Dr Ford Brewer - PrevMed

Verbucestat did not reduce cognitive or functional decline for Alzheimer's. This was the first big trial - and failure - of a BACE 1 Inhibitor. There was a lot of hope for decreases the production of Beta-Amyloid by decreasing the function of BACE - the Beta-Amyloid Precursor Enzyme.

On December 23, 2004, the New England Journal reported a breakthrough new colorectal cancer test: Fecal DNA. It was a breakthrough...somewhat.

It improved sensitivity by more than 400%. But that was only from 12.9% to 51% Unfortunately, sensitivity is still a major problem. Here's the problem; if the colorectal cancer is not bleeding or shedding DNA, you miss it with these home tests.

Colon Cancer is killing over 51,000 Americans each year. Over 30,000 of these deaths could be prevented. Why? Because over half of us are NOT getting proper colon cancer screening.

The major reason is the reticence to get the definitive screening test: colonoscopy.

This is the 3rd video in a series on Metformin and dementia. I review the details of several articles describing original research. The details of the science would indicate that metformin is probably neuroprotective.

Any study showing metformin as a risk for neurodegeneration would have to go into detail about how it avoided the obvious potential confounding of diabetes, the major known cause of dementia.

Scientific American recently covered the association of Metformin and dementia. The essence of the story was to show that Metformin is protective of dementia. The article then covers the ADA New Orleans presentation by Dr. Qian Shi of Tulane.

In studying over 6,000 US Vets with diabetes. Her research team demonstrated a significantly decreased risk for dementia for those on metformin. In fact, adjustment for age, level of disease, and other diabetes drugs - such as insulin - held true for metformin being protective.

This article covered lab animal research by Jing Wang and Freda Miller of the Toronto Hospital for Sick Children. They demonstrated increased spatial cognition by lab mice. Steven Arnold, a neurologist at Mass General (Harvard) demonstrated improved cognitive performance - and imaging evidence - in the brains of human mild cognitive impairment - when taking metformin.

Why isn't Dr. Arnold doing a larger, more definitive study of this issue? Metformin is very inexpensive. Because there is extremely little Pharma money to be made on Metformin, there is little funding available.

This is reminiscent of the TAME study (TArgetting Aging with Metformin) study. There is significant evidence that Metformin slows the general aging process. Yet funding for a study of this concept has suffered.

Wei Qi Wei, a researcher at Vanderbilt, recently used GWAS and PWAS studies to demonstrate residual risk for heart attack due to Lp(a). GWAS stands for Genome-Wide Association Studies. And PWAS stands for Phenome Wide Association Studies.

Vanderbilt has a significant advantage in these research techniques due to EMERGE, their coordinated Electronic Medical Record and Genetics research system.

A patient of mine asked about getting a Hydration Angle test. Dr. Mercola has interviewed Dr. Bush several times. There are several good points to the scientific story, like mitochondrial health and aging, cv inflammation and aging, and even the leaky gut story. Since so few have heard the leaky gut/haptoglobin/zonulin story, I review it. It has been well researched by a professor at Harvard, Allesio Fasano, who runs the pediatric GI and Zonulin research programs.

But there are some gaps I'm seeing in Dr. Zach Bush's story. They have to do with:

the connection between skin impedance and aging,

the connection between skin impedance and mitochondrial health;

the connection between gut tight junctions and distal mitochondrial function; and

the connection between Bush's product (RESTORE), (made from the earth) and mitochondrial function.

I look forward to being proven wrong; I'd love to stay young, even if it requires eating this dirt-based product.

Tumor growth rate or evolution of cancer is critical to the CRC screening process. It usually takes years for the development of an adenomatous polyp. And then from a polyp to an adenocarcinoma. That's important because it allows us time to continue screening over and over. If you do use the home screening methods, it takes years - and multiple samples to reliably pick up these samples. That's because these polyps are friable (meaning parts break off and bleed). But they don't bleed with every touch by feces. So, again, multiple samples are usually required - even if you're using DNA.

What's the difference between FIT and FOBT ( fecal immunochemical testing vs fecal occult blood testing)? FOBT is looking at the heme molecule. It's a chemical test. There are a lot of cross-reactions that cause false positives. These range from red meats to even some plant components. The FIT test is an immunochemical test is an antibody test to human globin, the protein seat of the heme molecule. This makes a much better test and deals with false positives. Even upper gi bleeding doesn't cause a false positive. That's because upper gi blood is digested by the stomach and small intestine.

Tumor growth rate or evolution of cancer is critical to the CRC screening process. It usually takes years for the development of an adenomatous polyp. And then from a polyp to an adenocarcinoma. That's important because it allows us time to continue screening over and over. If you do use the home screening methods, it takes years - and multiple samples to reliably pick up these samples. That's because these polyps are friable (meaning parts break off and bleed). But they don't bleed with every touch by feces. So, again, multiple samples are usually required - even if you're using DNA.

What's the difference between FIT and FOBT ( fecal immunochemical testing vs fecal occult blood testing)? FOBT is looking at the heme molecule. It's a chemical test. There are a lot of cross-reactions that cause false positives. These range from red meats to even some plant components. The FIT test is an immunochemical test is an antibody test to human globin, the protein seat of the heme molecule. This makes a much better test and deals with false positives. Even upper gi bleeding doesn't cause a false positive. That's because upper gi blood is digested by the stomach and small intestine.

SENSITIVITY and SPECIFICITY can be confusing. But they are important parameters of biomedical testing. In Colorectal Cancer (CRC), it's critical. More than 30,000 people die in the US each year due to failure to screen for CRC. Why?

The definitive screen is colonoscopy. It requires putting the patient to sleep, using an operating room, and days of bowel preparation requiring drinking gallons of fluid.

So many home tests have been developed, ranging from FOBT (fecal occult blood testing), FIMT ( fecal immunochemical blood testing), and fecal DNA testing. The FOBT and FIMT tests are inexpensive and practical. But they are not sensitive.

Test sensitivity equals the number of true positive tests over the total with the disease. ( Total with disease includes TRUE POSITIVES plus FALSE NEGATIVES).

The reason is simple; colorectal cancers do not always bleed. If they are not bleeding, the FOBT will be a false negative. FIMT is often a false negative as well.

TMAO (TriMethyl Amine Oxide) is a recognized risk factor for heart attack and stroke. Most functional medicine and plant-based diet fans are aware of this. But we usually don't screen for, at least at first.

Choline, which is found in animal products, is broken down by the gut microbiome to TMA ( TriMethyl Amine). As the TMA passes through the liver, it is oxidized to TMAO.

Elevated TMAO has been shown multiple times to be associated with increased all-cause mortality, and has been associated with CV inflammation and plaque.

The above link is to an article published in Nature Magazines Scientific Reports 7, Article number: 13781 (2017). It is a follow-up on serum and data collected in Groningen, Netherlands using the PREVENT study.

The study supported a significant increase in all-cause mortality with increased TMAO. But this association was seen only in patients with kidney disease, not with those without kidney disease.

So it raises again the question of causality. Is it the TMAO, or kidney disease, or (more likely) an intertwined mechanism? And the fact that kidney disease is most often associated with diabetes raises again the comorbidities question.