Create a biochemical savings account for your body. Just like every disease is linked to a negative, biochemical deficiency prodrome, your vital operating systems are linked to a positive, biochemical reserve prodrome. Strategic biochemical reserves can be created with plasmalogen supplementation to help the body maintain vitality, resist the entropy of aging, and achieve longevity. Prodrome plasmalogen supplements contain 100-900x more plasmalogen than other plasmalogen supplement brands available!
Click Here to order Plasmalogen Supplements or keep reading to learn more about the science behind the supplements and why we're so passionate to share with you this exciting research into prodomes and plasmalogens!
“Even if you do have a high genetic risk for Alzheimer’s, our research suggests this may be reduced by increasing your levels of important lipids called plasmalogens... Someday soon we could be getting our plasmalogen levels checked, just like a regular cholesterol check.” Professor Peter Meikle, senior author of a new Australian study in Alzheimer's & Dementia: The Journal of the Alzheimer's Association. To read more Click Here
Prodromes and Plasmologens
In this video Dr. Dayan Goodenowe explains his clinical background, the incredible technology he created to study the development of disease, the positive and negative prodromes of disease and vitality he discovered, and how plasmalogens can be used to manipulate these prodromes in order to protect against disease and promote longevity.
How to Elevate Blood Plasmalogen Levels
Death, Disease, Vitality, and Immortality
Dr. Dayan Goodenowe is pioneering a new field of optimal health and longevity based on deep science and technology. This new field is the concept of biochemical reserve and moves beyond the focus of disease and prevention and towards true health and vitality. He is a neuroscientist and inventor. His research has made him an expert on the biochemical basis of disease.
What Is A Prodrome?
Prodromes are states of biochemical imbalance that occur before disease symptoms appear. Prodrome Sciences develops blood tests to detect prodromes of diseases and therapeutics to restore unhealthy biochemical imbalances to a healthy state. The goal is to reduce the number of people that develop and die from disease and to promote optimal health and longevity.
Biochemical Mechanisms of Plasmalogens
Plasmalogens are unique lipid molecules that are a critical part of nerve, heart, lung, eye, and kidney cells. They are necessary for optimal neurotransmitter performance. Plasmalogen levels decrease with disease and age as the body is no longer able to make enough to keep up with demand and the body depletes plasmalogens as an antioxidant and anti-inflammatory molecule as well as a building block to repair cells and to build other molecules. Plasmalogens are concentrated in the brain, heart, lungs, eyes, and kidneys.
It is not possible to get enough plasmalogens through the diet as they are degraded in the gut.
The Science Linking Low Plasmalogens with Disease
The Scientific Evidence Linking Low Brain Plasmalogen Levels to Alzheimer's and Dementia
Scientific Evidence Linking Low Plasmalogens with Aging, Dementia, and Mortality
The Scientific Evidence Linking Plasmalogen Supplementation to Neuroprotection
Detailed Webinar - Plasmalogens and the Biochemical Basis of Dementia
Dr. Dayan Goodenowe, Founder and CEO of Prodrome Sciences, presents detailed scientific information about dementia and the genetic risk factor ApoE as well as another risk factor - plasmalogen deficiency.
Click Here for even more videos!
Lipids unlock opportunity for dietary supplement to reduce risk of Alzheimer’s disease
Published in Alzheimer's & Dementia: The Journal of the Alzheimer's Association, a new study shows that changing your metabolism could reduce your genetic risk of Alzheimer’s disease. The study’s senior author, Head of the Baker Institute’s Metabolomics Lab, Professor Peter Meikle, said the findings combined what we know about genetics – the predisposition to certain diseases like Alzheimer’s that we have from birth – with the growing understanding of how our metabolism plays a role in driving disease.
“While you cannot change your genetics, you can change your metabolism through your diet. So even if you do have a high genetic risk for Alzheimer’s, our research suggests this may be reduced by increasing your levels of important lipids called plasmalogens.” Professor Meikle said.
The most common gene associated with late-onset Alzheimer's disease is called apolipoprotein E (APOE), and it has three common forms: e2, e3 and e4.
Most Australians are born with only the e3 form, which carries a neutral risk of developing Alzheimer’s. But people with an e2 form (about 15 per cent of the population) have a lower risk and those born with e4 (about 25 per cent) have a higher risk. In analysing more than 6000 human samples from Australian and US longitudinal studies, Professor Meikle’s team identified that higher levels of plasmalogens, or related lipids, were responsible for up to 30 per cent of the e2 protective effect.
“We don’t fully understand what dictates an individual’s natural plasmalogen levels, but we want to bring everyone up to that higher level, and we think that can be done through dietary supplementation,” Professor Meikle said. “Given the global scale of Alzheimer’s disease, we see a simple lipid supplement as something that could potentially help millions.”
It’s hoped that this type of oral supplementation may also help with the prevention of other common metabolic diseases such as fatty liver disease and heart attacks, where Professor Meikle’s team has also determined plasmalogens play a protective role. “Someday soon we could be getting our plasmalogen levels checked, just like a regular cholesterol check,” Professor Meikle said.
ProdromeNeuro™ Improves Oxidative Stress Biomarkers in Cognitively Impaired Persons
Supplementation with ProdromeNeuro was observed to elevate blood DHA-plasmalogen levels. ProdromeNeuro is a plasmalogen supplement designed to specifically elevate DHA plasmalogen levels. An escalating dose study was performed in persons diagnosed with various degrees of cognitive impairment to determine the optimal dose for elevating blood plasmalogen levels.
In addition to clinical evaluations of cognition and mobility, blood samples were collected at baseline and after each month of supplement dosing for biomarker analyses.
Blood DHA-Plasmalogen levels were observed to be increased in all participants in a dose-dependent manner. After month 1 there was a 30% increase, after months 2 and 3 there was a 60% increase and after month 4 there was a 90% increase in the target DHA-plasmalogen levels. Persons with low baseline DHA-plasmalogen levels (quartiles 1 and 2) experienced a greater increase in blood DHA-plasmalogen levels (50%, 90%, and 120%, respectively).
The results of the oxidative stress biomarker analyses indicate that increasing blood DHA-plasmalogen levels using ProdromeNeuro has a profound positive effect on oxidative stress biomarkers.
For more details of the study and to see Dr. Goodenowe explain the trial design and biomarker analyses in detail Click Here
ProdromeNeuro™ Improves Cognition and Mobility in Cognitively Impaired Persons
Participants were clinically evaluated for cognition and mobility at baseline and after each month of supplement dosing. Cognitive status was evaluated using the Quick Dementia Rating System (QDRS), which was used to derive the participant’s Clinical Dementia Rating (CDR) score. Mobility was evaluated using the 30 second sit-stand test. Blood samples were collected for plasmalogen analyses at each clinical visit.
Three of the four participants with moderate dementia exhibited significant improvements in mobility (4 or 5 additional sit-stands) and one had a decline of 2 sit-stands. Of the participants with mild dementia, two exhibited improvement, one no change, and one declined. Of the 13 participants (one participant was unable to perform the test) with questionable or very mild dementia (CDR 0.5), 7 exhibited significant improvement, 4 were stable, and two declined. Using a random prediction model based upon the observed decline rate, the observed improvement was statistically significant (p=2.9e-05).
For more details of the study and to see Dr. Goodenowe explain the trial design and biomarker analyses in detail Click Here
Deficiency of Specific Phospholipid May Lead To Alzheimer’s
Alzheimer’s is characterized by neuropathologies such as β-amyloid plaques and neurofibrillary tangles. However, pharmacological therapies designed to lower β-amyloid plaques have not yielded any clinical benefits. This suggests there are events happening “upstream” of β-amyloid plaque formation that represent the early preclinical stages of neurodegenerative diseases like Alzheimer’s (AD). Scientists are beginning to recognize that this upstream event may be abnormal lipid metabolism. In fact, changes in lipid metabolism precede the abnormalities and clinical symptomology associated with AD. Specifically, a special type of phospholipid may be the missing link between biochemical and functional abnormalities occurring in AD and hallmarks such as β-amyloid deposition. A recent study found that a key plasmalogen (EPA-pPE) exerted neuroprotection at least partly through inhibiting neuronal apoptosis and enhancing the BDNF/TrkB/CREB pathway, "which suggests that EPA-enriched plasmalogen can be explored as a potential therapeutic agent in long-term Alzheimer's disease therapy" (Che, H., et al. 2020).
Deficiency of this specific type of phospholipid (plasmalogen):
- Impairs brain function
- Leads to increased deposition of β-amyloid plaques
- Mediates the effects of APOE on AD and dementia. The APOE ε4 allele is the second strongest risk factor after aging for AD.
In fact, levels of this phospholipid decline years before clinical symptoms of Alzheimer’s develop. To discover more about a blood test that determines levels of this critical phospholipid and the most effective way to replenish it, click here.
To discover more about this intriguing phospholipid, click here to read the full article published in Alzheimer’s & Dementia: Translational Research & Clinical Interventions.
A New Test To Detect Biochemical Risk Factors for Multiple Sclerosis and Autism
Multiple sclerosis (MS) and autism are caused by an underlying, pre-existing mitochondrial insufficiency – specifically in neuronal support cells, the glia. When a naturally occurring inflammation event occurs, the body responds by activating microglia. These microglia target damaged cells by exporting glutamate, which in high concentrations is a mitochondrial toxin. Weak or damaged cells will succumb and die. Healthy surrounding cells survive. However in MS and autism, the surrounding healthy cells are not as healthy as they should be (due to weak mitochondria). This results in the area of inflammation spreading. Some of the healthy cells actually become damaged, which further elicits an inflammatory response. This is the reason inflammation persists – in some cases indefinitely.
In events leading up to MS and autism, mitochondrial insufficiency results in three main consequences:
- Mitochondrial leakage. The purpose of the mitochondria is to burn a little hydrocarbon molecule called acetyl-CoA into carbon dioxide and water, just like your car engine. The energy released from one acetyl-CoA molecule is used to create 36 ATP energy molecules! When mitochondria are weak or stressed, they cannot process this fuel and so it leaks out and is then used by other biochemical processes (it has to go somewhere…)
- Reduced mitochondrial fatty acid oxidation. Mitochondria chop up fat to create their acetyl-CoA fuel. When they are stressed, they stop doing this or do less of it.
- Imbalanced peroxisomal metabolism. Peroxisomes are the mitochondria’s best friends. Always there in times of need. They pick up the slack when the mitochondrial are sick. However, when they are helping the mitochondria, their own work gets neglected.
The end result is that an excess of pro-inflammatory very long chain fatty acids (VLCFA) get made as a result of the acetyl-CoA leakage and the peroxisomes, which normally metabolize VLCFA, are busy metabolizing mitochondrial fatty acids, so these VLCFA metabolites increase. Also, since the peroxisomes are working overtime, they make more plasmalogens than normal and generate more reactive oxygen species (ROS) than normal. This is how mitochondrial insufficiency results in prolonged inflammation.A Ground-Breaking Blood Test Measures Biomarkers
Detecting the inflammation and mitochondrial stress that damages glial cells can be done through the ProdromeScan Blood Test from Prodrome Sciences that measures serum metabolic biomarkers that become imbalanced long before the development of MS or autism. Testing of the blood supply can measure the overall system – not just the local glial system being damaged. This type of test reveals:
- The biochemical imbalances that occur in persons before they get MS or autism
- Inflammation in the central nervous system
- Mitochondrial stress
- Plasmalogen imbalances.
The Solution for a Healthy Inflammatory Response in the Brain
Once the rate of inflammation and mitochondrial stress is determined through testing, you can support a healthy inflammatory response and mitochondrial health in your patients by delivering and keeping in reserve excess glial plasmalogen building material. The local need for plasmalogens is much greater than the minor increase caused by the mitochondrial insufficiency. This ensures that the surrounding glial cells can rebuild the white matter in the healthy cells as fast as the inflammation damages it. This results in a dramatic increase in glial cell recovery rate, which in turn results in a healthy inflammatory response and the inhibition of inflammation-mediated white matter loss. Want to know more about the Prodrome Scan blood test, which detects metabolic imbalances that may occur in people before they develop autism and MS? Click here.
To read more about the research on this type of testing in this BMC Neurology article, click here.
A Novel Way To Detect Elevated Colon Cancer Risk
Colorectal cancer (CRC) doesn’t just happen. Approximately 80% of all CRC cases occur in persons without genetic or family history risk factors. New evidence is emerging that acquired biochemical dysfunctions are the leading risk factors for CRC. Before someone can get CRC, they first must contract an unhealthy biochemical environment inside their body.
A group of potent anti-inflammatory and anti-cancer metabolites produced by a healthy gut microbiome has recently been observed to be deficient in persons with CRC. These molecules are called Gastrointestinal Tract Acids (GTAs). In fact, approximately 90% of all CRC cases occur in persons with GTA levels below the 10th percentile. Levels of this fatty acid metabolite also decline during aging, suggesting that age-related declines in GTAs may explain the increased incidence of CRC in older patients. GTAs are also low in persons with Inflammatory Bowel Disease. Testing for GTA levels can help to create a more accurate clinical picture of your patients’ risk of developing colorectal cancer.
Prodrome Sciences offers a ground-breaking blood test that is a clinically relevant means to determine GTA levels along with 80 other markers. Our ProdromeScan will report deficiencies in GTAs so that you can support your colon health with effective supplementation shown to raise GTA levels.
To read more about GTAs and how it can predict CRC risk click here to read a study published in the International Journal of Cancer.
A Revolutionary Method To Detect and Fix the Underlying Cause of Pancreatic Cancer
Pancreatic cancer, like all disease, does not just appear out of nowhere. There is a reason why a person gets pancreatic cancer. The detection of pancreatic cancer is challenging and usually only occurs after the existence of symptoms serious enough to justify imaging techniques such as endoscopic ultrasonography (EUS) or helical CT scan. Because pancreatic cancer is rare and these imaging methods are invasive, many patients are not screened for the disease. Consequently, more than 80% of pancreatic cancer cases are detected at an advanced stage, at which point the five-year survival rate is less than 3%. However, >90% of all persons who get pancreatic cancer have specific underlying biochemical deficiencies.
Now, there is a non-invasive screening test from Prodrome Sciences that measures these biochemical systems so that only high risk persons need to undergo invasive screening and more importantly, they can proactively correct their biochemistry and reduce their risk of pancreatic cancer. Click here to discover more about our ProdromeScan™ blood test.
To discover more about the science behind this test, click here to read the article in BMC Cancer.
An Alzheimer’s Risk Factor More Important Than Apolipoprotein E
Apolipoprotein E (APOE) is the primary lipoprotein in the brain and is considered the most important genetic risk factor for Alzheimer’s disease (AD). There are three common APOE genetic variants (APOE-2, 3, and 4). Up to 70% of people over the age of 60 with APOE-4,4 have AD. This is compared to only 3% of people with the APOE-2,3 genotype. A recent study has found that in order for APOE-4,4 to lead to the onset of AD, there must be a deficiency in a special type of phopholipid. In fact, the net effect of APOE genotype on cognition and the prevalence of dementia depends upon the person’s level of this type of phospholipid. Lower levels lead to increased susceptibility to the cognitive-impairing effects of APOE-4,4. Conversely, augmenting levels of this specific phospholipid may dramatically reduce the risk of AD to at least that of the APOE-2,3 genotype. This would result in a reduction of AD cases by 75% or more.
What is this powerful cognitive-supporting phospholipid? Click here to the read the full study in Brain Sciences.
Or to discover more about a ground-breaking test that detects levels of this critical brain health phospholipid click here.
Plasmalogen Supplement Publications
- Plasmalogen deficiency and neuropathology in Alzheimer’s disease: Causation or coincidence? Alzheimer’s & Dementia TRCI 5: Doi 10.1016/j.trci.2019.08.003
- Relation of Serum Plasmalogens and APOE Genotype to Cognition and Dementia in Older Persons in a Cross-Sectional Study. Brain Sci 9: Doi 10.3390/brainsci9040092
- Plasmalogen Augmentation Reverses Striatal Dopamine Loss in MPTP Mice. PLoS One. 2016 Mar 9;11(3):e0151020. doi: 10.1371/journal.pone.0151020.
- Metabolic dysfunctions in multiple sclerosis: implications as to causation, early detection, and treatment, a case control study. BMC neurology, 15, 154. doi:10.1186/s12883-015-0411-4
- Plasmalogen precursor analog treatment reduces levodopa-induced dyskinesias in parkinsonian monkeys. Behav Brain Res. 2015 Jun 1;286:328-37. doi: 10.1016/j.bbr.2015.03.012.
- Oral bioavailability of the ether lipid plasmalogen precursor, PPI-1011, in the rabbit: a new therapeutic strategy for Alzheimer’s disease. Lipids in health and disease, 10, 227. doi:10.1186/1476-511X-10-227