Plasmalogen Supplements

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.

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:

1. 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…)
2. 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.
3. 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.

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.