Unraveling oxytocin – is it nature’s medicine?

This 2020 review attempted to consolidate thousands of research papers on oxytocin:

“Chemical properties of oxytocin make this molecule difficult to work with and to measure. Effects of oxytocin are context-dependent, sexually dimorphic, and altered by experience. Its relationship to a related hormone, vasopressin, have created challenges for its use as a therapeutic drug.

Widely used medical interventions i.e.:

  • Exogenous oxytocin, such as Pitocin given to facilitate labor;
  • Opioid medications that block the oxytocin system; or
  • Cesarean sections that alter exposure to endogenous oxytocin:

have lasting consequences for the offspring and/or mother.

Such exposures hold the potential to have epigenetic effects on the oxytocin systems, including changes in DNA methylation. These changes in turn would have lasting effects on the expression of receptors for oxytocin, leaving individuals differentially able to respond to oxytocin and also possibly to the effects of vasopressin.

Regions with especially high levels of OXTR [oxytocin receptor gene] are:

  • Various parts of the amygdala;
  • Bed nucleus of the stria terminalis;
  • Nucleus accumbens;
  • Brainstem source nuclei for the autonomic nervous system;
  • Systems that regulate the HPA axis; as well as
  • Brainstem tissues involved in pain and social attention.

Oxytocin protects neural cells against hypoxic-ischemic conditions by:

  • Preserving mitochondrial function;
  • Reducing oxidative stress; and
  • Decreasing a chromatin protein that is released during inflammation;

which can activate microglia through the receptor for advanced glycation end products (RAGE). RAGE acts as an oxytocin-binding protein facilitating the transport of oxytocin across the blood-brain barrier and through other tissues.

Directionality of this transport is 5–10 times higher from the blood to the brain, in comparison with brain to blood transport. Individual differences in RAGE could help to predict cellular access to oxytocin and might also facilitate access to oxytocin under conditions of stress or illness.

Oxytocin and vasopressin and their receptors are genetically variable, epigenetically regulated, and sensitive to stressors and diet across the lifespan. As one example, salt releases vasopressin and also oxytocin.

Nicotine is a potent regulator of vasopressin. Smoking, including prenatal exposure of a fetus, holds the potential to adjust this system with effects that likely differ between males and females and that may be transgenerational.

Relative concentrations of endogenous oxytocin and vasopressin in plasma were associated with:

These studies support the usefulness of measurements of both oxytocin and vasopressin but leave many empirical questions unresolved.

The vast majority of oxytocin in biosamples evades detection using conventional approaches to measurement.”

https://pharmrev.aspetjournals.org/content/pharmrev/72/4/829.full.pdf “Is Oxytocin Nature’s Medicine?”


I appreciate attempts to ferret out worthwhile research from countless poorly performed studies, research that wasted resources, and research that actually detracted from science.

Although these reviewers didn’t provide concrete answers to many questions, they did point the way toward promising research areas, such as:

  • Improved approaches to oxytocin measurements;
  • Prenatal epigenetic experience associations with oxytocin and OXTR; and
  • Possible transgenerational transmission of these prenatal epigenetic experiences.

No honorable intentions

Catching up with Martin Armstrong:

“What’s going on here? It seems to be more that government is realizing that they’re in trouble.

Everybody has deficits year after year after year. The social programs are failing. They have no intention of ever paying anything back!

This idea that they’ve going to change the economy…this is an academic utopia. This is never going to work. This is not the way things work.

When you lose your job, your future, your future is very much in flux. The Great Reset is just not going to happen.

Our model is not talking about what people talk about on Facebook, Twitter, whatever. Our models focus on what creates that to begin with. The U.S. Army, etc., are focusing on that [FB etc.] to predict what people are going to start throwing bricks at. Our model focuses on the origin, not the end game.”

https://www.armstrongeconomics.com/world-news/civil-unrest/how-socrates-predicts-civil-unrest/



“Lifting the restrictions means they have a very serious problem.

The majority are just sheep. They wear their masks and surrender all rights today and those of their children into the future. They are incapable of waking up and think the government really cares. They will be the ones with a devastating blow that will come all at once.”

https://www.armstrongeconomics.com/armstrongeconomics101/economics/world-has-gone-mad/


Take responsibility for your one precious life – DHEA

This 2020 meta-analysis subject was DHEA:

“Twenty-four qualified trials were included in this meta-analysis. Statistically significant increases in serum IGF-1 levels were found only in participants who were:

  1. Women; or
  2. Supplementing 50 mg/d; or
  3. Undergoing intervention for > 12 weeks; or
  4. Without an underlying comorbidity; or
  5. Over the age of 60 years.

DHEA supplementation led to an overall increase of ~16 ng/ml in serum IGF-1 levels, as well as increases of ~23 [women] and ~20 ng/ml [age > 60]. Diseased and healthy subjects ages ranged from 20 to 72 years old.”

Discussion section explanations of the above:

  1. “Women are more susceptible to biochemical and clinical shifts caused by DHEA supplementation.
  2. The majority of investigations tested DHEA at a dose of 50 mg/d.
  3. The majority of studies were performed for > 12 weeks.
  4. Participants with no comorbidities were also older in many studies.
  5. Older patients have a natural decline in the production of IGF-1 and DHEA.

Additional rigorous RCTs are warranted to better define whether and to what extent changes in IGF-1 levels caused by DHEA supplementation are relevant for health benefits.”

https://www.sciencedirect.com/science/article/abs/pii/S0531556520302977Impact of dehydroepianrosterone (DHEA) supplementation on serum levels of insulin-like growth factor 1 (IGF-1): A dose-response meta-analysis of randomized controlled trials” (not freely available)


More on IGF-1 from The influence of zinc supplementation on IGF-1 levels in humans: A systematic review and meta-analysis which was cited for “Previous studies have demonstrated that IGF-1 levels can be affected by several factors.”

“IGF-1 is a growth factor synthesized in the liver, and elicits a myriad of effects on health due to its participation in the GH-IGF-1 axis, where it:

  • Is involved in tissue homeostasis;
  • Has anti-apoptotic, mitogenic, anti-inflammatory, antioxidant and metabolic actions;
  • Contributes to skeletal muscle plasticity, maintenance of muscle strength and muscle mass;
  • Neural and cardiovascular protection;
  • Development of the skeleton;
  • Possesses insulin-like effects, and
  • Is a key factor in brain, eye and lung development during fetal development.

IGF-1 plays important roles in both growth and development, and its levels vary depending on age, with peaks generally observed in the postnatal period and at puberty. IGF-1 levels influence the release of GH [growth hormone] from the hypophysis [pituitary gland] via a negative feedback loop.

A rapid decrease in IGF-1 levels is registered during the third decade of life. Levels gradually decrease between the third and the eighth decade of life.”


The Group 3 “> 12 weeks” finding was reinforced by perspectives such as:

Group 4 “with no comorbidities” was narrowly defined. All of us have degrees of diseases in progress. Consider aging effects:

  • Aging as a normal disease “Aging and its diseases are inseparable, as these diseases are manifestations of aging. Instead of healthy aging, we could use the terms pre-disease aging or decelerated aging.”
  • Aging as an unintended consequence “Epigenetic ageing begins from very early moments after the embryonic stem cell stage and continues uninterrupted through the entire lifespan. Ageing is an unintended consequence of processes that are necessary for development of the organism and tissue homeostasis thereafter.”
  • Organismal aging and cellular senescence “If we assume that aging already starts before birth, it can be considered simply a developmental stage, required to complete the evolutionary program associated with species-intrinsic biological functions such as reproduction, survival, and selection.”
  • An environmental signaling paradigm of aging “The age-phenotype of a cell or organ depends on its environment and not its history. Organisms, organs, and their cells can be reset to different age-phenotypes depending on their environment.”

These perspectives are less important than what each of us choose to do about our own problems. Take responsibility for your one precious life.

Get serious about advanced glycation end products (AGEs)

Ever heard about AGEs? Here are three papers that describe how AGEs affect humans.

First is a 2020 Italian review Common Protective Strategies in Neurodegenerative Disease: Focusing on Risk Factors to Target the Cellular Redox System:

“Neurodegenerative disease is an umbrella term for different conditions which primarily affect the neurons in the human brain. Currently, neurodegenerative diseases are incurable, and the treatments available only control the symptoms or delay the progression of the disease.

Neurotoxicity can be induced by glycation reactions. Since glycation is a nonenzymatic process, proteins characterized by a slow turnover are those that more easily accumulate AGEs.

Methylglyoxal (MG) can occur as glycolysis by-product, but it is also present in foods (especially cooked and baked), beverages (mainly those fermented), and cigarette smoke, and it is considered the most potent precursor of AGE formation. More than 20 different AGEs have been identified in foods and in human tissues.

AGE accumulation, oxidative stress, and inflammation are related to AGE ability to bind specific receptors called RAGE. RAGE expression increases during aging, cancer, cardiovascular diseases, AD [Alzheimer’s], PD [Parkinson’s], and other neurodegenerative diseases.”


A 2015 study by some of the same authors Antiglycative activity of sulforaphane: a new avenue to counteract neurodegeneration? was cited for a treatment in addition to changing one’s diet to be AGE-less.

“When MG production is increased by high glucose or oxidative stress, glycated proteins accumulate in the brain and lead to glycative stress, playing a fundamental role in the establishment of different neurodegenerative disorders.

Our results indicated that SF [sulforaphane] counteracts ROS by two possible mechanisms of action: an increase of intracellular GSH [glutathione] levels and an enhancement of MG-detoxification through the up-regulation of the glyoxalase (GLO1) systems. GLO1 up-regulation is mediated by the transcription factor Nrf2. SF has been demonstrated to activate Nrf2.

Another mechanism by which SF exerts its neuroprotective activity against MG-induced glycative damage is the modulation of mitogen-activated protein kinase (MAPK) signaling pathways involved in apoptotic cell death. All MAPK signaling pathways are activated in AD.

Brain-derived neurotrophic factor (BDNF) is associated with neuronal survival through its interactions with the tyrosine receptor kinase B (TrkB) and p75 cellular receptors. BDNF expression levels are reduced in the brain of AD patients. SF pre-treatment, before MG addition, not only further increased BDNF levels, but also significantly induced TrkB protein levels reverting MG negative effect on this receptor.

SF totally reverts the reduction of glucose uptake caused by MG exposure. SF can be defined as a multitarget agent modulating different cellular functions leading to a pro-survival frame of particular importance in the prevention / counteraction of multifactorial neurodegenerative diseases.”


A 2020 review Non-enzymatic covalent modifications: a new link between metabolism and epigenetics investigated glycation:

“Non-enzymatic covalent modifications (NECMs) by chemically reactive metabolites have been reported to manipulate chromatin architecture and gene transcription. Unlike canonical post-translational modifications (PTMs), NECMs accumulate over time and are much more dependent on the cellular microenvironment.

A. Guanine residues in DNA and RNA can undergo methylglyoxal glycation, thereby inducing DNA and RNA damage. This DNA damage has few corresponding repair pathways.

B. Histones are primary glycation substrates because of their long half-lives and abundant lysine and arginine residues. Histone glycation was found to induce epigenetic dysregulation through three distinct mechanisms:

  1. Competition with essential enzymatic PTMs for sites (e.g., glycation adducts replace H3K4me3 and H3R8me2);
  2. Changing the charge states of histone tails and subsequently affecting the compaction state of the fiber; and
  3. Altering three-dimensional chromatin architecture by inducing both histone-histone and histone-DNA crosslinking.

Epigenetic impacts of histone glycation were shown to be dependent on sugar concentration and exposure time. Histone and DNA glycation may lead to long term epigenetic impacts on immune responses.

C. Glycation of multiple lysine residues of NRF2 inhibits its oncogenic function. Sugar molecules can influence epigenetic events through glycation of transcription factors and/or their associated regulatory proteins.”

The Transcription factor glycation section referenced a 2011 paper Regulation of the Keap1/Nrf2 system by chemopreventive sulforaphane: implications of posttranslational modifications:

“Nrf2 mRNA level is unaffected by treatment with sulforaphane, suggesting that cellular expression of Nrf2 protein is posttranscriptionally regulated. Posttranslational modifications of Keap1 and Nrf2 proteins seem to play an important role in the regulation of ARE‐dependent gene expression.”


Other curated AGEs papers include:

Part 3 of Do broccoli sprouts treat migraines?

This 2019 Swedish review subject was the role of inflammation in migraines:

“In this article, we argue that inflammation could have an important role in migraine chronification through a mechanism termed neurogenic neuroinflammation, a phenomenon whereby activation of trigeminal sensory pathways leads to an orchestrated inflammatory response involving immune cells, vascular cells and neurons.

No studies to date have directly linked hypothalamic neuroinflammation with migraine, and we therefore looked to other studies. Overactivity of the NF-κB–IKKβ signalling pathway has been shown to be a critical modulator of hypothalamic inflammation.

We do not believe that CNS inflammation is involved in the triggering of migraine attacks, as BBB alterations, glial cell activation and leukocyte infiltration have not been observed in individuals with this condition. Peripheral sensitization is an important factor in migraine chronification, as opposed to migraine triggering.”

https://www.nature.com/articles/s41582-019-0216-y “Does inflammation have a role in migraine?” (not freely available)

See Reevaluate findings in another paradigm for other views of hypothalamic inflammation.


I came across this review through its citation in the 2020 medical paper The fifth cranial nerve in headaches with the same lead author:

“Reduced serotonergic transmission seems to be involved in medication overuse headache development, possibly through a facilitation of the sensitization process via a maladaptive plasticity. In humans, common neurophysiological investigation of central sensitization shows an abnormal cortical response to repetitive sensory stimuli, with an increased response amplitude after low numbers of stimuli and a lacking habituation, suggesting an altered plasticity.

Neurons, under repetitive, persistent nociceptive, become sensitized and produce exaggerated and prolonged responses to lower threshold stimuli. Over time, a neuroplastic adaptation in medullary and cortical pain areas causes a shift in the pain modulatory system creating a new threshold and favouring a net pain facilitation rather than pain alleviation.

Targets are almost exclusively found in the nerves of trigeminal ganglion; the hub of the fifth cranial nerve. Although we believe that the headache-trigger most likely have the origin in the CNS, this review underscores the importance of trigeminal neurons in the perception of pain.”

This second paper listed various treatments of symptoms. Remarkable for no focus on treatments of causes.


Per Parts 1 and 2, I rarely get headaches anymore, much less migraines. 23 weeks of eating a clinically relevant amount of broccoli sprouts every day resolved causes for me. I didn’t appreciate how migraines and many other things changed until awakening during Week 9.

Broccoli sprout synergies

I was asked for examples of broccoli sprout synergies with supplements mentioned in Week 19 of Changing to a youthful phenotype with broccoli sprouts. I take them together an hour or two before meals to keep meal contents from lowering sulforaphane bioavailability. Sulforaphane peaks in plasma between 1 and 2 hours after ingestion.

sulforaphane peak plasma

I started splitting broccoli sprout doses after reading the first study of A pair of broccoli sprout studies. The second study was Untargeted metabolomic screen reveals changes in human plasma metabolite profiles following consumption of fresh broccoli sprouts.

Those subjects ate only “a single dose of fresh broccoli sprouts (providing 200 μmol SFN equivalents) at 8 AM on study day 1.” A 200 μmol amount of sulforaphane is a 35 mg weight.

For comparison, my daily consumption is a worst-case 52 mg sulforaphane from microwaving 131 g of 3-day-old broccoli sprouts per Estimating daily consumption of broccoli sprout compounds. Every day for 22 weeks now. 🙂

The second study’s measurements through 48 hours produced this informative graphic and text:

“Of the features we identified using metabolite databases and classified as endogenous, eleven were significantly altered.

  • Glutathione (GSH) – a major intracellular antioxidant that conjugates with SFN during metabolism – was significantly decreased in plasma at 6, 12 and 24 hours following sprout intake.
  • GSH precursors glutamine (3 and 24 hours) and cysteine (12 and 24 hours) also decreased.
  • We observed significant decreases in dehydroepiandrosterone (DHEA) at 3, 6 and 12 hours.
  • Decreases in fatty acids reported here suggest that even a single dose of broccoli sprouts may alter plasma lipids in healthy adult populations.

While this study focuses largely on potential effects of SFN, broccoli sprouts contain many other bioactive components (e.g., indoles) that could be responsible for our observations as well as additional health benefits.”

Supplements I take twice daily with broccoli sprouts:

  • 1 gram L-glutamine for replenishment and other purposes;
  • 25 mg DHEA to replenish and other effects;
  • 15 mg then 50 mg zinc, which has a role in GSH metabolism;
  • 500 mg glucosamine (anti-inflammatory, crosstalk with Nrf2 signaling pathway);
  • 500 mg acetyl-L-carnitine (induces Nrf2-dependent mitochondrial biogenesis); and
  • 1400 IU then 2000 IU Vitamin D. A major portion of its effects is Nrf2 activation, like sulforaphane. A virtuous circle develops when taken with broccoli sprouts in that the Vitamin D receptor is a Nrf2 target gene inducible by sulforaphane, which then upregulates Nrf2 expression levels.

One of the things eating Boring Chicken Vegetable Soup twice a day does is replenish cysteine. I eat that and steel-cut oats (another cysteine source) separately from broccoli sprouts.

I take 1 gram flax oil with breakfast and dinner instead of with broccoli sprouts. Haven’t found relevant research on whether broccoli sprout compounds decrease omega-3 polyunsaturated alpha linolenic acid C18:3 as they do these six endogenous fatty acids.


Both studies investigated effects of fresh broccoli sprouts. Timing of their measured decreases and increases are different for me because I microwave broccoli sprouts up to but not exceeding 60°C (140°F).

A section of Microwave broccoli seeds to create sulforaphane highlighted metabolic differences among fresh broccoli sprouts, microwaved broccoli sprouts, and broccoli sprout supplements.

“A metabolic profile resulting from my current practices is probably between the Sprout and BSE (broccoli sprout extract) divided-dose statistics:

  1. Sulforaphane intake is greater than eating raw broccoli sprouts because microwaving 3-day-old broccoli sprouts creates an increased amount of sulforaphane in them before eating.
  2. Sulforaphane uptake from microwaved broccoli sprouts is quicker than eating raw broccoli sprouts. It may not be as immediate as taking sulforaphane supplements, which are usually powders.
  3. Sulforaphane dose from microwaved broccoli sprouts is less dependent on an individual’s metabolism than eating raw broccoli sprouts.
  4. Sulforaphane release from microwaved broccoli sprouts continues on to the gut as does eating raw broccoli sprouts. Sulforaphane release from supplements typically ends in the stomach.”

One thing I didn’t mention in that blog post was that glucoraphanin also increased by microwaving per Microwave broccoli to increase sulforaphane levels. A coauthor clarified a chart’s 60°C (140°F) glucoraphanin amount increased by 27% (2.78 / 2.18 μmol).

Metabolism of broccoli sprout glucoraphanin and other glucosinolates that aren’t preferentially hydrolyzed by microwaving and thorough chewing is assisted in the gut twice a day by:

  • 6 billion IU acidophilus; and
  • 750 mg fructo-oligosaccharides.

Take responsibility for your one precious life – Trained immunity

This 2020 review subject was the normal progression of our immune systems:

“Age-related alterations in the immune system result in high susceptibility to infections, increased risk of hospitalization and mortality. Defects in adaptive immunity underlie the markedly low vaccine efficiency in the elderly. Despite reduced cellular functions, a systemic increase in inflammatory markers, so-called inflammaging, is observed in aged individuals.

Trained immunity is a newly emerging concept that showed that innate immune cells possess non-specific immunological memory established through epigenetic and metabolic reprogramming upon encountering certain pathogenic stimuli.

Novel approaches targeting innate immunity to improve host responses are crucial to evade the consequences of the aged immune system. It is an emerging concept that innate immune cells can manifest memory-like properties that are not antigen-specific and exhibit enhanced responsiveness upon later challenges with heterologous stimuli. Whether trained immune responses change as people age is yet to be explored.”

https://academic.oup.com/intimm/advance-article/doi/10.1093/intimm/dxaa052/5885077 “Overcoming immune dysfunction in the elderly: trained immunity as a novel approach”


Previous papers by this review’s corresponding coauthor were curated in:

There’s no reason to rely entirely on the review’s elaborate vaccination schemes to develop trained immunity. Take responsibility for your one precious life and Train your immune system every day!

Eat broccoli sprouts for your hair!

This 2017 review explored broccoli sprout compounds effects on head hair:

“Skin appendages, notably hair follicles (HFs), can be exposed to high levels of reactive oxygen species (ROS), which are generated through metabolic reactions occurring mostly in the mitochondria, peroxisomes and the endoplasmic reticulum as well as in the plasma membrane. Despite their involvement in redox stress and cellular damage, ROS also have key roles in physiological signalling processes, including but not limited to, control of stem cell quiescence / differentiation, regulation of innate and adaptive immune responses and importantly, normal HF development.

HFs are composed of a series of concentric keratinocyte layers with a central hair shaft, all of which are encapsulated by a mesenchymal connective tissue sheath. Within this structure is an area known as the ‘bulge’, housing a population of epithelial and melanocyte stem cells. The hair bulb, the lowermost portion of the HF, contains transient amplifying cells that produce the rapidly proliferating matrix keratinocytes that give rise to the various cell types of the inner root sheath and hair shaft itself.

Putative impact of NRF2 activation on protection against hair disorders:

  1. Accumulation of excess ROS within crucial HF compartments (i.e. bulb and bulge) can be induced by endogenous and exogenous stressors associated with androgenetic alopecia (AGA), alopecia areata (excessive mast cell degranulation), chemotherapy, UV exposure and even physiological processes such as melanogenesis.
  2. In the HFSCs [hair follicle stem cells] of the bulge, this can lead to reduced FOXP1 signaling, increased senescence and P21-mediated telogen retention, contributing the hair ageing.
  3. In the hair bulb, negative consequences of excessive ROS can include reduced matrix keratinocyte proliferation and Bcl-2 expression, coupled to increased p53 activity and apoptosis. This redox imbalance may also stimulate the dermal papilla-derived TGF-b1 release associated with AGA.
  4. NRF2 activation via SFN [sulforaphane] can induce the expression of numerous downstream targets, hence suggesting the potential to counteract excessive ROS and associated pathologies, for example via enhanced clearance of reactive species, detoxification, NADPH generation and GSH maintenance.
  5. In addition, NRF2 may down-regulate genes that would negatively impact on proliferation and stimulate apoptosis.
  6. Ultimately, the activation of NRF2 has the potential to protect against HF miniaturization, chemotherapy-induced apoptosis, HFSC aging and hair greying, through maintenance of normal redox homeostasis.

Whereas eumelanin (black) is involved in natural UV protection by reducing generation of free radicals, pheomelanin (red) can trigger generation of ROS. It would certainly be interesting to determine whether NRF2 activity is therefore higher in individuals with red as opposed to black hair, in order to mitigate any negative impact from higher ROS generation.

Modulation of NRF2 activity is an attractive approach for further study in the prevention of hair greying and HFSC ageing. The remarkable prospect for NRF2 activators in modulating other oxidative stress-linked disease states, strongly advocates for the development of NRF2 targeting as a novel strategy in modulating redox-associated disorders of the HF.”

https://onlinelibrary.wiley.com/doi/abs/10.1002/bies.201700029 “Oxidative stress management in the hair follicle: Could targeting NRF2 counter age‐related hair disorders and beyond?” (not freely available)


This review was cited in a 2020 Exploring the possibility of predicting human head hair greying from DNA using whole-exome and targeted NGS data:

“This study aimed to assess the potential of genetic data to predict hair greying in a population of nearly 1000 individuals from Poland. Most of the prediction information was brought by age alone. Genetic variants explained < 10% of hair greying variation and the impact of particular SNPs on prediction accuracy was found to be small.

Study population included 673 males (67.4%) and 325 (32.6%) females. The mean age of the participants was 30.5 ± 8.8.

Hair greying was recorded in 14.3% of individuals aged 18–30 and the prevalence of grey hair was noted to be significantly higher in young males when comparing to young females (17.8 and 9.2%, respectively). The incidence of grey hair increased to 29.5% in the group of people aged 18–40 years and was 84.2% when people aged ≥40 years were considered.

Because pleiotropy is so common, it would be impossible to predict natural phenotypes avoiding genes involved in determination of pathological phenotypes. The penetrance of individual SNP variants is usually low and they altogether can only explain a small fraction of the predisposition to the disease.

Prediction of hair greying status solely based on genetic information is currently impossible.”


A 2020 review had a pertinent evaluation scheme:

“Geroprotectors are pharmacological agents that decrease the rate of aging and extend lifespan. We proposed a set of primary and secondary selection criteria for potential geroprotectors. Primary criteria:

  1. The life extension in experiments with wild type animal models. The geroprotector should prolong the life of the model beyond the intact maximum lifespan, protecting it from one or more mechanisms of aging.
  2. Improvement of molecular, cellular, and physiological biomarkers to a younger state or slow down the progression of age-related changes in humans.
  3. Most potential geroprotectors are preventive only when applied at relatively high concentrations. The lifespan-extending dose should be several orders of magnitude less than the toxic dose.
  4. Minimal side effects at the therapeutic dosage at chronic application.
  5. The potential benefit of taking a geroprotector may come after a long period. Potential geroprotectors should initially improve some parameters of health-related quality of life: physical, mental, emotional, or social functioning of the person.”

https://www.mdpi.com/2076-3921/9/6/529/htm “Terpenoids as Potential Geroprotectors”


IMG_20200822_064852

Aging as a normal disease

This 2018 review explained:

“Aging is the sum of all age-related diseases. Aging and its diseases are inseparable, as these diseases are manifestations of aging.

An aged appearance (e.g., grey hair, wrinkles, cushingoid body types and loss of muscles) are manifestations of pre-diseases. For example, an aged appearance may reflect hypercortisolism, sarcopenia, osteoporosis, skin pre-diseases.

Instead of healthy aging, we could use the terms pre-disease aging or decelerated aging. Treatments are generally more effective at pre-disease stages, associated with hyper-function, than at disease stages, associated with functional decline.

The decision to treat or not to treat is often determined by whether it is possible to treat.

A treatment that slows aging increases both healthspan (subclinical period) and lifespan, whereas a treatment that increases lifespan (e.g., coronary bypass, defibrillation) is not necessarily increase healthspan. The goal of both anti-aging therapies and preventive medicine is to extend healthspan (by preventing diseases), thus extending total lifespan.

The fact that aging is an obligatory part of the life of all organisms is not important. Aging can be treated as a pre-disease to prevent its progression to diseases. Aging does not need to be defined as a disease to be treated.”

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6286826/ “Disease or not, aging is easily treatable”