Brain Health

Alzheimers or Brain Diabetes

Alzheimer's or Brain Diabetes?

Ronald Grisanti D.C., D.A.B.C.O., D.A.C.B.N., M.S.

A growing body of research suggests there's a powerful connection between your diet and your risk of Alzheimer's disease via similar pathways that cause type 2 diabetes.

Back in 2005, a published medical paper introduced a new disease tentatively dubbed "type 3 diabetes".

The researchers learned that, in addition to the pancreas, your brain also produces insulin.

They discovered that without the insulin your brain cells will die.

A drop in insulin production in your brain may contribute to the degeneration of your brain cells, and studies have found that people with lower levels of insulin and insulin receptors in their brain often have Alzheimer's disease.

Studies since 2005 have continually documented that insulin has a much greater role in the brain than previously expected.

Insulin is directly responsible for neuron glucose-uptake, and the regulation of neurotransmitters like acetylcholine, which are crucial for memory and learning.

Scientists have come to understand that cognition is impaired when insulin levels are reduced.

The clinical research has made it quite clear that the same pathological process that leads to insulin resistance and type 2 diabetes may also hold true for your brain.

The take away from these studies make a strong point that the over-consumption of sugars and "grains" which are also detrimental to the the development of diabetes may also result in Type 3 Diabetes (brain diabetes).

When the brain becomes overwhelmed by the consistently high levels of glucose, the insulin signaling will eventually become blunted or desensitized. This will lead to impairments in your thinking and memory abilities, eventually causing permanent brain damage.

Healthcare clinicians trained in functional medicine have the training and knowledge to investigate what is at the root of the pathological process that leads to Type 2 diabetes and the new diagnosis of Type 3 diabetes.

The one size fits all approach of prescriptive medications for diabetes, although of some value, will not shut down the physiological cascade of the consequences of poor sugar/insulin control. 

Functional Medicine University

www.functionalmedicineuniversity.com

Link Between the Gut and Brain and Inflammation

The Gut-Brain Axis in Health and Disease

Robert G. Silverman, DC, DACBN, DCBCN, MS, CCN, CNS, CSCS, CIISN, CKTP, CES, HKC, SASTM

 

The brain is the most nutrient-dependent, energy-dependent and toxin- and stress-vulnerable organ in the body. The gut and the brain are very tightly linked. In the gut-brain axis, damage to one is often damage to the other.

 

 

Concussion is a good example. When a blow to the head or severe jolt causes a concussion, the damage to the neurons has a parallel in damage to the gut lining. The tight junctions of the lining almost immediately open up and become permeable. This produces inflammatory cytokines that can penetrate the blood-brain barrier, leading to additional brain inflammation. In other words, when the gut is on fire, so is the brain.

If the sudden intestinal permeability caused by a concussion goes untreated, the concussion symptoms will be worse, due to the additional inflammation. The gut permeability may not resolve by itself, which could contribute to making the concussion symptoms linger on for weeks instead of days. Intestinal permeability may also play a role in those patients who go on to develop post-concussion syndrome by causing ongoing brain inflammation.

So, in addition to treating the concussion itself with nutrition, the intestinal permeability, particularly the release of occludin and zonulin, needs to be immediately addressed.

The intercellular permeability of the gut lining can be treated through repair and regeneration with xanthohumol. A natural phenol derivative of hops, xanthohumol has a very extensive (more than 250 publications in preclinical science) record of efficacy and safety. In the brain, xanthohumol acts as an antioxidant and anti-inflammatory; it also helps with the biogenesis of mitochondria in damaged neurons. In the gut, the polyphenols are strongly anti-inflammatory. They modify the inflammatory kinases in favor of antioxidant pathways and, just as important, block the kinases in the cell-damaging inflammatory pathways for tumor necrosis factor, COX-2, and others.

On a chronic level, we know that neurodegenerative diseases such as Alzheimer's, depression, and anxiety may not be exclusively triggered within the brain. When the intestinal barrier is breached, so is the blood-brain barrier. Inflammation from circulating gut-derived lipopolysaccharides (LPS) pass through the blood-brain barrier and have been linked to a number of neurodegenerative disorders. In particular, LPS stimulates the production of IgA, IgG, and IgM antibodies that can cross-react with tissues and induce autoimmune disease and neurodegeneration. 

Treating brain inflammation caused by gut inflammation starts with removing the cause through a modified elimination food plan and the removal of pathogens. Anti-inflammatory supplements, such as berberine, and digestive enzymes, such as lipase and amylase, help restore the gut lining. The next step is to reinoculate and regenerate the gut with a powdered nutritional supplement if needed, continuation of the modified elimination diet, and the addition of probiotics, vitamin D, alpha-lipoic acid, and specialized pro-resolving mediators (SPMs). Xanthohumol is also very helpful for regenerating intestinal mucosa.

Once the process is underway, retesting is important to see the gains and make any necessary adjustments to the treatment plan. As healing progresses, retaining the gains with a better diet and appropriate supplements becomes the focus of treatment.

Healing the intestinal barrier is only half the equation. The brain inflammation needs to be treated as well. Low-level laser therapy (LLLT) is a valuable tool for improving neurological function. In concussion patients, it has been shown to help reduce inflammation, modulate oxidative stress and nitric oxide production, and down-regulate pro-inflammatory microglial cytokine expression.

LLLT is also valuable for reducing inflammation of the vagus nerve. The longest of the cranial nerves, the vagus is often called the great wanderer for the way is wanders through the visceral organs. A major function of the vagus nerve is preventing inflammation. In the gut, the vagus nerve endings sense the chemical signals of inflammation, such as cytokines and tumor necrosis factor, and send messages to the brain telling it to release anti-inflammatory neurotransmitters via the cholinergic anti-inflammatory pathway. When the brain-gut axis is disrupted, the vagus nerve is affected and the messages back and forth are garbled or don't get through at all. Decreased vagal nerve activity has some serious effects on the gut. Hydrochloric acid and pancreatic enzyme secretion is reduced, as is bile secretion. The parietal cells in the stomach, which are responsible for producing intrinsic factor, don't work as well, leading to reduced absorption of B vitamins. 

We know that post-injury vagal nerve stimulation (VNS) after a concussion can help prevent the breakdown of epithelial cells in the gut and keep the tight junctions from opening. This only works when administered within 90 minutes of the injury, however. Later on, stimulation of the vagus nerve with LLLT using 405 nm violet lightcan help to restore communications and reduce inflammation.

Treatment modalities such as those discussed here help repair the integrity of the gut lining and the blood-brain barrier. They're a hopeful new approach to restoring the functionality of the gut-brain axis and returning the body to harmony.  

Compliments of Functional Medicine University

www.functionalmedicineuniversity.com

 

Vitamin Deficiency Linked to Stroke and Plaque Buildup in Carotid Artery

Vitamin Deficiency Linked to Stroke and Plaque Buildup in Carotid Arteries

Ronald Grisanti D.C., D.A.B.C.O., D.A.C.B.N., MS

A study published in the the Canadian Medical Association Journal revealed that people low in vitamin B12 had an increase risk of a fatal heart attack and stroke.

The study focused on the relationship between homocysteine, B-12 and carotid artery plaque.

The study showed that higher blood levels of B vitamins are related to lower concentrations of homocysteine leading to decrease plaquing in the carotid arteries. However, an elevated blood homocysteine level revealed a strong risk factor for heart disease and stroke.

How the Study was Conducted
The study examined 421 people with the average age being 66. Vitamin B12, homocysteine levels and degree of plaque in the carotid arteries (via ultrasound) were evaluated.

The Results

Seventy-three patients (17%) had vitamin B12 deficiency with significant elevation of homocysteine. In addition and most important, carotid plaque was significantly larger among the group of patients who had deficiency of vitamin B12 In conclusion, the authors found that low blood vitamin B12 levels are a major cause of elevated homocysteine levels and increased carotid plaque area.

Dr. Grisanti's Comments
Have your physician order a blood homocysteine test and a methylmalonic acid (MMA) test. This is the most specific test for B12 status NOT the serum B-12 blood test.


Reference

Robertson J, Iemolo F, Stabler SP, Allen RH, Spence JD. Vitamin B12, homocysteine and carotid plaque in the era of folic acid fortification of enriched cereal grain products. CMAJ. 2005 Jun 7;172(12):1569-73.

compliments of Functional Medicine University

www.functionalmedicineuniversity.com

 

 

Medications That Contribute to Alzheimer's and Natural Ways to Improve Memory

Alzheimer's: Why is the Brain Deteriorating?

Ronald Grisanti D.C., D.A.B.C.O., D.A.C.B.N., M.S.

After considerable research it is interesting to bring you up to speed on documented evidence of things which answer the question. "Why is the human brain deteriorating faster than the rest of the body?”

There are a multitude of factors and today's article will touch on a few and also provide some solutions.

For starters I find it disturbing and somewhat criminal that a common blood pressure medication called calcium channel blockers has been proven radiologically on MRI to cause brain shrinking. Research has shown that these drugs cause deterioration of the I.Q. within 5 years' use.

Another medication used to lower cholesterol called Lipitor causes a decline in brain function. It is important to know that statin cholesterol-lowering drugs like Lipitor poison the liver's synthesis of cholesterol. This in turn will starve the brain of cholesterol needed to repair the brain, renew worn out membranes, and stave off Alzheimer's.

In fact, an excellent book, “Lipitor Thief of Memory” written by the respected medical doctor, former astronaut, aerospace medical research scientist, flight surgeon, and family doctor, Dr. Duane Graveline, shares his rapid mental decline after taking the drug Lipitor. Worth reading.

Even with all this hard evidence can you believe the pharmaceutical industry has created a potent drug which combines both the calcium channel blocker and a statin called Atorvastatin/Amlodipine (Caduet). Talk about a double punch to optimal brain function!

Moving on to another documented contributor of Alzheimer's, we can't forget the unavoidable heavy metals. We all have them in us and they poison brain repair enzymes, leading to Alzheimer's.

For example, there is no one who doesn't have aluminum in them, from eating out, aluminum cookware, aluminum flocculation agents in municipal drinking waters, aluminum in baking powders used in breads, processed and restaurant foods cooked in aluminum vats, industrial and vehicular exhausts, deodorants, antacids, and many other sources.

Aluminum causes the nerves in the brain to actually get tangled up (neurofibrillary tangles) as well as make a glue-like substance (called amyloid) to gum up the normal workings of the delicate brain electricity..

Now to provide some nutritional answers to reduce amyloid production we need to look no further than Phosphatidylserine (PS). This nutritional powerhouse has shown to perk up memory, and stave off Alzheimer's.  One interested case showed PS in 3 months return the memory back to where it was 12 years earlier.

Most recently there has been evidence how DHA is an amyloid eater.

Well here is something even easier: green tea. Real organic green tea has over 3 catechins or polyphenols. They have been found to be potent preventers of amyloid deposition in the brain. Sencha Premium Organic Green Tea is by far the best I have found.

This short article is simply a glimpse of the research you won't see promoted on CNN or Fox News. Of course this is sad. There is another side of the clinical management of many diseases that the public will rarely if ever be shown unless you are a reader of my weekly health reports or other alternative or functionally oriented heath professional reports or journals.

The take away from today's article is to “NOT” be your own doctor but seek out the assistance and help from someone trained and skilled in functional medicine who can properly evaluate you and outline a personalized program to help you get well.  

To find a healthcare professional certified in functional medicine, go to www.FunctionalMedicineDoctors.com.These are clinicians who have been trained at Functional Medicine University (www.FunctionalMedicineUniversity.com)

COMPLIMENTS OF FUNCTIONAL MEDICINE UNIVERSITY
 

 



Reference

Haque A, et al, Green tea catechins prevent cognitive deficits caused by AB1-40 in rats, J Nutr Biochem, 19:619-26, 2008

Behl C, et al, Vitamin E protects nerve cells from amyloid B protein toxicity, Biochem Biophys Res Commun, 186:944-52, 1992

Hashimoto M, et al, Docosahexaenoic acid provides protection from impairment of learning ability in Alzheimer's disease model rats, J Neurochem, 81:1084-91, 2002

Rezai-Zadeh K, et al, Green tea epigallocatechin-3-gallate (EGCG) modulates amyloid precursor protein cleavage and reduces cerebral amyloidosis in Alzheimer transgenic mice, J Neurosci, 25:8807-14, 2005

Crook T1, Petrie W, Wells C, Massari DC.Effects of phosphatidylserine in Alzheimer's disease.Psychopharmacol Bull. 1992;28(1):61-6.

http://www3.scienceblog.com/community/older/1997/B/199702039.html (Calcium Channel Blocker reference)

 

Alzheimer's or Brain Diabetes

Alzheimer's or Brain Diabetes?

Ronald Grisanti D.C., D.A.B.C.O., D.A.C.B.N., M.S.

 

A growing body of research suggests there's a powerful connection between your diet and your risk of Alzheimer's disease via similar pathways that cause type 2 diabetes.

Back in 2005, a published medical paper introduced a new disease tentatively dubbed "type 3 diabetes".

The researchers learned that, in addition to the pancreas, your brain also produces insulin.

They discovered that without the insulin your brain cells will die.

A drop in insulin production in your brain may contribute to the degeneration of your brain cells, and studies have found that people with lower levels of insulin and insulin receptors in their brain often have Alzheimer's disease.

Studies since 2005 have continually documented that insulin has a much greater role in the brain than previously expected.

Insulin is directly responsible for neuron glucose-uptake, and the regulation of neurotransmitters like acetylcholine, which are crucial for memory and learning.

Scientists have come to understand that cognition is impaired when insulin levels are reduced.

The clinical research has made it quite clear that the same pathological process that leads to insulin resistance and type 2 diabetes may also hold true for your brain.

The take away from these studies make a strong point that the over-consumption of sugars and "grains" which are also detrimental to the the development of diabetes may also result in Type 3 Diabetes (brain diabetes).

When the brain becomes overwhelmed by the consistently high levels of glucose, the insulin signaling will eventually become blunted or desensitized. This will lead to impairments in your thinking and memory abilities, eventually causing permanent brain damage.

Healthcare clinicians trained in functional medicine have the training and knowledge to investigate what is at the root of the pathological process that leads to Type 2 diabetes and the new diagnosis of Type 3 diabetes.

The one size fits all approach of prescriptive medications for diabetes, although of some value, will not shut down the physiological cascade of the consequences of poor sugar/insulin control.


Reference:

Steen E, Terry BM, Rivera EJ, Cannon JL, Neely TR, Tavares R, Xu XJ, Wands JR, de la Monte SM. Impaired insulin and insulin-like growth factor expression and signaling mechanisms in Alzheimer's disease--is this type 3 diabetes? J Alzheimers Dis. 2005 Feb;7(1):63-80.

de la Monte, Wands.Alzheimer's Disease Is Type 3 Diabetes–Evidence Reviewed, J Diabetes Sci Technol. 2008 Nov; 2(6): 1101–1113.

COMPLIMENTS OF FUNCTIONAL MEDICINE UNIVERSITY