounds should be taken in early age to gain maximum benefits, as it’s easier to slow down the aging process in healthy young individuals then it is to reverse age in the elderly.

Written by Luke Pavasovic
Director and Naturopath at Alchemic Health
Alchemic Health
www.alchemichealth.com

References:
1. https://pubmed.ncbi.nlm.nih.gov/24494192/
2. https://pubmed.ncbi.nlm.nih.gov/20716914/
3. https://pubmed.ncbi.nlm.nih.gov/16968850/
4. https://pubmed.ncbi.nlm.nih.gov/31392470/
5. https://pubmed.ncbi.nlm.nih.gov/19628408/
6. https://pubmed.ncbi.nlm.nih.gov/22000973/
7. https://onlinelibrary.wiley.com/doi/full/10.1111/acel.1213
8. https://pubs.rsc.org/en/content/articlehtml/2019/ra/c9ra03313k
9. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5635249/
10. https://www.biorxiv.org/content/10.1101/2021.01.01.425058v1
11. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6696481/
12. https://nutritionj.biomedcentral.com/articles/10.1186/s12937-016-0179-4

A Holistic Approach to Discover Your Optimal State of Health

04/06/2021

Thank you Ryan Kennedy for the invitation to be on your podcast. We discuss topics such as hacks for increased longevity, addictions and ways to address it and touching on how to increase the brains health, function and motivation through specific nootropic compounds.

It was an absolute pleasure to talk to Ryan, he is a wealth of knowledge and I look forward to conversing with him more in the near future.

My guest on today’s show is Dr. Luke Pavasovic who’s a naturopath and clinician based in Australia. Tune into this amazing interview to learn more about:How...

26/03/2021

Ketamine – The Good, The Bad, The Ugly

The story of ketamine begins with the synthesis of phencyclidine, which was first synthesized in 1956 and found to have remarkable anesthetic effects on monkeys but in human trails it demonstrated to have unwanted side effects such as loss of sensation in limbs, producing sensory deprivation syndrome. Hoping to find an alternative drug, Dr Calvin Lee Stevens of Wayne State University synthesized numerous phencyclidine derivatives one of them being titled CI-581 which we now call ketamine. On August 3rd, 1964 the first human trials were conducted with subjects given intravenous ketamine and describing the experience like floating in space, disconnected from their body and environment. After its approval by the FDA in 1970, it was used on injured soldiers in the Vietnam War due to its large margin of safety. In the last two decades, clinical trials have found ketamine to be not only be useful for short term pain and chronic pain but also eases pain of a psychological nature such as PTSD, OCD, anxiety, depression and suicidal ideation. Due its mind altering and blissful nature, ketamine has also grown in popularity as a reactional drug sold on the black market.

Ketamine’s primary action is as a noncompetitive N-methyl-D-aspartate (NMDA) and glutamate receptor antagonist (meaning it inhibits these receptors) and also blocks HCN1 receptors. It partially agonizes (partially activates) op**te mu-receptors which provides its pain relieving properties(1). The antidepressants effects of ketamine are hypothesized to be caused from an increase in synaptic connectivity (increasing brain cell connections). Clinical trials suggested NMDA receptors play a significant role in depression and through ketamine’s NMDA antagonistic action, it works rapidly to control symptoms(1)(2). This may be due to an increase in glutamate levels, leading to synaptogenesis (the growth of new brain cell connections) and elevating levels of brain-derived neurotrophic factor (BNDF) which is an important growth factor within our brain and peripheral nervous system(1). In recent clinical applications of ketamine to patients with depression, 80% have shown an improvement in symptoms(3). Through these actions, ketamine may play an important role in helping people with specific neurological issues.

Even though ketamine is showing beneficial effects, the dose and duration makes it either a medicine or a poison. Ketamine usage has grown exponentially within the recreational market within the last decade and we are beginning to see some of the detrimental effects it may cause for the user if used in the wrong way. A recent study which conducted magnetic resonance imaging (MRI) on ketamine addicts of 0.5-12 years illustrated the possible brain damage that can occur from ketamine abuse. Even though the study was small with only 21 people recruited, the results demonstrate that lesions within the brain of ketamine addicts appeared within 2-4 years of usage(4). Cortical atrophy was usually evident in the frontal, parietal and occipital cortices, confirming that many brain regions in humans are susceptible to ketamine induced injury. Most patients consumed ketamine daily, with only a few consuming it 2-3 times per week, dosage ranged from 0.2g-3g per day, but on average they were consuming 1g per day(4). The damage was also increased when the patient mixed ketamine with other drugs such as alcohol, amphetamine and ecstasy(4). We also do not know the health status of these patients, how much they exercised, fluid intake, diet, sleep patterns etc., and it can be hypothesized that if they followed unhealthy lifestyle factors along with ketamine abuse then this would of most likely exacerbated the brain damage. So, with all this information we are able to see that ketamine is able to be very detrimental to neurological structures if abused recreationally.

Ketamine can further begin to become uglier the more it is abused, effecting numerous organs within the body. It has been shown in rare cases to cause chronic biliary colic, where patients present with biliary symptoms (nausea, vomiting, loss of appetite, fatigue and abdominal pain/cramps usually in the upper right quadrant) without evidence of gallbladder stones(5). This is due to ketamine’s effect on the gallbladder causing dilation in bile ducts, but once usage ceased the gallbladder returned to normal(5). Ketamine may cause renal (kidney) failure, and also lead to liver toxicity and damage(8). It also shown to cause severe lower urinary tract symptoms (LUTS) with CT scans on patients revealing decreased bladder volume, bladder wall thickening, mucosal enhancement and perivesical inflammation, with advanced cases identifying ureteric narrowing and strictures(6)(7). The damage to the liver, kidneys and lower urinary tract are primarily due to the metabolites of ketamine (norketamine, dehydronorketamine and hydroxylated ketamine metabolites with glucuronic acid) and not solely caused by ketamine alone(9). This clearly demonstrates the harmful and possibly irreversible effects of ketamine on numerous organs and that it is important to recognise symptoms in recreational users before it becomes too late.

As we can see, ketamine has its place within medicine and when used correctly can greatly help those with numerous conditions but when used incorrectly may wreak havoc on numerous parts of the body causing irreversible damage. I urge people to be responsible with usage if consuming this substance in a recreational setting, be mindful of your dosage and frequency of use. If any negative side effects occur, please reframe from usage and seek medical help if symptoms persist. If you decide to use this substance recreationally, may I suggest you consume enough fluids to flush your liver, kidneys and bladder frequently and consider consuming antioxidants (vitamin C and E, astaxanthin, R-alpha lipoic acid) to help mitigate the toxicity and damage of this substance. Be smart, be safe and be responsible with your health.

Written by Luke Pavasovic
Director and Naturopath at Alchemic Health
Alchemic Health
www.alchemichealth.com

References:
1. https://www.ncbi.nlm.nih.gov/books/NBK470357/
2. https://pubmed.ncbi.nlm.nih.gov/10686270/
3. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4810965/
4. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3713393/
5. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4898409/
6. https://pubmed.ncbi.nlm.nih.gov/20797465/
7. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4544340/
8. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4421282/
9. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6197107/

17/03/2021

Thank you Lucas Auon from Ergogenic_Health for having me on your Boost Your Biology podcast. We discuss various nootropics, herbal therapies, and the famous racetam family of compounds. I also share my experiences with psychedelic substances and how they can influence the course of one’s life. It was great to talk about subjects I am immensely passionate about and more podcasts will be coming soon in the near future.

For those of your who want to just listen to the audio please click the link the Spotify link below.
https://open.spotify.com/episode/52ZsswWB7wIN3KqN1adrEF

17/02/2021

A Toxic Relationship - When Alcohol Meets Co***ne

Alcohol and co***ne are two of the most popular recreational substances on the planet. Alcohol is legal and easily accessible to anyone; co***ne is illegal but a highly sought after with the image of it being a high-end drug for the rich and famous. Both substances are toxic in their own way but what happens when they are taken together?

From a general perspective these two substances are usually consumed together. Co***ne is the most abused psychostimulant known to man, and it gives the user a euphoric confident high due to its ability to directly inhibit the reuptake of dopamine, serotonin and norepinephrine into pre-synaptic neurons(1). This inhibition elevates synaptic concentrations of these neurotransmitters, which is responsible for the high co***ne provides. Although the high can be euphoric, co***ne does also come with sides effects such as edginess, paranoia and irritability which is generally due to its effects on norepinephrine. Due to this, it is very common for people to add alcohol to the equation to level out the high and bring some calming effects to their neurological system - but is this safe?

Alcohol is used as a catalyst in chemistry, meaning it enables a chemical reaction and speeds these reactions up where they would usually take a long time. When we consume alcohol and it enters the liver, it can alter the chemical reactions thus changing the way some drugs work within the body. When a person consumes alcohol while co***ne is in their system, it changes its kinetics and metabolism which creates a new byproduct called cocaethylene. Cocaethylene is an ethyl ester of benzoylecgonine and is a psychoactive substance which has pharmacological properties similar to co***ne but has a half-life three to five times that of co***ne(2)(7). It has been shown to be more potent, increasing aspects of the high for the consumer but also the dangers, exerting more cardiovascular toxicity than either alcohol or co***ne alone(3). Because cocaethylene has a slower rate of elimination from the body, it makes it more attractive to the user due to its duration along with its increased potency. However, it greatly increases the risks of seizures, liver damage and compromises the function of the immune system(4).

Cocaethylene causes hypertension and increased systemic vascular resistance, while at high concentrations decreases myocardial function, slows cardiac conduction and is arrhythmogenic(5). The LD50 of cocaethylene is significantly lower than that of co***ne, carrying a 18-25 fold increase in risk for immediate death than co***ne alone(6)(7). Experiments suggest cocaethylene depresses the myocardium which is the muscular center layer of the heart between the outer layer (epicardium) and the inner layer (endocardium). This demonstrates how it’s a major contributor to cardiotoxicity(8).

Human studies show that when co***ne is ingested with ethonal in the system, 17% of the co***ne is converted to cocaethylene with subjects said to of experienced more intoxication with this combination(10). Alcohol also increased peak concentrations of co***ne by about 20%, this is due to alcohol increasing the absorption of co***ne(11). So it’s not just cocaethylene that is possibly dangerous but the fact that alcohol also increases the absorption of co***ne at the same time, this combination increases the potential of toxicity along with overdose. Higher blood concentrations of co***ne along with the presence of cocaethylene was associated with elevated heart rate, increased plasma cortisol concentration and higher cardiotoxicity(11). Some good news is most users of co***ne do not ingest enough alcohol to produce significant amounts of cocaethylene, but when excess alcohol is consumed along with co***ne, concentrations of cocaethylene are very modest according to postmortem studies(11).

I have personally seen people mix this combination of drugs in the past. With my understanding of its toxicity, I worry what this may be doing to people not only in the immediate future but also in the distant. It may increase the ricks of cardiovascular disease (CVD being the number one killer worldwide, taking an estimate of 17.9 million lives each year)(9). With CVD being caused primarily from lifestyle choices, this combination is a factor that may to increase the risks. I want people to be aware of this toxic combination and byproduct, so that they understand what they are potentially doing to their body, allowing them to make changes to avoid these dangers. So next time you are out and having a drink, take a second thought before you do that line, think of your health and heart before you start.

Written by Luke Pavasovic
Director and Naturopath at Alchemic Health
Alchemic Health
www.alchemichealth.com

1. https://pubmed.ncbi.nlm.nih.gov/11920678/
2. https://pubmed.ncbi.nlm.nih.gov/9243342/
3. https://pubmed.ncbi.nlm.nih.gov/1432406/
4. https://pubmed.ncbi.nlm.nih.gov/9243342/
5. https://pubmed.ncbi.nlm.nih.gov/12215047/
6. https://pubmed.ncbi.nlm.nih.gov/7501674/
7. https://drugs.ncats.io/substance/FJO3071W5Y
8. https://pubmed.ncbi.nlm.nih.gov/8606535/
9. https://www.who.int/health-topics/cardiovascular-diseases =tab_1
10. https://pubmed.ncbi.nlm.nih.gov/14636972/
11. https://www.sciencedirect.com/topics/neuroscience/cocaethylene

11/02/2021

A Call for a Change of Perspective and Education

Let’s be honest, the war on drugs has failed and continues to fail. After decades of prohibition, recreational substances are still rampant and more accessible then ever before with the rise of Silk Road (an online black market) and other darknet sites. The common encouragement of “just say no” has shown time after time not to work, and in fact may increase the urge to try substances just because it is forbidden. Humans throughout history have shown their innate desire to seek altered states of consciousness, with most cultures having a sacred medicine which could be a concoction of plants or mushrooms. These medicines allowed them access to spiritual visions and essentially having a psychedelic experience. Unfortunately, in these modern times, such things are not as widely accepted and are outlawed in most countries and states, but humans still seek altered states on the daily through drinking our morning coffee for stimulation or having a glass of wine at dinner to finish off the day.

At the end of the day, if someone wants to seek and take a drug they will do so despite the law and we see this within our society. Due to it being so taboo and outlawed, we lack true unbiased drug education. There is and always has been an immense push of scare tactics to deter people from taking drugs, but we can see that this also does not work as it’s causing more misinformation and harm to the user. I am a true believer that if we want to save people’s lives from the dangers of drugs, rather than to scare them away, we need to educate so that people truly understand how these substances work and their possible interactions with other drugs and how to mitigate the toxicity. Please note that I am not condoning the use of drugs by all means, but I am all for true unbiased education so that people have the knowledge to make the right choices which inevitably will save lives and create a safer environment for the user. When we change our perspective on drugs, we will change our reality and how our society approaches the subject. Instead of pushing the subject away and turning a blind eye to it, we need to face it and understand why people want to seek them and how these substances work.

At Alchemic Health we are dedicated to helping people with addiction and offer drug rehabilitation. Alongside this we are also here to spread unbiased information about drugs and how to counter their toxicity (if there is any) through natural therapies. Knowledge is power and we want to grant people the power to understand themselves and what they are consuming so that they may make the right choices for themselves. We need to be compassionate to all walks of life as each person is unique and has a different life experience. I endorse all of us to stop demonizing people and actually take the time to understand each other.

In the near future, I will be bringing you true drug education and ways to bio-hack your recreational experience to create a safer environment. I hope to bring a new perspective and paradigm shift to the way we view and address this subject. Stay tuned!

Written by Luke Pavasovic
Director and Naturopath at Alchemic Health
Alchemic Health
www.alchemichealth.com

03/12/2020

Nootropics: Brain Restorative Properties of Plant Flavonoid 7,8-Dihydroxyflavone

Cognitive impairment is something no one wants to go through, but we will all suffer from it at some stage in our lives. There are many reasons why one would start to suffer cognitive decline, but a major contributing factor is synaptic loss. The synapses are the junctions between neurons where chemical information is exchanged. Sensory, motor and cognitive impairments are associated with the increased destruction of synapses, which can lead to neurodegenerative conditions such as major depressive disorder, Huntington disease, schizophrenia, dementia, Alzheimer’s disease and amyotrophic lateral sclerosis.

Reduced levels of brain-derived neurotrophic factor (BDNF) have been detected in those suffering from neurodegenerative diseases. This important brain protein promotes the survival of neurons as it plays a role in the growth, maturation and maintenance of brain cells. BNDF serves as a neurotransmitter modulator and participates in neuronal plasticity, making it essential for learning and memory(1). It binds to its high affinity receptor TrkB (tyrosine kinase B), where its activation signals transduction cascades (IRs1/2, PI3K, Akt), crucial for CREB and CBP production, which encode proteins involved in β cell survival. Similar to insulin-like growth factor 1, BNDF has downstream signaling mechanisms incorporating both p-CAMK and MAPK that increase the expression if pro-survival genes(1). This signaling through TrkB receptor plays a central role in promoting synaptic transmission, synaptogenesis and facilitating synaptic plasticity, making it an attractive candidate for targeted therapies(3). BNDF is vital for optimal brain health and functionality, but as we age the expression of this protein decreases, further leading to cognitive decline and neurological diseases. Although through increasing BNDF signaling, pre-clinical studies demonstrate that this may be a potent way to prevent, arrest and even reverse abnormal neurodevelopmental disorders(4).

Recent studies into 7,8-dihydroxyflavone (7,8 DHF), a small TrkB agonist that mimics BNDF function, has shown similar effects as BNDF in promoting neuronal survival and regeneration following traumatic brain injury(2). 7,8 DHF is a naturally occurring plant flavonoid that has a longer half-life in comparison to BNDF, as well as being much smaller in molecular size, allowing it to pe*****te the blood-brain barrier(2). It has been found to decrease cortical Aβ plaque deposition and protect cortical neurons against reduced dendritic arbor complexity, but has no impact on the density of dendritic spines. In addition to this it also protects against hippocampal increase in the level of choline-containing compounds and glutamate loss(3). 7,8 DHF promotes axon regeneration, inhibits the loss of hippocampal synapses, restores synapse number and synaptic plasticity, which prevents memory deficits(5)(8).

Huntington’s disease (HD) is a fatal neurodegenerative disease. Research has demonstrated a link between HD and reduced levels of striatal BNDF with an imbalance between its TrkB receptors and p75(NTR)(6). Thus, molecules with activity on the BNDF/TrkB/p75 system can potentially have therapeutic effects. After chronic 7,8 DHF administration, analyses revealed improved striatal levels of enkephalin, prevention of striatal volume loss, TrkBY816 phosphorylation recovery in striatum, normalized striatal levels of induced and neuronal nitric oxide synthase while ameliorating the imbalance of p75/TrkB(6). This supports its potential therapeutic role in those suffering with HD and other neurological ailments.

7,8 DHF has shown to protect people suffering from severe stress and traumatic brain injury (TBI). Post-traumatic stress disorder (PTSD) occurs after being exposed to a traumatic situation; this is characterized by cognitive deficits which include impaired explicit memory. 7,8 DHF significantly reverted spatial memory impairment and the increased long-term potentiation, supporting the idea that the activation of BNDF/TrkB pathway fulfills a protective role(7). When 7,8 DHF was taken alongside exercise, it has shown to improve brain function in those with traumatic brain injury. This combination enhances hippocampal functional connectivity, promoting enhanced levels of cell metabolism, synaptic plasticity and increases brain circuit function that facilitates greater rehabilitation after TBI(9).

Parkinson’s disease is caused by the destruction of dopamine producing neurons within part of the midbrain called substantia nigra. Studies show 7,8 DHF has potent neuroprotective effects through the activation of TrkB, which significantly improves dopamine-mediated behaviours and prevented the loss of dopaminergic neurons in the substantia nigra(10).

Due to the suspected low-water solubility, chemical instability, and poor bioavailability of 7,8 DHF, further research is on the way into increasing its absorption, thus potentially increasing its therapeutic effects. To overcome this, scientists fabricate stable 7,8 DHF loaded zein/lactoferrin composite nanoparticles which increases the chemical stability, water solubility and bioaccessibility(11). 7,8 DHF has an array of positive effects on numerous conditions and diseases, which warrants great interest in this natural compound. Even with its poor bioavailability, it still has noticeable cognitive enhancing effects and would work well in anyone’s nootropic stack to increase the brains overall health and functionality, warding off age related cognitive disorders.

Written by Luke Pavasovic
Director and Naturopath at Alchemic Health
Alchemic Health
www.alchemichealth.com

References:
1. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4697050/
2. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5319242/
3. https://pubmed.ncbi.nlm.nih.gov/29510124/
4. https://pubmed.ncbi.nlm.nih.gov/26220903/
5. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3895241/
6. https://pubmed.ncbi.nlm.nih.gov/28541476/
7. https://pubmed.ncbi.nlm.nih.gov/27068341/
8. https://pubmed.ncbi.nlm.nih.gov/24043773/
9. https://pubmed.ncbi.nlm.nih.gov/28315455/
10. https://pubmed.ncbi.nlm.nih.gov/27019033/
11. https://www.sciencedirect.com/science/article/abs/pii/S0141813019401244

13/11/2020

Longevity: Thymus Health and Regeneration

The thymus is an amazing little gland in the body that does some very important things. It’s part of the lymphatic system along with adenoids, spleen and tonsils and is also part of the endocrine system. It is located in the center of the chest behind the sternum and is responsible for producing progenitor cells which mature into T-cells (thymus-derived cells). The thymus also produces immune regulating compounds, hormones such as thymosin, thymopoietin and thymulin, as well as other peptides and interleukins. It is one organ that reaches maturity in utero and involutes as we age. The involution of the thymus changes it’s architecture, causing it to lose its organized structure and is replaced with adipose tissues as it becomes functionally less active(1). As we age, our thymus regresses and increases our susceptibility to disease and further aging due to the decline in T-cell output(1)(2). Advance aging correlates with a reduced ability of the immune system to generate antigen specific responses to pathogens. This profound change exhibited by the aging immune system is termed immunosenescence, affecting both innate and adaptive immunity(2). We can help slow down this regression or even regenerate the thymus gland through a number of interventions. By doing this we can reestablish a stronger and healthier immune system, helping ward off aging and age-related diseases.

A number of vitamins and minerals can help the health and functionality of the thymus as we age. High vitamin C intake has shown to suppress age-related thymic atrophy whilst promoting maturation of T-cells(3)(4). Vitamin A deficiency has shown to effect the production of thymosin-β4 and CD4 but high vitamin E intake enhances T-cell differentiation via TEC functions in the thymus(5)(6). Exogeneous melatonin leads to a marked reduction in signs of thymic aging, while being zinc deficient causes age related immunological dysfunction, including thymic failure(9)(10). However, when it comes to increasing thymus health and regeneration, one of the best tools for this job are bioregulatory peptides such as thymalin.

Thymalin is a synthetic version of thymulin (H-Pyr-Ala-Lys-Ser-Gln-Gly-Gly-Ser-Asn-OH). It was first isolated from the thymus gland in 1977 and has been studied for its geroprotective effects, meaning it aims to affect the root cause of aging and age-related diseases. It regulates immune function via increased T-cell activity, lowering inflammation, raising immunoglobulin A and has shown to be neuroprotective. One study researched the effects thymalin has on the elderly (60yrs+) over a 6-8 year period, receiving the peptide for the first 2-3 years of observation(7). The results showed the ability for bioregulators to normalize functions in cardiovascular, endocrine, immune and nervous systems. This restoration of homeostasis was accompanied by a 2.0-2.4-fold decrease acute respiratory disease, ischemic heart disease, hypertension disease, osteoarthrosis and osteoporosis(7). There was a significant improvement in the overall health state of the peptide treated patients which correlated with a decreased mortality rate during observations by 2.0-2.1 fold, demonstrating prevention in age related pathology and prolonging active longevity(7).

Other studies show it has pronounced antitumor effects, causing tumor growth arrest and also regression, some seeing growth suppression by 78%(8). Thymalin induced a significant increase in lymphoproliferative activity and the content of tissue basophils and plasmocytes in the thymus lobules(8). The results of other studies shows that thymalin significantly enhances immunological resistance to viral infections(11). Research demonstrates thymalin’s ability to regenerate the thymus gland, helping increase immunity whilst warding off age-related diseases.

A healthy lifestyle is the best way to attain a long and healthy life. If we want to help slow the onset of aging and age-related diseases, we need to incorporate lifestyle and nutritional factors into our life, supporting the body’s organs and systems as we get older. A healthy thymus is vital to longevity and if we support it throughout life with the right nutrients and even peptide technology, we can greatly affect and combat this major factor of aging. Living younger and longer without the diseases that primarily come with advanced age.

Written by Luke Pavasovic
Director and Naturopath at Alchemic Health
Alchemic Health
www.alchemichealth.com

References:
1. https://www.ncbi.nlm.nih.gov/books/NBK539748/
2. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3791471/
3. https://pubmed.ncbi.nlm.nih.gov/25608928/
4. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3869442/
5. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6296595/
6. https://pubmed.ncbi.nlm.nih.gov/9523031/
7. https://pubmed.ncbi.nlm.nih.gov/14523363/
8. https://www.pubfacts.com/detail/29797130/Effect-of-Thymalin-on-the-Tumor-and-Thymus-under-Conditions-of-Activation-Therapy-In-Vivo
9. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5995606/
10. https://pubmed.ncbi.nlm.nih.gov/8582782/
11. https://pubmed.ncbi.nlm.nih.gov/8067076/