New Research & Discoveries from 2024
As the end of the year approaches Dr. Dominique Fradin-Read thought it helpful to summarize new research discoveries that were published during the past year, and new testing or treatments that are now offered at VitaLifeMD.
Rapamycin
In February, a review of the literature summarizing the effect of Rapamycin on aging was published in the Lancet (Targeting aging with rapamycin and its derivatives in humans: a systematic review). A thorough search across five databases yielded 18,400 unique articles, resulting in 19 included studies, results showed that “Rapamycin and its derivatives improved physiological parameters associated with aging in the immune, cardiovascular, and integumentary systems (skin, hair and nails) of healthy individuals or individuals with aging-related diseases.” No serious adverse events were reported in these studies.
The physiological action of Rapamycin was previously described in our January 2024 blog. As a reminder, the molecule works at the mTOR gene complex that is responsible for the initiation of several disease processes as we age, it decreases inflammation, and it activates autophagy known as “the trash removal” of the body, lowering the toxic burden that could cause illnesses.
An article “Antiaging enthusiasts are taking a pill to extend their lives. Will it work?” was published in September on the first page of the New York Times increasing the general public interest in the product. The evidence is clear that Rapamycin increases lifespan in animal studies and promising data are coming out for its use on humans that will hopefully be confirmed in further trials.
New Indication for the Peptides GHK and GHK-CU
Since its discovery in 1973, the human peptide GHK-Cu (also known as copper peptide) established itself as a powerful protective and regenerative ingredient, which is currently widely used in skin and hair products.
Dr. Dominique Fradin-Read is always curious to look at other potential and not well-known benefits of peptides; while researching the physiological actions of GHK peptide, she found interesting results on the effect of this peptide at the gene level.
GHK can affect gene expression in a number of ways:
GHK increases the expression of 14 antioxidant genes resulting in a potent antioxidant effect
GHK expresses strong anti-inflammatory action by suppressing two prooxidant genes and modifying several genes involved in the inflammatory process.
GHK appears to support the remodeling and restructuring of connective tissue, modulating expression of numerous genes, including up-regulation of genes of the TGF-β pathway. It increases collagen, elastin, and glycosaminoglycan synthesis, as well as supports the function of dermal fibroblasts. GHK’s ability to improve tissue repair has been demonstrated for skin and hair in several studies.
GHK can restore the function of lung fibroblasts in COPD patients and can protect lung tissue from acute lung injury
GHK is a neuroprotector: it promotes nerve growth by activating the production of neurotrophic factors, which can help protect against oxidative damage. It has been shown to have anti-anxiety effects in animal experiments.
A major concern for any substance, that activates cell growth and tissue remodeling, is whether it can also increase or not the risk of cancer. What is very reassuring about the GHK peptide is that it possesses potent anti-cancer properties. Various studies confirmed the findings that GHK affected 84 genes associated with DNA repair and other processes, relevant to anti-cancer effects. It also stimulated apoptosis, the mechanism of programmed cell death that occurs when a cell's DNA and the cellular skeleton break down, leading to the cell's death. It's a normal process that helps the body get rid of damaged or unneeded cells and plays a role in preventing cancer.
GHK peptide (with or without CU) ability to reset gene expression patterns to a healthier state may be a useful preventative measure and treatment for various conditions associated with aging.
Pentadecapeptide Arginate versus BPC157
Pentadecapeptide arginate(PDA) is a peptide very similar to BPC157. The two peptides contain the same 15 amino acid sequence that has healing and protective benefits in the body.
PDA has an additional arginine amino acid attached, which enhances its stability and bioavailability when used therapeutically. Due to its increase in stability, PDA appears to be more effective than BPC 157 for its therapeutic benefits.
Its properties are the same as BPC157:
Tissue repair and wound healing: PDA increases blood flow to damaged tissues and accelerates the healing of different types of wounds- including tendon-to-bone healing, damaged ligaments, and bone fractures- which helps in faster recovery post-injury.
Anti-inflammatory action and pain reduction: PDA helps decrease pain in damaged areas by regulating local production of inflammatory cytokines, making it useful for those suffering from discomfort due to muscle sprains, tears, and damage
Muscle mass support: PDA enhances the effects of growth hormone on the muscles by increasing the expression of growth hormone receptors on the tissues. This is beneficial for muscle growth and overall sports performance.
Anti-aging properties and collagen synthesis: PDA increases collagen synthesis, which is important for skin health and overall tissue strength.
Cardiovascular protection: PDA has shown valuable therapeutic effects in recent studies for patients suffering from heart disease (heart attack and arrhythmia).
It is however important to note that, when taken orally, PDA will not have the same action on the digestive tract as the basic BPC 157. For this indication, oral BPC 157 will still need to be prescribed.
Pentadecapetide Arginate improves many physiological pathways involved in the aging process. It is a very safe peptide with an excellent safety profile and minor side effects making it a key component in anti-aging protocols.
Two New Blood Tests for Early Detection of Alzheimer Disease (AD)
Early diagnosis of AD is challenging. Yet early intervention and treatment are essential to slow down the progression of the disease. An estimated 6.7 million Americans aged 65 or older were living with AD in 2023. Patients who develop AD will initially present mild cognitive decline such as memory loss and attention deficit disorders.
What is important to remember is that, among patients with documented cognitive decline, about one-third will progress to a diagnosis of AD. Knowing that a person starting to suffer from memory issues and cognitive decline -even mild- is at risk of AD can help patients and their families to better prepare for future care needs and enable eligibility for new treatments. On the opposite knowing that the cause for cognitive decline is not AD can help identify other causes of brain dysfunction such as vascular dementia, autoimmune conditions, toxic exposure….
Unfortunately, until now the gold-standard method for the diagnosis of AD is post-mortem measurement of amyloid plaques in the brain of the deceased patient. The most well-established methods for diagnosis of AD in living individuals are cognitive assessments with positron emission tomography (PET) and the measurement of biomarker analysis of cerebrospinal fluid (CSF). These methods are complex, invasive and expensive and not adapted to primary care settings. In recent years blood-based biomarkers of AD have been an active area of research and are now available for clinical practice.
Two new blood tests are now offered to patients at VitaLifeMD.
Alzheimer's disease (AD) patients develop extracellular deposits of beta amyloid plaques and neurofibrillary tangles observed in the cortex and the limbic brain region. The major molecular components of beta amyloid plaques and neurofibrillary tangles are beta amyloid 1-42 and tau proteins, respectively.
Beta-Amyloid 42/40 Ratio (Aβ42/40).
Two kinds of beta amyloid products are produced naturally by the body: beta amyloid 1-42 and beta amyloid 1-40. We want a high ratio of 42/ 40 as this protects against the accumulation of the amyloid plaques in the brain.
A high Aβ42/40 ratio suggests a lower risk of having AD pathology compared to lower values and may prompt investigation of non-AD causes of cognitive decline or dementia.
A moderately high Aβ42/40 ratio suggests an intermediate risk of having AD pathology.
A low Aβ42/40 ratio suggests a higher risk of having AD pathology compared to higher values.
In both cases of moderately high and low ratios, follow-up testing (eg, PET, CSF biomarkers) is warranted to investigate AD pathology as the cause of cognitive decline or dementia.
Phosphorylated tau217 (p-tau217)
In addition to the amyloid plaques, Alzheimer's patients develop neurofibrillary tangles in the brain with an accumulation of a protein called phosphorylated tau (p-tau) protein.
Plasma p-tau217 has a particularly strong association with amyloid plaque pathology and increases early in AD progression. Plasma p-tau217 can differentiate AD from many other neurodegenerative diseases causing cognitive decline.
Normal plasma p-tau217 levels are inconsistent with cognitive decline and dementia caused by AD. Further investigation of other causes of cognitive symptoms may be considered.
Increased plasma p-tau217 levels are consistent with cognitive decline and dementia caused by AD. Follow-up biomarker assessment using PET or CSF analysis to confirm the presence of AD pathology will be recommended.
Note: Plasma p-tau217 levels can be increased in those with chronic kidney disease or a history of myocardial infarction or stroke and should be reevaluated in the patient-specific past history context.
These tests are recommended for any adult exhibiting signs of mild cognitive decline or dementia. While these tests bring a great tool in the early diagnosis of Alzheimer’s, the results of these assays should be considered in conjunction with the findings from medical and family history, nutritional deficiency biomarkers, neuroimaging, and physical, neurological, and neuropsychological examination.
Prolonged Chronic Intermittent Fasting (16 Hours) is Detrimental to Health
In March this year, a study of over 20,000 adults found that those who followed an 8-hour time-restricted eating schedule, a type of intermittent fasting, had a 91% higher risk of death from cardiovascular disease.
In addition, compared with a standard schedule of eating across 12-16 hours per day, limiting food intake to less than 8 hours per day was not associated with living longer.
Dr. Dominique Fradin-Read has always been opposed to the idea of prolonged intermittent fasting. Her reasoning is that it is completely anti-physiological, forcing the body to operate in a “metabolic stress mode” with the constant use of glycolysis for hours (repeatedly depleting the liver from its reserve of glycogen to provide energy to the body in between meals) and functioning under high cortisol production when the level of sugar drops. This causes ups and downs in metabolism and in the production of enzymes from the digestive tract which is the opposite of “homeostasis”. Homeostasis is the ability of an organism to maintain a stable internal environment, despite changes in its external environment. This process allows organisms to survive and function properly. When homeostasis is unsuccessful, it can lead to imbalance, disease, or death. For example, without regular circadian rhythms, the body's ability to maintain homeostasis is severely compromised. No wonder why people who practice intermittent fasting will end up developing heart disease (and maybe other illnesses?) as they get older!
Stay tuned as 2025 seems very promising in terms of research and new treatments for anti-aging and optimal health. The era of precision medicine has come: "an emerging approach for disease treatment and prevention that takes into account individual variability in genes, environment, and lifestyle for each person."
Our providers at VitaLifeMD have long avoided the one-fits-all approach of standard of care and offered personalized treatment to our patients. A brand-new study was published recently in collaboration between Yale University and the epigenetics company Tru Diagnostic. The researchers analyzed the impact on DNAm biological aging clocks of 51 longevity interventional trials - including lifestyle changes (Mediterranean diet, exercise, smoking cessation…) as well as the benefits of pharmacological medications (metformin, senolytic agents) and therapeutic modifications. This was the first large meta-analysis of aging interventions based on 110 biomarkers including biological age clocks and epigenetic biomarkers to identify which are most effective at slowing aging. The results were stunning, showing the benefits of targeted interventions to improve one’s health and increase longevity.
Dr. Dominique Fradin-Read has recommended the TruDiagnostic test for years and has found it to be a great tool to help identify her patients’ biological age and to determine the best program suited to improve their health.
The future will allow us to use new genetic information that can provide an even more accurate evaluation of one’s health risk and greater individualization of recommendation and treatment for prevention and longevity.
Dr. Dominique Fradin-Read and her team at VitaLifeMD wish you a wonderful holiday season and a healthy and happy 2025!